Uniaxial cyclic stretch stimulates TRPV4 to induce realignment of human embryonic stem cell-derived cardiomyocytes

Yan, Qi; Li, Zhichao; Kong, Chi-Wing; Tang, Nelson Leung Sang; Huang, Yü; Tse, Gary; Yao, Xiaoqiang

doi:10.1016/j.yjmcc.2015.08.005

Cited by 28 publications

(23 citation statements)

References 30 publications

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“…The cytosolic Ca 2+ was measured as described elsewhere (Qi et al, 2015). Briefly, NRCMs were loaded with 5 μmol/L Fluo-4/AM (Invitrogen, Waltham, MA, USA) for 40 min in normal Tyrode’s solution that contained in mmol/L, 140 NaCl, 5.4 KCl, 1 MgCl 2 , 2 CaCl 2 , 5.5 glucose and 5 HEPES at pH 7.4.…”

Section: Methodsmentioning

confidence: 99%

Gastrodin Inhibits Store-Operated Ca2+ Entry and Alleviates Cardiac Hypertrophy

Zheng

Meng

et al. 2017

Front. Pharmacol.

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Cardiac hypertrophy is a major risk factor for heart failure, which are among the leading causes of human death. Gastrodin is a small molecule that has been used clinically to treat neurological and vascular diseases for many years without safety issues. In the present study, we examined protective effect of gastrodin against cardiac hypertrophy and explored the underlying mechanism. Phenylephrine and angiotensin II were used to induce cardiac hypertrophy in a mouse model and a cultured cardiomyocyte model. Gastrodin was found to alleviate the cardiac hypertrophy in both models. Mechanistically, gastrodin attenuated the store-operated Ca2+ entry (SOCE) by reducing the expression of STIM1 and Orai1, two key proteins in SOCE, in animal models as well as in cultured cardiomyocyte model. Furthermore, suppressing SOCE by RO2959, Orai1-siRNAs or STIM1-siRNAs markedly attenuated the phenylephrine-induced hypertrophy in cultured cardiomyocyte model. Together, these results showed that gastrodin inhibited cardiac hypertrophy and it also reduced the SOCE via its action on the expression of STIM1 and Orai1. Furthermore, suppression of SOCE could reduce the phenylephrine-induced cardiomyocyte hypertrophy, suggesting that SOCE-STIM1-Orai1 is located upstream of hypertrophy.

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Section: Methodsmentioning

confidence: 99%

Gastrodin Inhibits Store-Operated Ca2+ Entry and Alleviates Cardiac Hypertrophy

Zheng

Meng

et al. 2017

Front. Pharmacol.

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“…Various experiments have been developed to determine the physiological function of MSCs, which have exposed cells to various mechanical loads in situ. In such electrophysiological experiments, cells have been exposed to cell stretch, 42 – 45 shear flow, 46 – 48 membrane indentation, 49 – 51 osmotic challenges, 52 , 53 hydrostatic pressure 54 – 56 and other loading conditions. In line with these experiments, mechanical unloading, as experienced in microgravity, represents an interesting condition, since exposure to microgravity leads to a series of physiological adaption processes (reviewed in refs.…”

Section: Mechanosensitivity Of Ion Channelsmentioning

confidence: 99%

Electrophysiological experiments in microgravity: lessons learned and future challenges

et al. 2018

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Advances in electrophysiological experiments have led to the discovery of mechanosensitive ion channels (MSCs) and the identification of the physiological function of specific MSCs. They are believed to play important roles in mechanosensitive pathways by allowing for cells to sense their mechanical environment. However, the physiological function of many MSCs has not been conclusively identified. Therefore, experiments have been developed that expose cells to various mechanical loads, such as shear flow, membrane indentation, osmotic challenges and hydrostatic pressure. In line with these experiments, mechanical unloading, as experienced in microgravity, represents an interesting alternative condition, since exposure to microgravity leads to a series of physiological adaption processes. As outlined in this review, electrophysiological experiments performed in microgravity have shown an influence of gravity on biological functions depending on ion channels at all hierarchical levels, from the cellular level to organs. In this context, calcium signaling represents an interesting cellular pathway, as it involves the direct action of calcium-permeable ion channels, and specific gravitatic cells have linked graviperception to this pathway. Multiple key proteins in the graviperception pathways have been identified. However, measurements on vertebrae cells have revealed controversial results. In conclusion, electrophysiological experiments in microgravity have shown that ion-channel-dependent physiological processes are altered in mechanically unloaded conditions. Future experiments may provide a better understanding of the underlying mechanisms.

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“…Neuronal TRPV4 channels may therefore be an important therapeutic target for cognitive, motor and ageing-related disorders. TRPV4 inhibitors have been described and were recently described as orally available compounds (Jia et al 2004;Krause et al 2005;Phan et al 2009;Vincent et al 2009;Morty & Kuebler, 2014;Feetham et al 2015;Qi et al 2015) and also as 'dual inhibitors' of TRPV4 and TRPA1 (Kanju et al 2016), which might be an attractive possibility given the postulated function of astrocytic TRPA1 (Lee et al 2012;Shigetomi et al 2012Shigetomi et al , 2013Wei et al 2016). Such inhibitors, if they are intended for oral use, will have to pass through the blood-brain barrier (although, for example, the blood-brain barrier is more penetrable in certain CNS disorders, such as multiple sclerosis).…”

Section: Role Of Trpv4 In Cns Neuronsmentioning

confidence: 99%

“…; Qi et al . ) and also as ‘dual inhibitors’ of TRPV4 and TRPA1 (Kanju et al . ), which might be an attractive possibility given the postulated function of astrocytic TRPA1 (Lee et al .…”

Section: Introductionmentioning

confidence: 99%

Pleiotropic function of TRPV4 ion channels in the central nervous system

Kanju

Liedtke

2016

Experimental Physiology

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TRPV4 ion channels are osmo-mechano-TRP channels with pleiotropic function and expression in many different types of tissues and cells. They have also been found involved in pain and inflammation. Studies have focused on the role of TRPV4 in peripheral sensory neurons, but its expression and function in central nervous glial cells and neurons has also been documented. In this overview, based on the senior author’s lecture at the recent physiology meeting in Dublin, we concisely review evidence of TRPV4 expression and function in the CNS, and how TRPV4 function can be modulated for therapeutic benefit of neuro-psychiatric disorders. Novel TRPV4-inhibitory compounds developed recently in the authors’ lab will also be discussed

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Uniaxial cyclic stretch stimulates TRPV4 to induce realignment of human embryonic stem cell-derived cardiomyocytes

Cited by 28 publications

References 30 publications

Gastrodin Inhibits Store-Operated Ca2+ Entry and Alleviates Cardiac Hypertrophy

Gastrodin Inhibits Store-Operated Ca2+ Entry and Alleviates Cardiac Hypertrophy

Electrophysiological experiments in microgravity: lessons learned and future challenges

Pleiotropic function of TRPV4 ion channels in the central nervous system

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