scholarly journals Role of extracellular calcium and calcium efflux in the activation of hepatic glycogenolysis by calcium-dependent hormones.

1985 ◽  
Vol 32 (2) ◽  
pp. 317-326 ◽  
Author(s):  
YOSHINOBU KOIDE ◽  
NOBUTAKA DEMURA ◽  
SATOSHI KIMURA ◽  
NOBUO KUGAI ◽  
KAMEJIRO YAMASHITA
Keyword(s):  
Extracellular Calcium ◽  
Calcium Efflux ◽  
Calcium Dependent

scholarly journals Calcineurin Activity Is Required for the Initiation of Skeletal Muscle Differentiation

2000 ◽  
Vol 149 (3) ◽  
pp. 657-666 ◽  
Author(s):  
Bret B. Friday ◽  
Valerie Horsley ◽  
Grace K. Pavlath
Keyword(s):  
Skeletal Muscle ◽  
Cell Fusion ◽  
Transcriptional Activation ◽  
Active Form ◽  
Extracellular Calcium ◽  
Molecular Signaling ◽  
Phenotypic Differentiation ◽  
Calcium Dependent ◽  
Sequence Of Events

Differentiation of skeletal muscle myoblasts follows an ordered sequence of events: commitment, cell cycle withdrawal, phenotypic differentiation, and finally cell fusion to form multinucleated myotubes. The molecular signaling pathways that regulate the progression are not well understood. Here we investigate the potential role of calcium and the calcium-dependent phosphatase calcineurin in myogenesis. Commitment, phenotypic differentiation, and cell fusion are identified as distinct calcium-regulated steps, based on the extracellular calcium concentration required for the expression of morphological and biochemical markers specific to each of these stages. Furthermore, differentiation is inhibited at the commitment stage by either treatment with the calcineurin inhibitor cyclosporine A (CSA) or expression of CAIN, a physiological inhibitor of calcineurin. Retroviral-mediated gene transfer of a constitutively active form of calcineurin is able to induce myogenesis only in the presence of extracellular calcium, suggesting that multiple calcium-dependent pathways are required for differentiation. The mechanism by which calcineurin initiates differentiation includes transcriptional activation of myogenin, but does not require the participation of NFAT. We conclude that commitment of skeletal muscle cells to differentiation is calcium and calcineurin-dependent, but NFAT-independent.

scholarly journals Extracellular Calcium-Dependent Modulation of Endothelium Relaxation in Rat Mesenteric Small Artery: The Role of Potassium Signaling

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Lise Hangaard ◽  
Peter B. Jessen ◽  
Dmitrii Kamaev ◽  
Christian Aalkjaer ◽  
Vladimir V. Matchkov
Keyword(s):  
Extracellular Calcium ◽  
Small Artery ◽  
Small Arteries ◽  
Calcium Dependent ◽  
Dependent Pathway

The nature of NO- and COX-independent endothelial hyperpolarization (EDH) is not fully understood but activation of small- and intermittent-conductance Ca2+-activated K+channels (SKCaandIKCa) is important. Previous studies have suggested that the significance ofIKCadepends onCa2+out. Also it has been suggested that K+is important through localizedK+outsignaling causing activation of the Na+,K+-ATPase and inward-rectifying K+channels (Kir). Here we tested the hypothesis that the modulating effect ofCa2+outon the EDH-like response depends onK+out. We addressed this possibility using isometric myography of rat mesenteric small arteries. WhenK+outwas 4.2 mM, relaxation to acetylcholine (ACh) was stronger at 2.5 mMCa2+outthan at 1 mMCa2+out. Inhibition ofIKCawith TRAM34 suppressed the relaxations but did not change the relation between the relaxations at the low and highCa2+out. ThisCa2+out-dependence disappeared at 5.9 mMK+outand in the presence of ouabain or BaCl2. Our results suggest thatIKCaare involved in the localizedK+outsignaling which acts through the Na+,K+-ATPase andKirchannels and that the significance of this endothelium-dependent pathway is modulated byCa2+out.

Effect of Annexins Translocated in Extracellular Vesicles on Tumorigenesis

2020 ◽  
Vol 20 ◽  
Author(s):  
Qionghui Wu ◽  
Haidong Wei ◽  
Wenbo Meng ◽  
Xiaodong Xie ◽  
Zhenchang Zhang ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Extracellular Vesicles ◽  
Immune Cell ◽  
Epithelial Mesenchymal Transition ◽  
Main Role ◽  
Tumor Cell Adhesion ◽  
Mesenchymal Transition ◽  
Calcium Dependent ◽  
Tumor Neovascularization

: Annexin, a calcium-dependent phospholipid binding protein, can affect tumor cell adhesion, proliferation, apoptosis, invasion and metastasis, as well as tumor neovascularization in different ways. Recent studies have shown that annexin exists not only as an intracellular protein in tumor cells, but also in different ways to be secret outside the cell as a “crosstalk” tool for tumor cells and tumor microenvironment, thus playing an important role in the development of tumors, such as participating in epithelial-mesenchymal transition, regulating immune cell behavior, promoting neovascularization and so on. The mechanism of annexin secretion in the form of extracellular vesicles and its specific role is still unclear. This paper summarizes the main role of annexin secreted into the extracellular space in the form of extracellular vesicles in tumorigenesis and drug resistance and analyzes its possible mechanism.

scholarly journals A CACNA1A variant associated with trigeminal neuralgia alters the gating of Cav2.1 channels

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Eder Gambeta ◽  
Maria A. Gandini ◽  
Ivana A. Souza ◽  
Laurent Ferron ◽  
Gerald W. Zamponi
Keyword(s):  
Trigeminal Neuralgia ◽  
Missense Mutation ◽  
Neurotransmitter Release ◽  
Trigeminal System ◽  
Wild Type ◽  
Calcium Dependent ◽  
Whole Cell Patch Clamp ◽  
C Terminus ◽  
Dependent Inactivation

AbstractA novel missense mutation in the CACNA1A gene that encodes the pore forming α1 subunit of the CaV2.1 voltage-gated calcium channel was identified in a patient with trigeminal neuralgia. This mutation leads to a substitution of proline 2455 by histidine (P2455H) in the distal C-terminus region of the channel. Due to the well characterized role of this channel in neurotransmitter release, our aim was to characterize the biophysical properties of the P2455H variant in heterologously expressed CaV2.1 channels. Whole-cell patch clamp recordings of wild type and mutant CaV2.1 channels expressed in tsA-201 cells reveal that the mutation mediates a depolarizing shift in the voltage-dependence of activation and inactivation. Moreover, the P2455H mutant strongly reduced calcium-dependent inactivation of the channel that is consistent with an overall gain of function. Hence, the P2455H CaV2.1 missense mutation alters the gating properties of the channel, suggesting that associated changes in CaV2.1-dependent synaptic communication in the trigeminal system may contribute to the development of trigeminal neuralgia.

A Drosophila mutant defective in extracellular calcium-dependent photoreceptor deactivation and rapid desensitization

Nature ◽  
1991 ◽  
Vol 354 (6350) ◽  
pp. 230-232 ◽  
Author(s):  
Rama Ranganathan ◽  
Greg L. Harris ◽  
Charles F. Stevens ◽  
Charles S. Zuker
Keyword(s):  
Extracellular Calcium ◽  
Calcium Dependent ◽  
Drosophila Mutant

Role of the cytoskeleton in extracellular calcium-regulated PTH release

2007 ◽  
Vol 354 (1) ◽  
pp. 8-13 ◽  
Author(s):  
Stephen J. Quinn ◽  
Olga Kifor ◽  
Imre Kifor ◽  
Robert R. Butters ◽  
Edward M. Brown
Keyword(s):  
Extracellular Calcium

The role of extracellular calcium in the pathophysiology of myotonic dystrophy

1993 ◽  
Vol 41 (4) ◽  
pp. 370-374 ◽  
Author(s):  
L. Oz ◽  
M.E. Dinc ◽  
M.E. Oz ◽  
G.B. Frank
Keyword(s):  
Myotonic Dystrophy ◽  
Extracellular Calcium

scholarly journals Role of Phosphopantetheinyl Transferase Genes in Antibiotic Production by Streptomyces coelicolor

2008 ◽  
Vol 190 (20) ◽  
pp. 6903-6908 ◽  
Author(s):  
Ya-Wen Lu ◽  
Adrianna K. San Roman ◽  
Amy M. Gehring
Keyword(s):  
Antibiotic Production ◽  
Streptomyces Coelicolor ◽  
Morphological Development ◽  
Phosphopantetheinyl Transferase ◽  
Calcium Dependent ◽  
Actinorhodin Production

ABSTRACT The phosphopantetheinyl transferase genes SCO5883 (redU) and SCO6673 were disrupted in Streptomyces coelicolor. The redU mutants did not synthesize undecylprodigiosin, while SCO6673 mutants failed to produce calcium-dependent antibiotic. Neither gene was essential for actinorhodin production or morphological development in S. coelicolor, although their mutation could influence these processes.

MO092THE ROLE OF CALCIUM IN UROMODULIN EXPRESSION AND SECRETION FROM RENAL MEDULLARY EPITHELIAL CELLS OF HYPERTENSIVE AND NORMOTENSIVE RATS

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Philipp Boder ◽  
Sheon Mary ◽  
Lesley Graham ◽  
Christian Delles
Keyword(s):  
Blood Pressure ◽  
Epithelial Cells ◽  
Mrna Level ◽  
Extracellular Calcium ◽  
Female Rats ◽  
Thick Ascending Limb ◽  
Molecular Signaling ◽  
Extracellular Secretion ◽  
Wistar Kyoto

Abstract Background and Aims Uromodulin (UMOD) is the most abundantly secreted protein found within the urine, primarily produced by medullary thick ascending limb (mTAL) epithelial cells of the kidneys. There is accruing genetic evidence implicating UMOD in blood pressure regulation and consequently hypertension. The molecular signaling induced by calcium in the kidney and its influence on blood pressure are not well understood. The aim of this study was to investigate the potential role of extracellular calcium and the calcium-sensing receptor (CaSR) in mTAL on UMOD production and secretion in TAL cells with the hope of defining novel clinical targets for the treatment of hypertension. Method Kidneys were harvested from normotensive Wistar-Kyoto (WKY) and stroke-prone spontaneously hypertensive (SHRSP) female rats. To determine the effect of extracellular calcium on UMOD secretion, mTAL tubules were incubated in media with and without 1mM calcium, nifedipine (10µM), NPS2143 (1 or 5 µM) and spermine (2mM). Extracellular and intracellular UMOD protein levels were detected by Western blot. Gene expression of Umod was determined by qRT-PCR. Results Calcium increased mTAL tubule UMOD secretion in WKY and SHRSP. Nifedipine slightly decreased UMOD secretion in WKY without calcium. In both strains, NPS2143 increased calcium-induced UMOD secretion, with an enhanced effect in SHRSP. Stimulation of CaSR with spermine decreased UMOD secretion in WKY. Analysis of intracellular UMOD levels in these conditions demonstrated increased accumulation when extracellular secretion was low, and vice versa. Incubation of primary mTAL cells with calcium confirmed increased localisation of UMOD at the membrane compared to the cytosol, without any major differences in cell morphology. The Umod mRNA level changes were not statistically significant among conditions. Conclusion Trafficking of UMOD in the mTAL is influenced by the type of CaSR ligand and the biased nature of G-protein coupled CaSR signalling. Unravelling the signalling events post-calcium will be necessary for identification of key regulators of UMOD secretion and provide new sites for therapeutic intervention in hypertension.

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