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Calcium signalling in endothelial cells
Q K Tran1, K Ohashi, H Watanabe
1Department of Internal Medicine III, Hamamatsu University School of Medicine, 3600 Handa-cho, 431-3192, Hamamatsu, Japan.
Insights
Vascular endothelial cells rely on calcium signaling for many functions. This review details intracellular calcium stores, channels, and the critical store-operated calcium entry mechanisms.
Area of Science:
- Cardiovascular Biology
- Cell Physiology
- Endothelial Cell Function
Background:
- Vascular endothelial cells are vital for numerous physiological processes.
- Intracellular calcium concentration (Ca²⁺) changes significantly regulate endothelial cell functions.
- Understanding calcium signaling pathways is crucial for comprehending endothelial cell behavior.
Purpose of the Study:
- To review the key components of endothelial calcium signaling.
- To elucidate the mechanisms governing store-operated calcium entry (SOCE).
- To highlight the importance of transplasmalemmal calcium entry in endothelial functions.
Main Methods:
- Literature review of endothelial calcium signaling pathways.
- Analysis of intracellular calcium stores and channels.
- Examination of ligand-binding, store depletion, and calcium influx.
Main Results:
- Endothelial cells possess diverse intracellular Ca²⁺ stores and channels.
- Store-operated Ca²⁺ entry (SOCE) is a critical mechanism for endothelial Ca²⁺ homeostasis.
- Multiple factors, including Ca²⁺ influx factor and conformational coupling, regulate SOCE.
Conclusions:
- Calcium signaling is fundamental to endothelial cell multifunctionality.
- Store-operated calcium entry is a key pathway for regulating endothelial functions.
- Further research into SOCE mechanisms can reveal therapeutic targets for vascular diseases.
Abstract:
Vascular endothelial cells are ubiquitous for their presence in each and every vessel and unique for their multifunctional nature. A large number of endothelial functions depend to various extents on changes in intracellular Ca(2+) concentration. Reviewed are endothelial Ca(2+) stores, Ca(2+) channels, and in-out-in Ca(2+) signalling events, from ligand-binding on the plasma membrane into depletion of intracellular Ca(2+) stores and therefrom out to transplasmalemmal Ca(2+) entry that is of prime importance for many endothelial functions. Special emphasis is placed on mechanisms regulating store-operated Ca(2+) entry including a Ca(2+) influx factor, the vesicle secretion-like model, the conformational coupling model, the membrane potential, cytochrome P450, protein tyrosine kinase, myosin light chain kinase and nitric oxide.