BioAssay record AID 225394 submitted by ChEMBL: Percent increase in intracellular calcium ion concentration ([Ca2+]i) using CHO cells, stably transfected with human muscarinic m3 acetylcholine receptor (AChR); nd=Not determined.
Purpose.: Previously, retinopetal axons containing histamine and dopaminergic neurons expressing histamine H1-receptor had been localized in mouse retinas using anatomic techniques. The goal of these experiments was to demonstrate that these receptors are functional. Methods.: Dopaminergic cells were acutely isolated from retinas of transgenic mice expressing red fluorescent protein under control of the tyrosine hydroxylase promoter and loaded with the calcium indicator Fura-2. Results.: Under control conditions, there were spontaneous oscillations in the levels of free intracellular calcium in dopaminergic cells. These oscillations were abolished in nominally calcium-free extracellular medium and in 1 μM tetrodotoxin, findings suggesting that the oscillations were mediated by calcium entry across the plasma membrane in response to sodium-dependent action potentials. Histamine increased the mean free intracellular calcium in the dopaminergic cells by increasing the frequency and/or amplitude of ...
TY - JOUR. T1 - Transmembrane Ca2+ gradient-mediated change of fluidity in the inner layer of phospholipids modulates Ca2+-ATPase of sarcoplasmic reticulum. AU - Tu, Yaping. AU - Xu, H.. AU - Yang, F. Y.. PY - 1994. Y1 - 1994. N2 - Sarcoplasmic reticulum (SR) vesicles with (1000 folds) or without transmembrane Ca2+ gradient have been prepared. Different fluorescence probes (DPH, TMA-DPH and n-AS), were used to determine the effect of transmembrane Ca2+ gradient on the lipid fluidity both in outer and inner layer of Ca2+-ATPase-containing SR vesicles. The results showed that transmembrane Ca2+ gradient could significantly decrease the fluidity of the inner layer of SR membrane, while no obvious change was monitored in the outer layer. This may be deduced that Ca2+-ATPase might be modulated mainly by the transmembrane Ca2+ gradient-mediated alteration of physical state of phospholipid in the inner layer of SR membrane.. AB - Sarcoplasmic reticulum (SR) vesicles with (1000 folds) or without ...
In endothelial cells, a bolus of hydrogen peroxide (H2O2) or oxygen metabolites generated by hypoxanthine-xanthine oxidase (HX-XO) increased the mitochondrial calcium concentration [Ca2+]m. Both agents caused a biphasic increase in [Ca2+]m which was preceded by a rise in cytosolic free calcium concentration [Ca2+]c (18 and 6 seconds for H2O2 and HX-XO, respectively). The peak and plateau elevations of [Ca2+] were consistently higher in the mitochondrial matrix than in the cytosol. In Ca2+-free/EGTA medium, the plateau phase of elevated [Ca2+] evoked by H2O2 due to capacitative Ca2+ influx was abolished in the cytosol, but was maintained in the mitochondria. In contrast to H2O2 and HX-XO, ATP which binds the P2Y purinoceptors induced an increase in [Ca2+]m that was similar to that of [Ca2+]c. When cells were first stimulated with inositol 1,4, 5-trisphosphate-generating agonists or the Ca2+-ATPase inhibitor cyclopiazonic acid (CPA), subsequent addition of H2O2 did not affect [Ca2+]c, but still ...
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Among different pathways coordinating intracellular signaling, the most prominent is intracellular calcium signaling (ICS), controlling various cellular processes including proliferation, motility, apoptosis and differentiation [1]. ICS is impressively diverse and consists of mechanisms that differ in frequency, amplitude and spatio-temporal patterning depending on an extensive molecular repertoire of signaling components. The free intracellular calcium concentration ([Ca2+i) of a resting cell is in the range of 10-100 nM. Following physiological stimulation, [Ca2+i levels can rise up to 1-2 μM concentrations. ICS is codified by the peak amplitude and frequency of [Ca2+i transients, promoted by the entry of external Ca2+ through Ca2+ channels or the release of Ca2+ from internal stores. These internal stores are deposited within internal membrane structures such as the endoplasmic reticulum (ER). Following activation of G-protein-coupled receptors, phospholipase C-β (PLC-β) cleaves ...
To examine the role of Ca2+ in early neuronal death, we studied the impact of free intracellular calcium concentration ([Ca2+]i) on survivability in populations of cultured mouse spinal neurons. We asked whether early neurotoxicity was triggered by Ca2+ influx, whether elevated [Ca2+]i was a predictive indicator of impending neuronal death, and whether factors other than [Ca2+]i increases influenced Ca2+ neurotoxicity. We found that when neurons were lethally challenged with excitatory amino acids or high K+, they experienced a biphasic [Ca2+]i increase characterized by a primary [Ca2+]i transient that decayed within minutes, followed by a secondary, sustained, and irreversible [Ca2+]i rise that indicated imminent cell death. We showed that in the case of glutamate-triggered neurotoxicity, processes triggering eventual cell death required Ca2+ influx, and that neurotoxicity was a function of the transmembrane Ca2+ gradient. Fura-2 Ca2+ imaging revealed a ceiling on measurable changes in ...
The sarcoplasmic reticulum (SR) is the major intracellular calcium storage depot in cardiac muscle. Cycling of calcium between the lumen of the SR and the myoplasmic space occurs repetitively during each heart beat. Excitation-contraction coupling in the heart begins when calcium entry through voltage-gated L-type calcium channels in the sarcolemma induces the opening of calcium release channels (also known as ryanodine receptors, or RyR) in the adjacent SR. The majority of the calcium that enters the cytosol during the early portion of each cycle is then resequestered into the SR lumen via the actions of the calcium uptake protein, (sarco)endoplasmic reticulum calcium adenosine triphosphatase (SERCA). Tight regulation of the timing and quantity of these intracellular calcium fluxes is critical to achieve graded contractility and relaxation of the heart muscle. Such control allows optimal matching of cardiac function to heart rate and metabolic needs of the body. The mechanisms of ...
The cytoplasmic free calcium concentration ([Ca2+]i) was studied in Fura-2/AM loaded granule neurones in acutely prepared cerebellar slices isolated from neonatal (6 days old) and adult (30 days old) mice. Bath application of elevated (10-50 mM) KCl-containing extracellular solutions evoked [Ca2+]i rise which was dependent on extracellular Ca2+. The K(+)-induced [Ca2+]i elevation was inhibited to different extends by verapamil, nickel and omega-conotoxin suggesting the coexpression of different subtypes of plasmalemmal voltage-gated Ca2+ channels. Bath application of caffeine (10-40 mM) elevated [Ca2+]i by release of Ca2+ from intracellular stores. Caffeine-induced [Ca2+]i elevation was inhibited by 100 microM ryanodine and 500 nM thapsigargin. Depletion of internal Ca2+ stores by caffeine, or blockade of Ca2+ release channels by ryanodine, did not affect depolarization-induced [Ca2+]i transients, suggesting negligible involvement of Ca(2+)-induced Ca2+ release in [Ca2+]i signal generation following
BioAssay record AID 270304 submitted by ChEMBL: Activity at human recombinant iGluR2 flip expressed in HEK293 cells measured as change in intracellular calcium ion concentration in presence of glutamate by FLIPR assay.
In many cell types, low concentrations of inositol 1,4,5-trisphosphate (IP3) release only a portion of the intracellular IP3-sensitive Ca2+ store, a phenomenon known as quantal Ca2+ release. It has been suggested that this effect is a result of reduced activity of the IP3-dependent Ca2+ channel with decreasing calcium concentration within the IP3-sensitive store ([Ca2+]s). To test this hypothesis, the properties of IP3-dependent Ca2+ release in single saponin-permeabilized HSY cells were studied by monitoring [Ca2+]s using the Ca(2+)-sensitive fluorescent dye mag-fura-2. In permeabilized cells, blockade of the sarco/ER Ca(2+)-ATPase pump in stores partially depleted by IP3 induced further Ca2+ release via an IP3-dependent route, indicating that Ca2+ entry via the sarco/ER Ca(2+)-ATPase pump had been balanced by Ca2+ loss via the IP3-sensitive channel before pump inhibition. IP3-dependent Mn2+ entry, monitored via quenching of luminal mag-fura-2 fluorescence, was readily apparent in filled ...
Intracellular calcium recycling plays a critical role in regulation of systolic and diastolic function in cardiomyocytes. Here, we...
Loss of the mitochondrial membrane potential results in a significant inhibition of calcium influx through calcium release-activated channels (CRAC) in Jurkat cells suspended in the medium of pH lower than 7.4. This effect disappears when the medium pH increases. Alkalinisation of the cytosol achieved by the addition of NH(4)Cl to the cells pretreated with thapsigargin, CCCP and CaCl(2), suspended in the medium of pH 7.2, does not affect CRAC activity, while alkalisation of the extracellular milieu by NaOH results in a strong stimulation of calcium entry. Thus, the mitochondrial effect on CRAC is exclusively related to the extracellular pH. Coupled mitochondria are able to take up Ca(2+) accumulated in the close proximity of CRAC. This protects these channels against feedback inhibition exerted by high [Ca(2+)](c). We conclude that CRAC may exist in two conformations: inhibitable and not inhibitable by cytosolic Ca(2+). Lower extracellular pH promotes the former one. This explains a much higher
Calcium plays an important role in several body functions, including muscle contractions, enzyme function, and nerve conduction. Calcium is stored in the bones.. Disorders affecting calcium metabolism require clinical care by a physician or other health care professional. Listed in the directory below are some of the disorders that affect calcium metabolism, for which we have provided a brief overview.. If you cannot find the information in which you are interested, please visit the Diabetes & Other Endocrine and Metabolic Disorders Online Resources page in this website for an Internet address that may contain additional information on that topic.. ...
Proper functioning of organelles such as the ER or the Golgi apparatus requires luminal accumulation of Ca2+ at high concentrations. Here we describe a ratiometric low-affinity Ca2+ sensor of the GFP-aequorin protein (GAP) family optimized for measurements in high-Ca2+ concentration environments. Transgenic animals expressing the ER-targeted sensor allowed monitoring of Ca2+ signals inside the organelle. The use of the sensor was demonstrated under three experimental paradigms: (1) ER Ca2+ oscillations in cultured astrocytes, (2) ex vivo functional mapping of cholinergic receptors triggering ER Ca2+ release in acute hippocampal slices from transgenic mice, and (3) in vivo sarcoplasmic reticulum Ca2+ dynamics in the muscle of transgenic flies. Our results provide proof of the suitability of the new biosensors to monitor Ca2+ dynamics inside intracellular organelles under physiological conditions and open an avenue to explore complex Ca2+ signaling in animal models of health and disease ...
Earlier studies have demonstrated that a high (mM) extracellular Ca2+ concentration triggers intracellular [Ca2+] signals with a consequent inhibition of bone resorptive activity. We now report that micromolar concentrations of the divalent cation, Ni2+, elicited rapid and concentration-dependent elevations of cytosolic [Ca2+]. The peak change in cytosolic [Ca2+] increased monotonically with the application of [Ni2+] in the 50-5,000 microM range in solutions containing 1.25 mM-[Ca2+] and 0.8 mM-[Mg2+]. The resulting concentration-response function suggested Ni(2+)-induced activation of a single class of binding site (Hill coefficient = 1). The triggering process also exhibited a concentration-dependent inactivation in which conditioning Ni2+ applications in the range 5-1,500 microM-[Ni2+] inhibited subsequent responses to a maximally effective [Ni2+] of 5,000 microM. Ni(2+)-induced cytosolic [Ca2+] responses were not dependent on extracellular [Ca2+]. Thus, when 5,000 microM-[Ni2+] was applied to
PTH, together with vitamin D and calcitonin, brings about mobilization of calcium and phosphate from the skeletal system and increases the uptake of calcium in the intestine and the excretion of phosphate via the kidneys. The constancy of the blood calcium level is ensured by the interaction of PTH and calcitonin. The secretion of PTH is inhibited by high calcium concentrations and promoted by low calcium concentrations ...
A patient has a total serum calcium level of 13.3 mg/dL (3.3 mmol/L). The nurse will anticipate the need to teach the patient about testing for
A patient has a total serum calcium level of 13.3 mg/dL (3.3 mmol/L). The nurse will anticipate the need to teach the patient about testing for
Optical mapping of intact cardiac tissue reveals that, in some cases, intracellular calcium (Ca) release can alternate from one beat to the next in a large-small-large sequence, also referred to as Ca transient (CaT) alternans. CaT alternans can also become spatially phase-mismatched within a single …
Figure 1: Study of Cellular Uptake of Modified Oligonucleotides by Using Time-Resolved Microspectrofluorimetry and Florescence Imaging
Sugar solutions taste sweeter when warm. Talavera et al. now provide a molecular mechanism for this phenomenon. They identified the transient receptor potential (TRP) family members TRPM5 and TRPM4 as thermally activated, calcium-dependent cation channels. TRPM5 and the related protein TRP4 are calcium-impermeable cation channels. When expressed in human embryonic kidney (HEK) 293 cells, these proteins exhibited a shift in voltage dependence in response to increased temperature in the range of 15°C to 35°C, such that at higher temperatures the channels were more active. Activation of the channels by heat required the presence of intracellular calcium, despite the fact that these channels do not conduct calcium ions. Therefore, they are poised to serve as coincidence detectors, sensing a stimulus that increases intracellular calcium concentrations, such as the presence of a taste ligand that activates a taste receptor, as well as temperature. Indeed, knockout mice lacking TRPM5 did not show any ...
Important element in road towards development of new drugs for neurodegenerative diseases All living cells keep their cellular calcium concentration at a very low level. Since a small increase in calcium can affect many critical cellular functions (an elevated calcium concentration over an extended period can induce cell death), powerful cellular mechanisms ensure that calcium concentration quickly returns to its low level.. It is known that impairments of cellular calcium regulation underlie almost all neurodegenerative diseases. For example, age-related loss of calcium regulation was shown to promote cell vulnerability in Alzheimers disease.. In a study recently published in the Journal of Neuroscience, Hebrew University of Jerusalem researchers, along with others from Israel and the US, presented their findings of a previously undescribed cellular mechanism which is essential for keeping cellular calcium concentration low. This mechanism operates together with other already characterized ...
Gomez-Ospina et al. provide evidence for an intriguing mechanism whereby voltage-dependent calcium channels modulate gene transcription. Calcium entry through voltage-gated channels in the plasma membrane provides a link between electrical activity and changes in gene expression. Gomez-Ospina et al. found that, whereas an antibody that recognized the full-length Cav1.2 calcium channel localized to membrane and cytosolic fractions of rat brain cortex, an antibody that recognized the C-terminal fragment, which is proteolytically cleaved, appeared in the nucleus. The C-terminal fragment was abundant in nuclei of GABAergic neurons; moreover, nuclear fluorescence was apparent in neurons or glioblastoma cells expressing a construct in which the Cav1.2 C terminus was fluorescently labeled. Treatments aimed at lowering cytoplasmic calcium increased nuclear abundance of the Cav1.2 fragment, whereas treatments that increase intracellular calcium decreased it. The Cav1.2 fragment immunoprecipitated with ...
We found a doubling of risk for fatal prostate cancer among men in the highest tertile of total serum calcium and a tripling of risk for men in the highest tertile of ionized serum calcium. The results for total serum calcium are consistent with our previous findings for prostate cancer mortality in NHANES I in which we observed a multivariable-adjusted RR of 2.68 (5). This is the first study to examine prostate cancer risk in relation to prediagnostic levels of ionized serum calcium.. Each individual is believed to have his or her own set point for serum calcium that is under genetic control (9). The concentration of ionized serum calcium in a given individual normally does not deviate by ,2% from its set point (10). Conversely, there is considerable variation in calcium levels between individuals, with normal levels of total serum calcium ranging from 8.5 to 10.5 mg/dL (2.1-2.6 mmol/L; ref. 11).. This study has several strengths. It is hypothesis testing, is prospective, and uses a population ...
Fig.: Fibre-optic recording of YC3.60 signals in barrel cortex. Schematics of a setup (left) and functional signals in a freely-moving mouse (right).. Image: Mazahir T. Hasan. Neurons communicate with one another via so-called action potentials. During an action potential, voltage-gated calcium channels are opened resulting in rapid calcium ion influx. Because of this tight coupling, fluorescent calcium indicator proteins can visualize action potentials. These proteins have two fluorescent subunits, one of which radiates yellow light and the other blue. When the proteins bind calcium, the proportion of yellow to blue light changes. Colour variation from blue light towards yellow thus reports different calcium levels - which is why the protein has been dubbed a cameleon.. Measuring action potentials optically. With the cameleon protein YC3.60, a fairly new variant, the scientists succeeded in recording the reaction of nerve cells to sensory stimuli in the intact brain of mice: every time the ...
In addition to transmitting involving extracellular free of charge contaminants, a generally accepted super model tiffany livingston of pathogen distribution is one wherein pathogen replicates in one cell, producing infectious contaminants that transmit to the following cell via cell junctions or induced polarized connections. outside the group had been bad for pathogen immediate-early phrase generally. We further display, using separated monolayer assays spatially, that at least one element of this activated migration is certainly the paracrine pleasure of a cytotactic response from contaminated cells to uninfected cells. The lifetime of this procedure adjustments our concept of pathogen transmitting and the potential features, pathogen, and web host elements included. Launch The systems included in the transmitting of contagious infections between cells are of fundamental importance for our general understanding of computer virus duplication, virulence, and pathogenesis and for long lasting ...
TY - JOUR. T1 - CXCL10-induced cell death in neurons. T2 - Role of calcium dysregulation. AU - Sui, Yongjun. AU - Stehno-Bittel, Lisa. AU - Li, Shanping. AU - Loganathan, Rajprasad. AU - Dhillon, Navneet K.. AU - Pinson, David. AU - Nath, Avindra. AU - Kolson, Dennis. AU - Narayan, Opendra. AU - Buch, Shilpa. PY - 2006/2. Y1 - 2006/2. N2 - Chemokines play a key role in the regulation of central nervous system disease. CXCL10 over-expression has been observed in several neurodegenerative diseases, including multiple sclerosis, Alzheimers disease and HIV-associated dementia. More recent studies by others and us have shown that CXCL10 elicits apoptosis in fetal neurons. The mechanism of CXCL10-mediated neurotoxicity, however, remains unclear. In this study, we provide evidence for the direct role of Ca2+ dysregulation in CXCL10-mediated apoptosis. We demonstrate that treatment of fetal neuronal cultures with exogenous CXCL10 produced elevations in intracellular Ca2+ and that this effect was ...
When detergent-extracted, demembranated cell models of Chlamydomonas were resuspended in reactivation solutions containing less than 10(-8) M Ca++, many models initially swam in helical paths similar to those of intact cells; others swam in circles against the surface of the slide or coverslip. With increasing time after reactivation, fewer models swam in helices and more swam in circles. This transition from helical to circular swimming was the result of a progressive inactivation of one of the axonemes; in the extreme case, one axoneme was completely inactive whereas the other beat with a normal waveform. At these low Ca++ concentrations, the inactivated axoneme was the trans-axoneme (the one farthest from the eyespot) in 70-100% of the models. At 10(-7) or 10(-6) M Ca++, cell models also proceeded from helical to circular swimming as a result of inactivation of one of the axonemes; however, under these conditions the cis-axoneme was usually the one that was inactivated. At 10(-8) M Ca++, most ...
Calcium stored in bone can be redistributed to serum when the calcium balance is negative, but to date, the skeletal adaptations and molecular mediators were still largely unknown. Here, we found that the shift of calcium from bone to serum depended on the control of calcium incorporation into the bone matrix as well as calcium release from bone, and that 1,25(OH)2D was a prime regulator of both processes. These data suggest that the cellular processes regulated by serum calcium will be guaranteed at the expense of skeletal integrity, even when these adaptations result in bone fractures. Insufficient intestinal calcium absorption caused by dietary restriction or intestinal-specific Vdr inactivation (Vdrint- mice) resulted in a negative calcium balance. Increased renal calcium reabsorption, mediated by the high levels of PTH and 1,25(OH)2D (data not shown), may partially counterbalance the impaired intestinal calcium absorption in Vdrint- mice. In addition, skeletal calcium can supply the serum ...
Under appropriate conditions macrophage cytosolic extracts can form a three-dimensional gel network of cross-linked actin filaments. These cytoplasmic gels are mainly composed of actin, filamin, alpha-actinin, and two new proteins of about 70,000 and 55,000 Mr (70 and 55 K). The behaviour of 70 K protein was found to be remarkably affected by Ca2+. Ca2+ treatment of isolated cytoplasmic gels led to the selective solubilization of the 70 K protein along with a 17 K polypeptide. Half-maximal recovery in the supernatant fraction was obtained from about 0.15 microM free Ca2+. The cytoplasmic gel constituents solubilized in high ionic strength buffer were able to re-assemble into an insoluble actin network when returned to near physiological ionic conditions. However, the inclusion of micromolar Ca2+ prevented the re-association of 70 K protein with actin in these complexes. As compared to the 70 K protein, alpha-actinin was fully resistant to any variations in Ca2+ concentrations. On the other hand, ...
By: Andy De Santis, RD and Dr. Kathleen Regan, ND. Andy De Santis is a Registered Dietician practicing at Innate Wellness High Park. He focuses on creating diet plans for patients of Innate Wellness. If you are interested in having a customized nutrition program created for you, please call the High Park Clinic. Calcium is one of the most abundant minerals found in the human body. Most calcium is stored either in our bones or our teeth, leaving a small amount found in other tissues or circulating through our blood. The way our bodies use and absorb calcium depends on the presence of specific nutrients, such as Vitamin D, and specific hormones, such as parathyroid hormone and calcitonin. Calcium levels are also influenced by specific female hormones such as estrogen (which increases calcium absorption).. Declining levels of estrogen as women age, through menopause, after hysterectomy, or via estrogen reducing drugs such as Tamoxifen (post-breast cancer treatment) can dramatically affect calcium ...
The present study reports a potentiating effect of glibenclamide on quantal catecholamine secretion evoked from individual PC-12 cells by exposure to solutions containing either 50 mmK+ or 30 mm caffeine. Using either stimulus, this secretion is Ca2+-dependent. For K+-evoked release, Ca2+ influx through voltage-gated Ca2+ channels is a prerequisite for exocytosis, and of the different channel types present in PC-12 cells (Liu et al., 1996), the N-type appear to be most closely coupled to depolarization-mediated release because ω-conotoxin GVIA causes profound inhibition of such release (Taylor and Peers, 1998). Caffeine has recently been demonstrated to evoke secretion from PC-12 cells (Koizume and Inoue, 1998), and the present study indicates that this release is quantal (i.e., because of exocytosis) (Fig. 6). Caffeine causes release of Ca2+ from intracellular stores (presumably via activation of ryanodine receptors), and this store depletion in turn activates CCE. Koizume and Inoue (1998) ...
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Cells have developed a variety of mechanisms to keep free calcium ion concentrations at very low levels in the cytosol. These mechanisms allow transient increases in cell calcium concentrations to be used as signals to trigger a variety of cellular processes, gene expression being one of them. Skeletal muscle relies on nerve activity both for contraction and also for the expression of genes related to pathways that include survival and the plastic changes required for adaptation to exercise. A particular pathway that involves Cav1.1 as a voltage sensor for nerve activity, pannexin-1 channels to release ATP to the extracellular milieu, purinergic P2Y receptors to link the signal ...
Video articles in JoVE about inositol 1 4 5 trisphosphate include Imaging Local Ca2+ Signals in Cultured Mammalian Cells, Direct Imaging of ER Calcium with Targeted-Esterase Induced Dye Loading (TED), Monitoring ER/SR Calcium Release with the Targeted Ca2+ Sensor CatchER+, PIP-on-a-chip: A Label-free Study of Protein-phosphoinositide Interactions, Radiolabeling and Quantification of Cellular Levels of Phosphoinositides by High Performance Liquid Chromatography-coupled Flow Scintillation, Preparation of Quality Inositol Pyrophosphates, Characterization of G Protein-coupled Receptors by a Fluorescence-based Calcium Mobilization Assay, Cytosolic Calcium Measurements in Renal Epithelial Cells by Flow Cytometry, Targeting Cysteine Thiols for in Vitro Site-specific Glycosylation of Recombinant Proteins, A Cell Culture Model of Resistance Arteries , Preparation of Pancreatic Acinar Cells for the Purpose of Calcium Imaging, Cell Injury Measurements, and Adenoviral Infection, Lignin Down
When the estrogen produced by the body is reduced, the bones inadequately absorb and utilize calcium. This resulting drop in calcium levels can lead to decreased bone mass and osteoporosis later in...
Ca2+ signals are probably the most common intracellular signaling cellular events, controlling an extensive range of responses in virtually all cells. Many cellular stimuli, often acting at cell surface receptors, evoke Ca2+ signals by mobilizing Ca2+ from intracellular stores. Inositol trisphosphate (IP3) was the first messenger shown to link events at the plasma membrane to release Ca2+ from the endoplasmic reticulum (ER), through the activation of IP3-gated Ca2+ release channels (IP3 receptors). Subsequently, two additional Ca2+ mobilizing messengers were discovered, cADPR and NAADP. Both are metabolites of pyridine nucleotides, and may be produced by the same class of enzymes, ADP-ribosyl cyclases, such as CD38. Whilst cADPR mobilizes Ca2+ from the ER by activation of ryanodine receptors (RyRs), NAADP releases Ca2+ from acidic stores by a mechanism involving the activation of two pore channels (TPCs). In addition, other pyridine nucleotides have emerged as intracellular messengers. ADP-ribose and 2
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In the present study we showed increased TRPV1 activity after prestimulation of TRPA1, both in HEK cells and DRG neurons. This was dependent on calcium, AC, and PKA. Mutation of the putative phosphorylation site serine 116 in TRPV1 also abolished increased TRPV1 activity after TRPA1 stimulation. Together, our findings suggest that TRPA1 activation causes an influx of calcium and increases calcium-sensitive AC activity, cAMP accumulation, and subsequent PKA activation. This results in phosphorylation and sensitization of TRPV1.. Although some studies showed direct activation of TRPV1 by MO at high concentrations (Ohta et al., 2007; Everaerts et al., 2011; Gees et al., 2013), our control experiments and other studies showed that MO at a concentration of 20 µM did not directly activate TRPV1 (Fig. 2D; Jordt et al., 2004; Everaerts et al., 2011).. Approximately 30% to 50% of TRPV1-expressing small- to medium-sized peripheral sensory neurons coexpress TRPA1, and almost all TRPA1-positive neurons ...
Regehrs laboratory studies the implication of calcium Ca2+ as it affects synaptic strength. Neurons communicate with one another via synapses. Regehr was one of the first to use fluorescent imaging to see the synaptic activity occurring in the brain. A dye alters the fluorenscence properties when attached to calcium, and changes in intracellular calcium are associated with neuronal activity (firing of action potentials). Using fluorescence-microscopy techniques, calcium levels are detected, and therefore the influx of calcium in the presynaptic neuron ...
MAIL VIA INTERNET FROM BIOSCI-REQUEST at genbank.bio.net THURSDAY 09/10/92 6:15:03 A.M. , , Received: from CU.NIH.GOV by NIHCU (Mailer) id 9613; , Thu, 10 Sep 92 06:15:03 EDT , Received: from GENBANK.BIO.NET by CU.NIH.GOV , with TCP; Thu, 10 Sep 92 6:15:00 EDT , Received: by genbank.bio.net (5.65/IG-2.0) , id AA05730; Thu, 10 Sep 92 03:15:24 -0700 , Received: by genbank.bio.net (5.65/IG-2.0) , id AA05723; Thu, 10 Sep 92 03:15:22 -0700 , Message-Id: ,9209101015.AA05723 at genbank.bio.net, , To: bio-soft at genbank.bio.net , From: Fergus_Doherty at vme.ccc.nottingham.ac.uk , Subject: Calculating free Ca2++ with EGTA buffers , Date: 10 Sep 92 10:00:35 GMT , Sender: list-admin at daresbury.ac.uk , Original-To: BIO-SOFT at uk.ac.daresbury , , Can anyone help me to calculate free Ca2++ in EGTA/CA buffers? Basically , I want to determine the effect of Ca on enzyme activity, and relatedly , translocation of an enzyme to membranes-which is Ca -dependent. I need , to include EGTA to completely inhibit the ...
Repolarization alternans has been considered a strong marker of electrical instability. The objective of this study was to investigate the hypothesis that ischemia-induced contrasting effects on the kinetics of membrane voltage and intracellular calcium transient (Ca(i)T) can explain the vulnerability of the ischemic heart to repolarization alternans. Ischemia-induced changes in action potential (AP) and Ca(i)T resulting in alternans were investigated in perfused Langendorff guinea pig hearts subjected to 10-15 min of global no-flow ischemia followed by 10-15 min of reperfusion. The heart was stained with 100 microl of rhod-2 AM and 25 microl of RH-237, and AP and Ca(i)T were simultaneously recorded with an optical mapping system of two 16 x 16 photodiode arrays. Ischemia was associated with shortening of AP duration (D) but delayed upstroke, broadening of peak, and slowed decay of Ca(i)T resulting in a significant increase of Ca(i)T-D. The changes in APD were spatially heterogeneous in contrast to a
Calcium is a universal second messenger present in all eukaryotic cells. The mobilization and storage of Ca2+ ions drives a number of signaling-related processes, stress-responses, or metabolic changes, all of which are relevant for the development of immune cells and their adaption to pathogens. Here, we introduce the Förster resonance energy transfer (FRET)-reporter mouse YellowCaB expressing the genetically encoded calcium indicator TN-XXL in B lymphocytes. Calcium-induced conformation change of TN-XXL results in FRET-donor quenching measurable by two-photon fluorescence lifetime imaging. For the first time, using our novel numerical analysis, we extract absolute cytoplasmic calcium concentrations in activated B cells during affinity maturation in vivo. We show that calcium in activated B cells is highly dynamic and that activation introduces a persistent calcium heterogeneity to the lineage. A characterization of absolute calcium concentrations present at any time within the cytosol is ...
Phospholipase C (PLC) regulates various cellular processes by catalyzing the formation of inositol-1,4,5-trisphosphate (IP3) and diacylglycerol from phosphatidylinositol-4,5-bisphosphate (PIP2). Here, we have investigated the influence of Ca2+ on receptor-triggered PLC activity in individual insulin-secreting β-cells. Evanescent wave microscopy was used to record PLC activity using green fluorescent protein (GFP)-tagged PIP2/IP3-binding pleckstrin homology domain from PLCδ1, and the cytoplasmic Ca2+ concentration ([Ca2+]i) was simultaneously measured using the indicator Fura Red. Stimulation of MIN6 β-cells with the muscarinic-receptor agonist carbachol induced rapid and sustained PLC activation. By contrast, only transient activation was observed after stimulation in the absence of extracellular Ca2+ or in the presence of the non-selective Ca2+ channel inhibitor La3+. The Ca2+-dependent sustained phase of PLC activity did not require voltage-gated Ca2+ influx, as hyperpolarization with ...
A: 1. by increasing open time of the calcium channels, and more calcium rush into the cardiac muscle cell. From the extracellular fluid. 2. Phosphorylate (activate) phospholamban, whch increases Calcium ATPase in the sarcoplasmic reticulum. This increases calcium stores in the SR, so more is released when needed, leading to forceful contractions. Calcium is also removed from the cytosol faster, shortening the calcium-troponin binding time, which causes shorter duration of contraction.. Q: What is the isovolumic systole ...
In this study, we provide in vivo evidence that SEL-12, a C. elegans PSEN homolog, is involved in regulating calcium homeostasis and impacts mitochondrial morphology and function. In addition, we have found that the calcium dysregulation observed in SEL-12-deficient animals arises from ER stores and that this defect leads to increased mitochondrial uptake of calcium, which drives the mitochondrial defects observed in sel-12 mutants. Furthermore, we show that the role of SEL-12 in regulating mitochondrial function is independent of its role in γ-secretase function and that the mitochondrial defects observed in sel-12 mutants are caused in part by the opening of the mPTP and elevated DRP-1-dependent mitochondrial fission.. Although the role of PSEN in AD progression remains unclear (Sherrington et al. 1995), similar to our findings, calcium dysregulation has been observed in various models of mutant PSEN function as well as tissue samples from AD patients (Ito et al. 1994; Leissring et al. 1999; ...
EMG - Force Relationship An EMG signal will not necessarily reflect the total amount of force (or torque) a muscle can generate The number of motor units recorded by electrodes will be less than the total number of motor units that are firing - electrodes cant pick-up all motor units
TY - JOUR. T1 - Vitamin D does not increase calcium absorption in young women. T2 - A randomized clinical trial. AU - Gallagher, J. Christopher. AU - Jindal, Prachi S.. AU - Smith, Lynette M.. PY - 2014/5. Y1 - 2014/5. N2 - It is commonly said that vitamin D should be used to increase calcium absorption. We tested this statement in a dose-response study of vitamin D on calcium absorption. A total of 198 white and African American women, aged 25 to 45 years, with vitamin D insufficiency, serum 25-hydroxyvitamin D (25OHD) 2D) amongst the lowest groups. Vitamin D doses up to 2400 IU daily did not increase calcium absorption. No threshold level of serum 25OHD for calcium absorption was found at baseline or in the longitudinal study, suggesting that active transport of calcium is saturated at very low serum 25OHD levels AB - It is commonly said that vitamin D should be used to increase calcium absorption. We tested this statement in a dose-response study of vitamin D on calcium absorption. A total of ...
New Delhi: June 18, 2016: Calcium is important for maintaining strong bones. It also helps in blood clotting, early developmental growth and muscle contraction and relaxation. Calcium can be easily obtained from natural food sources like leafy vegetables, yoghurt, nuts and cheese. However, the majority of the Indians, specifically in the age group of 14-20 years suffer from calcium deficiency due to lack of efficient absorption. Calcium deficiency disease, also known as hypocalcemia, occurs when you dont get enough calcium. It is crucial that people are educated about the effects of calcium deficiency on the overall health and wellbeing of people in the long run. Those suspected of suffering from calcium deficiency should not self-diagnose and treat themselves by consuming large amounts of calcium supplements. Instead, it is important that they consult their doctor and together devise a healthy eating plan supported by supplementation, said Padma Shri Awardee Dr KK Aggarwal - Honorary ...
In the latest Under the Microscope issue, Professor László Csernoch and his research group from the University of Debrecen (Hungary) explain their research into intracellular calcium homeostasis, which may seem like a simple statement. However, this fascinating area of research covers many areas, from arteriosclerosis to space travel.. They also explain how they rely on ratiometric calcium measurements, and the benefits they have experienced from their recent switch to the CoolLED pE-340fura LED Illumination System with their Zeiss Axio Vert microscope.. Read more about intracellular calcium homeostasis. This content was supplied by CoolLED.. ...
Aequorin, which luminesces in the presence of calcium, was injected into photoreceptor cells of Limulus ventral eye. A bright light stimulus elicited a large increase in aequorin luminescence, the aequorin response, indicating a rise of intracellular calcium ion concentration, Cai. The aequorin response reached a maximum after the peak of the electrical response of the photoreceptor, decayed during a prolonged stimulus, and returned to an undetectable level in the dark. Reduction of Cao reduced the amplitude of the aequorin response by a factor no greater than 3. Raising Cao increased the amplitude of the aequorin response. The aequorin response became smaller when membrane voltage was clamped to successively more positive values. These results indicate that the stimulus-induced rise of Cai may be due in part to a light-induced influx of Ca and in part to release of Ca from an intracellular store. Our findings are consistent with the hypothesis that a rise in Cai is a step in the sequence of ...
Oscillations in cytoplasmic calcium concentration ([Ca2+]i) in airway smooth muscle cells (ASMC), primarily mediated by repetitive openings and closings of inositol trisphosphate receptor (IP3R) channels situated in the sarcoplasmic reticulum membrane, have been found to be important in generating and maintaining airway contractile force. However, it has been unclear about the mechanisms accounting for such oscillations, especially how the IP3R behaves in living cells to perform its function. In light of the extensive existence of calcium oscillations in many other cell types, although this thesis focuses on modeling calcium oscillations in ASMC due to their importance for the study of pathology of asthma, it also aims to solve some major questions in a wider context: • What is the mechanism for the formation of the repetitive calcium releases? How is the mechanism connected to the dynamics of the IP3R? • How best (or simply) should the IP3R be modeled for performing its function? • Should ...
Microdomains of high intracellular calcium ion concentration, [Ca2+]i, have been hypothesized to occur in living cells exposed to stimuli that generate inositol 1,4,5-trisphosphate (IP3). Mitochondrially targeted recombinant aequorin was used to show that IP3-induced Ca2+ mobilization from intracellular stores caused increases of mitochondrial Ca2+ concentration, [Ca2+]m, the speed and amplitude of which are not accounted for by the relatively small increases in mean [Ca2+]i. A similar response was obtained by the addition of IP3 to permeabilized cells but not by perfusion of cells with Ca2+ at concentrations similar to those measured in intact cells. It is concluded that in vivo, domains of high [Ca2+]i are transiently generated close to IP3-gated channels and sensed by nearby mitochondria; this may provide an efficient mechanism for optimizing mitochondrial activity upon cell stimulation. ...
TY - JOUR. T1 - Intracellular free calcium increases in cultured cortical neurons deprived of oxygen and glucose.. AU - Goldberg, M. P.. AU - Choi, D. W.. PY - 1990/11/1. Y1 - 1990/11/1. N2 - Dissociated neocortical cultures from fetal mice exposed transiently to a medium lacking both glucose and oxygen developed neuronal degeneration without glial degeneration. We have found that this injury depends on extracellular calcium and is associated with uptake of calcium from the culture medium. We measured free cytoplasmic calcium in individual neurons using the fluorescent calcium indicator fluo-3 and provide evidence that oxygen and glucose deprivation injury increases the intracellular calcium signal. Both intracellular calcium elevation and subsequent neuronal loss could be blocked by the N-methyl-D-aspartate receptor antagonist dextrorphan.. AB - Dissociated neocortical cultures from fetal mice exposed transiently to a medium lacking both glucose and oxygen developed neuronal degeneration ...
In previous efforts to characterize sarcoplasmic reticulum function in human muscles, it has not been possible to distinguish the relative contributions of fast-twitch and slow-twitch fibers. In this study, we have used light scattering and 45Ca to monitor Ca accumulation by the sarcoplasmic reticulum of isolated, chemically skinned human muscle fibers in the presence and absence of oxalate. Oxalate (5 mM) increased the capacity for Ca accumulation by a factor of 35 and made it possible to assess both rate of Ca uptake and relative sarcoplasmic reticulum volume in individual fibers. At a fixed ionized Ca concentration, the rate and maximal capacity (an index of sarcoplasmic reticulum volume) both varied over a wide range, but fibers fell into two distinct groups (fast and slow). Between the two groups, there was a 2- to 2.5-fold difference in oxalate-supported Ca uptake rates, but no difference in average sarcoplasmic reticulum volumes. Intrinsic differences in sarcoplasmic reticulum function ...
Calcium is an essential mineral for several important functions in the body of an animal. Calcium is needed for the development of the fetal skeleton as well as for the secretion of milk in lactating females, making pregnant and nursing guinea pigs more prone to calcium deficiency if their increased nutritional needs are not being met. This related type of calcium deficiency usually develops in the one to two weeks before, or shortly after, giving birth. Also at higher risk of calcium deficiency are obese or stressed guinea pigs, or guinea pigs that have already been pregnant several times.
TY - JOUR. T1 - Stimulation of d2 dopamine receptors decreases intracellular calcium levels in rat anterior pituitary cells but not striatal synaptosomes. T2 - A flow cytometric study using indo‐1. AU - Wolf, Marina E.. AU - Kapatos, Gregory. PY - 1989. Y1 - 1989. N2 - An important question is whether all D2 dopamine (DA) receptors employ the same signal transduction mechanisms. Anterior pituitary cells and striatal synaptosomes, which possess pharmacologically similar D2 DA receptors, were compared with respect to the effect of D2 DA receptor stimulation on free intracellular Ca2+ levels ([Ca2+]i). Flow cytometry, in combination with either the fluorescent calcium indicator indo‐1 or fluorescent voltage‐sensitive dyes, was used to measure [Ca2+]i and to detect changes in membrane potential. In subpopulations of anterior pituitary cells, increases in [Ca2+]i were produced by elevated K+, veratridine, thyrotropin‐releasing hormone, and BAY K 8644. These increases were blocked by ...
Cellular stress responses often involve elevation of cytosolic calcium levels, and this has been suggested to stimulate autophagy. Here, however, we demonstrated that agents that alter intracellular calcium ion homeostasis and induce ER stress-the calcium ionophore A23187 and the sarco/endoplasmic reticulum Ca (2+)-ATPase inhibitor thapsigargin (TG)-potently inhibit autophagy. This anti-autophagic effect occurred under both nutrient-rich and amino acid starvation conditions, and was reflected by a strong reduction in autophagic degradation of long-lived proteins. Furthermore, we found that the calcium-modulating agents inhibited autophagosome biogenesis at a step after the acquisition of WIPI1, but prior to the closure of the autophagosome. The latter was evident from the virtually complete inability of A23187- or TG-treated cells to sequester cytosolic lactate dehydrogenase. Moreover, we observed a decrease in both the number and size of starvation-induced EGFP-LC3 puncta as well as reduced numbers of
What would we do if we had no bones? We would just be all skin, spineless. Could not even stand, cant even walk. That is why we need our bones strong and healthy. That is why calcium is the most abundant mineral in our body. 99% of calcium is found in our bones and in our teeth. Two or three pounds of it are mostly found in our bones and in our teeth. Imagine a world without bones. Imagine a world without teeth.. As much as calcium is very essential for our teeth and bones, we also use it in different ways. We use calcium to be an electrolyte for transmitting nerve signals, for water balance, for neutralizing acid/alkaline in our bodies and maintaining osmotic pressure. Calcium also helps in blood clotting, muscle contraction and heart muscle function.. So in order to prevent calcium deficiency we are listing whole foods that are a good calcium source. Other than food we are also listing other ways so we can avoid calcium deficiency. So, here they are.. ...
The secretion of ions and fluid plays a critical role in a variety of physiological activities that are vital to homeostatic mechanisms in animals. Control of such secretory activity is achieved by a range of neurotransmitters and hormones many of which act intracellularly by generating the second messenger inositol 1,4,5-trisphosphate (InsP3) and increasing cytosolic free calcium ion concentrations ([Ca2+]i). These increases are achieved by a combination of the InsP3-induced release of Ca2+ from specific intracellular stores and the activation of Ca2+ entry from the extracellular environment. The [Ca2+]i signal represents a balance between the adequate activation of components of the secretory mechanism and the avoidance of [Ca2+]i levels that are toxic to the cell. Resting [Ca2+]i is maintained low by the action of Ca2+ pumps on the intracellular stores and plasma membrane, with the result that gradients for Ca2+ movement into the cytosol from either of these two sources are very large and ...
Chronic hypertension remains a major cause of global mortality and morbidity. It is a complex disease that is the clinical manifestation of multiple genetic, environmental, nutritional, hormonal, and aging-related disorders. Evidence supports a role for vascular aging in the development of hypertension involving an impairment in endothelial function together with an alteration in vascular smooth muscle cells (VSMCs) calcium homeostasis leading to increased myogenic tone. Changes in free intracellular calcium levels ([Ca] ) are mediated either by the influx of Ca from the extracellular space or release of Ca from intracellular stores, mainly the sarcoplasmic reticulum (SR). The influx of extracellular Ca occurs primarily through voltage-gated Ca channels (VGCCs), store-operated Ca channels (SOC), and Ca release-activated channels (CRAC), whereas SR-Ca release occurs through inositol trisphosphate receptor (IPR) and ryanodine receptors (RyRs). IPR-mediated SR-Ca release, in the form of Ca waves, ...
Variations of free calcium concentration ([Ca2+]) are powerful intracellular signals, controlling contraction as well as metabolism in muscle cells. To fully understand the role of calcium redistribution upon excitation and contraction in skeletal muscle cells, the local [Ca2+] in different compartments needs to be taken into consideration. Fluorescent probes allow the determination of [Ca2+] in the cytosol where myofibrils are embedded, the lumen of the sarcoplasmic reticulum (SR) and the mitochondrial matrix. Previously, models have been developed describing intracellular calcium handling in skeletal and cardiac muscle cells. However, a comprehensive model describing the kinetics of the changes in free calcium concentration in these three compartments is lacking. We designed a new 3D compartmental model of the half sarcomere with radial symmetry, which accounts for diffusion of Ca2+ into the three compartments and simulates its dynamics at rest and at various rates of stimulation in mice ...
Serum calcium. Routine serum calcium assay measures the total serum calcium value. Total serum calcium contains about 50% bound calcium (literature range, 35%-55%) and about 50% nonbound calcium (literature range, 35%-65%). (Traditionally, nonbound calcium was called ionized calcium and is also known as free or dialyzable calcium.) Bound calcium is subdivided into calcium bound to protein and calcium complexed to nonprotein compounds. About 45% of total calcium (30%-50%) is protein-bound, of which 70%-80% is bound to albumin. The remaining 5% (5%-15%) of total calcium is complexed to ions such as citrate, phosphate, sulfate, and bicarbonate, which are not part of the serum proteins. Ionized calcium levels can be measured directly by ion-selective electrode techniques or less accurately can be estimated from total serum calcium and albumin or total protein values using certain formulas. The most commonly used calcium correction formula is that of R.B. Payne:. Adjusted calcium = (measured ...
Localized, transient elevations in cytosolic Ca2+, known as Ca2+ sparks, caused by Ca2+ release from sarcoplasmic reticulum, are thought to trigger the opening of large conductance Ca2+-activated potassium channels in the plasma membrane resulting in spontaneous transient outward currents (STOCs) in smooth muscle cells. But the precise relationships between Ca2+ concentration within the sarcoplasmic reticulum and a Ca2+ spark and that between a Ca2+ spark and a STOC are not well defined or fully understood. To address these problems, we have employed two approaches using single patch-clamped smooth muscle cells freshly dissociated from toad stomach: a high speed, wide-field imaging system to simultaneously record Ca2+ sparks and STOCs, and a method to simultaneously measure free global Ca2+ concentration in the sarcoplasmic reticulum ([Ca2+]SR) and in the cytosol ([Ca2+]CYTO) along with STOCs. At a holding potential of 0 mV, cells displayed Ca2+ sparks and STOCs. Ca2+ sparks were associated with STOCs;
Education. Dr. Keirstead received her Ph.D. in neurophysiology from Queens University, Kingston, Canada, where she studied the role of neck muscle motoneurons and sensory afferents in the control of head movement in the laboratory of Dr. P. Ken Rose. As a post-doctoral fellow in the laboratories of Dr. M. Rasminsky and Dr. A.J. Aguayo at McGill University, Dr. Keirstead examined the capabilities of retinal neurons to regenerate axons and form functional synaptic connections with central nervous system neurons. Dr. Keirstead came to the University of Minnesota as a research associate in the Department of Physiology where she used calcium imaging techniques to study the regulation of intracellular calcium ion concentration in glial cells by neurotransmitters in the laboratory of Dr. Robert Miller. She continued these studies as an assistant professor in the Department of Ophthalmology.. Dr. Keirstead is an assistant professor in the Department of Integrative Biology and Physiology, and the ...
Peter Gillham Natural Vitality - Calm Plus Calcium Calcium is an important nutrient essential for maintaining total body health. Your body needs it every day-not just to keep your bones and teeth strong, but to ensure proper functioning of muscles and nerves. It even helps your blood to clot. But can too much calcium be a problem? Yes, it can. Excess calcium can deplete its vital sister mineral, magnesium, from the body and, as a result, can bring about symptoms of magnesium depletion, listed on the green page of this brochure. Calcium acts to excite nerves and is necessary for muscle contraction. Magnesium, on the other hand, calms nerves and is needed for muscle relaxation. Calcium makes bones stiff and hard, but magnesium is needed to avoid their becoming brittle. An excess of unabsorbed calcium may result in kidney stones and deposits in soft tissues such as arteries and heart cells, where it can calcify or harden into insoluble calcium. You experience the tensing (calcium)
Peter Gillham Natural Vitality - Calm Plus Calcium Calcium is an important nutrient essential for maintaining total body health. Your body needs it every day-not just to keep your bones and teeth strong, but to ensure proper functioning of muscles and nerves. It even helps your blood to clot. But can too much calcium be a problem? Yes, it can. Excess calcium can deplete its vital sister mineral, magnesium, from the body and, as a result, can bring about symptoms of magnesium depletion, listed on the green page of this brochure. Calcium acts to excite nerves and is necessary for muscle contraction. Magnesium, on the other hand, calms nerves and is needed for muscle relaxation. Calcium makes bones stiff and hard, but magnesium is needed to avoid their becoming brittle. An excess of unabsorbed calcium may result in kidney stones and deposits in soft tissues such as arteries and heart cells, where it can calcify or harden into insoluble calcium. You experience the tensing (calcium)
We investigated the roles of sodium-calcium exchange, sarcoplasmic reticulum, and mitochondria in Cai homeostasis in cultured chick ventricular cells. Specifically, the influence of low sodium medium on contractile state, calcium fluxes, and cytosolic free [Ca] [( Ca]i) was examined. [Ca]i was measured using fura-2. Mean [Ca]i in control medium was 126 +/- 14 nM. Exposure of cells to sodium-free or sodium- and calcium-free medium (choline-substituted) resulted in contracture development, which returned toward the baseline level over 2-3 minutes. The Nao-free contracture was associated with a tenfold increase in [Ca]i (1,280 +/- 110 nM) followed by a gradual decrease to a level fourfold above control [Ca]i (460 +/- 58 nM). Nao- and Cao-free contracture was associated with a fivefold increase in [Ca]i (540 +/- 52 nM) followed by a rapid decrease to below 80 nM. Sodium-free medium failed to produce an increase in [Ca]i or contracture in cells preexposed to calcium-free medium, although caffeine, ...
CitationAlvarez-Lacalle, E. [et al.]. A General Equilibrium Model to Study Intracellular Calcium Homeostasis. New Insights on Ventricular Function. A: The Heart by Numbers: Integrating Theory, Computation, and Experiment to Advance Cardiology. The Heart by numbers: integrating theory, computation, and experiment to advance cardiology, Berlin, Germany: September 4-7, 2018: Biophysical Society Thematic Meeting: program & abstracts. 2018, p. 44 ...
TY - JOUR. T1 - Protamine augments stretch induced calcium increase in vascular endothelium. AU - Murase, Kichiro. AU - Naruse, Keiji. AU - Kimura, Akira. AU - Okumura, Kenji. AU - Hayakawa, Tetsuo. AU - Sokabe, Masahiro. PY - 2001. Y1 - 2001. N2 - Human umbilical vein endothelial cells cultured on a transparent silicone chamber were subjected to a short stretch pulse (ca. 1 s, 5 - 25% stretch) of their substrate and following increases in intracellular Ca2+ concentration ([Ca2+]i) were measured by fluorescence intensity ratiometry using fura-2. In response to mechanical stretch, the cells in HEPES buffered saline exhibited a Ca2+ transient in a dose dependent way. The response was completely dependent on external Ca2+ and inhibited by gadolinium (Gd3+), suggesting that ir was mediated by the activation of a stretch activated cation channel (SACatC). Interestingly, the stretch induced Ca2+ transient was significantly augmented in the presence of basic polypeptide, protamine. This augmented Ca2+ ...
Read Bending the MDCK Cell Primary Cilium Increases Intracellular Calcium, The Journal of Membrane Biology on DeepDyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips.
Calcium buffering describes the processes which help stabilise the concentration of free calcium ions within cells, in a similar manner to how pH buffers maintain a stable concentration of hydrogen ions. The majority of calcium ions within the cell are bound to intracellular proteins, leaving a minority freely dissociated. When calcium is added to or removed from the cytoplasm by transport across the cell membrane or sarcoplasmic reticulum, calcium buffers minimise the effect on changes in cytoplasmic free calcium concentration by binding calcium to or releasing calcium from intracellular proteins. As a result, 99% of the calcium added to the cytosol of a cardiomyocyte during each cardiac cycle becomes bound to calcium buffers, creating a relatively small change in free calcium. The regulation of free calcium is of particular importance in excitable cells like cardiomyocytes and neurons. Within these cells, many intracellular proteins can act as calcium buffers. In cardiac muscle cells, the most ...
Calcium homeostasis in cardiac myocytes results from the integrated function of transsarcolemmal Ca2+ influx and efflux pathways modulated by membrane potential and from intracellular Ca2+ uptake and release caused predominantly by SR function. These processes can be importantly altered in different disease states as well as by pharmacological agents, and the resulting changes in systolic and diastolic [Ca2+]i can cause clinically significant alterations in contraction and relaxation of the heart. It may be anticipated that a rapid increase in our understanding of the pathophysiology of Ca2+ homeostasis in cardiac myocytes will be forthcoming as the powerful new tools of molecular and structural biology are used to investigate the regulation of Ca2+ transport systems. ...
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Synaptic vesicle exocytosis in primary cultures of baroreceptor neurons is reduced during high-frequency stimulation. Calcium influx through voltage-gated calcium channels (VGCC) is a key step in neurotransmitter release. With the help of FM2-10, a marker of synaptic vesicle recycling, the present s …
Effects of extracellularly applied ATP (added as disodium salt) on stimulus-secretion coupling were investigated in clonal insulin-producing RINm5F cells. Cytoplasmic free Ca2+ concentration [( Ca2+]i), electrical activity, membrane potential, formation of InsP3 and insulin release were measured. Addition of ATP in a Ca2(+)-containing medium promoted a rapid rise in [Ca2+]i, which was followed by a slow decline towards the basal level. In a Ca2(+)-free medium, the ATP-induced increase in [Ca2+]i was smaller, but still enough to elicit insulin secretion. Upon normalization of the extracellular Ca2+ concentration, the response to ATP recovered instantaneously. The presence of glucose in the incubation medium was a prerequisite to obtain a pronounced effect of ATP in the absence of extracellular Ca2+. However, glucose did not enhance the response to ATP in a Ca2(+)-containing medium. The effect of ATP was dose-dependent, with a clearly detectable increase in [Ca2+]i at 1 microM and a maximal response being
Ca2+ flux into mitochondria is an important regulator of cytoplasmic Ca2+ signals, energy production and cell death pathways. Ca2+ uptake can occur through the recently discovered mitochondrial uniporter channel (MCU) but whether the MCU is involved in shaping Ca2+ signals and downstream responses to physiological levels of receptor stimulation is unknown. Here, we show that modest stimulation of leukotriene receptors with the pro-inflammatory signal LTC4 evokes a series of cytoplasmic Ca2+ oscillations that are rapidly and faithfully propagated into mitochondrial matrix. Knockdown of MCU or mitochondrial depolarisation, to reduce the driving force for Ca2+ entry into the matrix, prevents the mitochondrial Ca2+ rise and accelerates run down of the oscillations. The loss of cytoplasmic Ca2+ oscillations appeared to be a consequence of enhanced Ca2+-dependent inactivation of InsP3 receptors, which arose from the loss of mitochondrial Ca2+ buffering. Ca2+ dependent gene expression in response to
Weakness in bones? Grab a calcium supplement, advice the doctors. But have you thought about the way intake of extra calcium can affect your body. This important nutrient that is essential for healthy bones may become a reason for heart disease and other complications if taken in excess quantities.. Calcium and bone health. Bone health is dependent on calcium intake but research has indicated that large amounts of calcium consumed by older women may expose the women to heart disorders and even other complications like death.. The Swedish research study. A sample of women who were born in the period from 1914-1948 was collected, and a research study was done on them by Swedish Researchers. The follow-up research was carried out on almost 61,433 women for about 19 years. The researchers prepared a questionnaire to keep an account of the diet taken by the ladies and the intake of the calcium supplements they took. The study confirmed the reasons for death recorded by the Swedish government ...
One example of such an instability is alternans, which at the cellular level, is characterized by a beat-to-beat alternation in membrane potential and intracellular calcium dynamics. Alternans, which manifests on the surface electrocardiogram as T-wave alternans, is a putative trigger of some types of reentrant arrhythmias. Two possible mechanisms have been proposed for alternans - either transmembrane ionic currents or intracellular calcium dynamics fail to cycle completely during one beat, due to insufficient time, leading to the beat-to-beat alternations characteristic of alternans. Importantly, because the voltage and intracellular calcium dynamics are bidirectionally coupled, alternans in one system will lead to secondary alternans in the other. Because of this coupling it is difficult to determine which mechanism is the main source of the instability. In our laboratory, we attempt to disentangle the contributions of voltage and calcium dynamics leading to cellular alternans via a hybrid ...
Drug resistance is a fundamental problem in cancer chemotherapy. Intracellular calcium concentration ([Ca2+](i)) may play a role in the development of chemoresistance. We investigated the regulatory role of [Ca2+](i) in Taxol resistance in the non-small-cell lung cancer cell line A549 and its chemoresistant subclone A549-T24. Measurement of cytosolic calcium ([Ca2+](c)) in single cells and cell populations revealed similar levels of basal calcium in the two cell lines. However, a reduced response to thapsigargin (a sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) inhibitor) in A549-T24 cells compared to the parent cell line suggested a lower ER Ca2+ content in these cells. mRNA expression of SERCA2b and SERCA3, major Ca2+ pumps involved in ER Ca2+ homeostasis, did not significantly differ between the two cell lines, as revealed by RT-PCR. An altered calcium influx pathway in the Taxol-resistant cell line was observed. Modulation of the ER calcium pools using CMC (4-chloro-m-cresol) and ATP
Glucagon-like peptide-1 (GLP-1) elevates the intracellular free calcium concentration ([Ca2+]i) and insulin secretion in a Na+-dependent manner. To investigate a possible role of Na ion in the action of GLP-1 on pancreatic islet cells, we measured th
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Receptor-mediated Ca2+ signaling in many non-excitable cells initially induces Ca2+ release from intracellular Ca2+ stores, followed by Ca2+ influx across the plasma membrane. binding domain name 946128-88-7 manufacture and the SAM domain name, together with functional divergence 946128-88-7 manufacture studies, identified critical regions/residues likely underlying functional changes, and provided evidence for the hypothesis that STIM-1 and STIM-2 might have developed distinct functional properties after duplication. Introduction In response to appropriate stimuli, virtually all types of animal cells can initiate spatial and temporal changes of cytosolic free Ca2+ concentrations to regulate a wide range of physiological processes [1]. Accordingly, animal 946128-88-7 manufacture cells employ a repertoire of membrane transporters such as Ca2+ channels, Ca2+ ATPases, and cation/Ca2+ exchangers to control cytosolic Ca2+ [2], [3]. One important mode of Ca2+ influx across the plasma membrane involves ...
Is your body calcium deficient & are you searching for measures to prevent it? Your search ends here as weve got exhaustive tips to prevent calcium deficiency!
Eye twitching calcium deficiency - What kind of deficiency causes under eye twitching? Twitching. Mostly excess cafein nicotine low calcium.