Calcium-Release-Activated Calcium Influx in Endothelium

Davis, Michael J.; Sharma, N. R.

doi:10.1159/000159222

Cited by 25 publications

(20 citation statements)

References 26 publications

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“…A number of subsequent reports have supported our findings that tyrosine kinases are involved in regulating SOCE in many cell types (Marhaba et al, 1996;Davis and Sharma, 1997;Krutetskaia et al, 1997;Taketo et al, 1997). In addition, studies of platelets indicate that depletion of Ca 2+ from intracellular stores leads to the tyrosine phosphorylation of a 130 kD protein, which led to speculation that this protein is involved in the regulation of Ca 2+ entry (Vostal et al, 1991).…”

Section: Introductionsupporting

confidence: 69%

Tyrosine phosphatase and cytochrome P450 activity are critical in regulating store-operated calcium channels in human fibroblasts

Lee

Son²,

Babnigg³

et al. 2006

Exp Mol Med

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Diverse signaling pathways have been proposed to regulate store-operated calcium entry (SOCE) in a wide variety of cell types. However, it still needs to be determined if all of these known pathways operate in a single cell type. In this study, we examined involvement of various signaling molecules in SOCE using human fibroblast cells (HSWP). Bradykinin (BK)-stimulated Ca 2+ entry, previously shown to be via SOCE, is enhanced by the addition of vanadate, an inhibitor of tyrosine phosphatases. Furthermore, SOCE is regulated by cytochrome P-450, as demonstrated by the fact that the products of cytochrome P-450 activity (14,15 EET) stimulated SOCE while econazole, an inhibitor of cytochrome P450, suppressed BK-stimulated Ca 2+ entry. In contrast, Ca 2+ entry was unaffected by the guanylate cyclase inhibitor LY83583, or the membrane permeant cyclic GMP analog 8-bromo-cyclic GMP (8-Br-cGMP). Neither nitric oxide donors nor phorbol esters affected BK-stimulated Ca 2+ entry. SOCE in HSWP cells is primarily regulated by tyrosine phosphorylation and the cytochrome P-450 pathway, but not by cyclic GMP, nitric oxide, or protein kinase C. Thus, multiple pathways do operate in a single cell type leading to the activation of Ca 2+ entry and some of these signaling pathways are more prominently involved in regulating calcium entry in different cell types.

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Section: Introductionsupporting

confidence: 69%

Tyrosine phosphatase and cytochrome P450 activity are critical in regulating store-operated calcium channels in human fibroblasts

Lee

Son²,

Babnigg³

et al. 2006

Exp Mol Med

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“…[23][24][25] These large E m changes to SP and BK clearly contrast with the very slight hyperpolarizing responses to these peptides that we observed in current-clamped intact endothelial cells. They also contrast with the findings of Wang et al 19 in freshly isolated current-clamped endothelial cells of rat aorta studied by the perforated-patch method.…”

Section: Hyperpolarizing Responses To Sp and Bk Differ Between Culturmentioning

confidence: 43%

Rat Coronary Endothelial Cell Membrane Potential Responses During Hypertension

Gauthier

Rusch

2001

Hypertension

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Abstract-The purpose of this study was to provide the first membrane potential profile in coronary endothelial cells from normotensive sham-operated control and 1-kidney, 1-clip renal hypertensive rats. Dilator responses were assessed in cannulated coronary arteries from control and 1-kidney, 1-clip rats, and the perforated patch-clamp method was used to compare membrane potential responses between the intact endothelial cells. Under these conditions, acetylcholine (100 pmol/L to 10 mol/L) induced similar large dilations of coronary arteries from control and 1-kidney, 1-clip rats that were associated with endothelial cell hyperpolarizing responses of 16Ϯ3 and 18Ϯ2 mV, respectively. Substance P (10 fmol/L to 1 nmol/L) and bradykinin (100 fmol/L to 10 nmol/L) also substantially dilated coronary arteries from control rats but only induced small (2 to 4 mV) endothelial cell hyperpolarizing responses. These dilations, which appeared independent of membrane potential changes, were highly blunted or absent in arteries from 1-kidney, 1-clip rats. Thus, dilator responses to acetylcholine that are associated with large endothelial hyperpolarizing responses are normal in the small coronary arteries of 1-kidney, 1-clip rats. However, dilator response to substance P and bradykinin, which apparently are not heavily dependent on endothelial cell hyperpolarizations, are selectively targeted for impairment in the coronary arteries of this model of hypertension (Hypertension. 2001;37:66-71.)Key Words: endothelium Ⅲ hypertension, renal Ⅲ coronary artery disease Ⅲ muscle, smooth, vascular Ⅲ membranes Ⅲ potassium channels E ndothelium-mediated dilations are often blunted in isolated arteries from different rat models of experimental hypertension and in arteries of human subjects with essential hypertension. [1][2][3][4][5][6][7][8] Although the mechanisms that underlie this dilator dysfunction are complex, a reduced release of endothelium-derived relaxing factors appears to be a contributing factor. 9 In this regard, the signaling pathways by which dilator substances release relaxing factors from endothelial cells appear to involve changes in membrane potential (E m ). 10,11 Specifically, dilator molecules bind to endothelial membrane receptors to activate plasmalemmal Ca 2ϩ -dependent K ϩ channels, resulting in K ϩ efflux and membrane hyperpolarization. This enhanced electrical gradient for Ca 2ϩ influx, combined with the release of Ca 2ϩ from intracellular stores, elevates cytosolic Ca 2ϩ in the endothelial cell to activate the Ca 2ϩ -dependent enzymes required for the synthesis of dilator factors. 10 -12 Hence, hyperpolarization of the endothelial cell membrane is linked to the release of relaxing factors, and the failure of dilator substances to trigger hyperpolarizing responses may promote endothelial dilator dysfunction during hypertension.In this study, we directly investigated this hypothesis by characterizing vasodilator and endothelial cell E m responses to acetylcholine (ACH), substance P (SP), and bradykinin (BK) in iso...

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“…EDHF-type relaxations is thought to be capacitative Ca 2ϩ influx into the endothelial cell, whereby depletion of Ca 2ϩ stores in the endoplasmic reticulum results in K Ca channel activation, hyperpolarization, and enhanced electrochemical Ca 2ϩ entry (30,31). The role of these events in cAMP-mediated relaxation of intact SMA rings was evaluated using CPA (which depletes the endoplasmic reticulum Ca 2ϩ store by blocking its Ca 2ϩ -ATPase pump) and 5,6-EET (which activates store-operated Ca 2ϩ channels directly without the necessity for store depletion) (6,8,30,32).…”

Section: Resultsmentioning

confidence: 99%