Cross-Talk between Mechanosensitive Ion Channels and Calcium Regulatory Proteins in Cardiovascular Health and Disease

Wang, Yaping; Shi, Jing; Tong, Xiaoyong

doi:10.3390/ijms22168782

Cited by 26 publications

(21 citation statements)

References 157 publications

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“…In the cardiovascular system, myocardial contraction pumps blood into the arteries, and blood flow creates friction and pressure on the blood vessels ( 49 ). MSCs are widely expressed in the cardiovascular system, sensing changes in mechanical forces and transducing mechanical signals into chemical and electrical signals ( 50 ). Piezo1 is one of the cardiovascular sense and plays a crucial role in cardiovascular development, blood pressure regulation, hypertensive vascular remodeling, and other physiology and pathology ( 51 – 54 ).…”

Section: Piezo1 Channel-mediated Chronic Inflammationmentioning

confidence: 99%

Piezo1 Channels as Force Sensors in Mechanical Force-Related Chronic Inflammation

Liu

Zheng

et al. 2022

Front. Immunol.

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Mechanical damage is one of the predisposing factors of inflammation, and it runs through the entire inflammatory pathological process. Repeated or persistent damaging mechanical irritation leads to chronic inflammatory diseases. The mechanism of how mechanical forces induce inflammation is not fully understood. Piezo1 is a newly discovered mechanically sensitive ion channel. The Piezo1 channel opens in response to mechanical stimuli, transducing mechanical signals into an inflammatory cascade in the cell leading to tissue inflammation. A large amount of evidence shows that Piezo1 plays a vital role in the occurrence and progression of chronic inflammatory diseases. This mini-review briefly presents new evidence that Piezo1 responds to different mechanical stresses to trigger inflammation in various tissues. The discovery of Piezo1 provides new insights for the treatment of chronic inflammatory diseases related to mechanical stress. Inhibiting the transduction of damaging mechanical signals into inflammatory signals can inhibit inflammation and improve the outcome of inflammation at an early stage. The pharmacology of Piezo1 has shown bright prospects. The development of tissue-specific Piezo1 drugs for clinical use may be a new target for treating chronic inflammation.

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Section: Piezo1 Channel-mediated Chronic Inflammationmentioning

confidence: 99%

Piezo1 Channels as Force Sensors in Mechanical Force-Related Chronic Inflammation

Liu

Zheng

et al. 2022

Front. Immunol.

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“…Aside from this, some scientific reports recently indicated that Ca 2+ entry mediated by mechanosensitive channels is regulated by a diversity of major proteins which are located in the cellular membrane or endoplasmic reticulum. It was shown that mechanosensitive channels can be physically connected with some Ca 2+ regulatory proteins [ 49 ]. For example, Piezo and SERCA were discovered to cross-talk to each other through physical interaction in endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Store-Operated Ca2+ Entry Contributes to Piezo1-Induced Ca2+ Increase in Human Endometrial Stem Cells

Chubinskiy-Nadezhdin

Semenova

Vasileva

et al. 2022

IJMS

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Endometrial mesenchymal stem cells (eMSCs) are a specific class of stromal cells which have the capability to migrate, develop and differentiate into different types of cells such as adipocytes, osteocytes or chondrocytes. It is this unique plasticity that makes the eMSCs significant for cellular therapy and regenerative medicine. Stem cells choose their way of development by analyzing the extracellular and intracellular signals generated by a mechanical force from the microenvironment. Mechanosensitive channels are part of the cellular toolkit that feels the mechanical environment and can transduce mechanical stimuli to intracellular signaling pathways. Here, we identify previously recorded, mechanosensitive (MS), stretch-activated channels as Piezo1 proteins in the plasma membrane of eMSCs. Piezo1 activity triggered by the channel agonist Yoda1 elicits influx of Ca2+, a known modulator of cytoskeleton reorganization and cell motility. We found that store-operated Ca2+ entry (SOCE) formed by Ca2+-selective channel Orai1 and Ca2+ sensors STIM1/STIM2 contributes to Piezo1-induced Ca2+ influx in eMSCs. Particularly, the Yoda1-induced increase in intracellular Ca2+ ([Ca2+]i) is partially abolished by 2-APB, a well-known inhibitor of SOCE. Flow cytometry analysis and wound healing assay showed that long-term activation of Piezo1 or SOCE does not have a cytotoxic effect on eMSCs but suppresses their migratory capacity and the rate of cell proliferation. We propose that the Piezo1 and SOCE are both important determinants in [Ca2+]i regulation, which critically affects the migratory activity of eMSCs and, therefore, could influence the regenerative potential of these cells.

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“…The plasma membrane Ca 2+ ATPase (PMCA) expels Ca 2+ outside the cell [ 83 ]. The sarco-endoplasmic reticulum Ca 2+ ATPase (SERCA) displaces Ca 2+ into internal stores [ 84 , 85 ]. These stores are remnants given to platelets from the endoplasmic/sarcoplasmic reticulum (ER/SR) of megakaryocytes [ 86 , 87 ] known as the dense tubular system (DTS) [ 88 ].…”

Section: Cytosolic Ion Fluxes In Procoagulant Coat Plateletsmentioning

confidence: 99%

Mechanisms Underlying Dichotomous Procoagulant COAT Platelet Generation—A Conceptual Review Summarizing Current Knowledge

Veuthey

Aliotta

Calderara

et al. 2022

IJMS

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Procoagulant platelets are a subtype of activated platelets that sustains thrombin generation in order to consolidate the clot and stop bleeding. This aspect of platelet activation is gaining more and more recognition and interest. In fact, next to aggregating platelets, procoagulant platelets are key regulators of thrombus formation. Imbalance of both subpopulations can lead to undesired thrombotic or bleeding events. COAT platelets derive from a common pro-aggregatory phenotype in cells capable of accumulating enough cytosolic calcium to trigger specific pathways that mediate the loss of their aggregating properties and the development of new adhesive and procoagulant characteristics. Complex cascades of signaling events are involved and this may explain why an inter-individual variability exists in procoagulant potential. Nowadays, we know the key agonists and mediators underlying the generation of a procoagulant platelet response. However, we still lack insight into the actual mechanisms controlling this dichotomous pattern (i.e., procoagulant versus aggregating phenotype). In this review, we describe the phenotypic characteristics of procoagulant COAT platelets, we detail the current knowledge on the mechanisms of the procoagulant response, and discuss possible drivers of this dichotomous diversification, in particular addressing the impact of the platelet environment during in vivo thrombus formation.

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Cross-Talk between Mechanosensitive Ion Channels and Calcium Regulatory Proteins in Cardiovascular Health and Disease

Cited by 26 publications

References 157 publications

Piezo1 Channels as Force Sensors in Mechanical Force-Related Chronic Inflammation

Piezo1 Channels as Force Sensors in Mechanical Force-Related Chronic Inflammation

Store-Operated Ca2+ Entry Contributes to Piezo1-Induced Ca2+ Increase in Human Endometrial Stem Cells

Mechanisms Underlying Dichotomous Procoagulant COAT Platelet Generation—A Conceptual Review Summarizing Current Knowledge

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