Transient receptor potential vanilloid-3 (TRPV3) activation plays a central role in cardiac fibrosis induced by pressure overload in rats via TGF-β1 pathway

Liu, Yan; Qi, Hanping; Mingyao, E; Shi, Pilong; Zhang, Qianhui; Li, Shuzhi; Wang, Ye; Cao, Yonggang; Chen, Yunping; Ba, Lina; Gao, Jingli; Huang, Wei; Sun, Hai‐Ying

doi:10.1007/s00210-017-1443-7

Cited by 27 publications

(36 citation statements)

References 31 publications

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“…Our previous studies have found that activation of TRPV3 channels can aggravate cardiac fibrosis in the pressure-overloaded rat hearts. 20 The present study further indicated that the expression of TRPV3 protein was signifi- | 1937 of autophagy after TRPV3 knockdown. As we all know, intracellular calcium is an important regulator of autophagy.…”

Section: Trpv3 Gene Is a Target Of Mir-103supporting

confidence: 63%

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MiR‐103 inhibiting cardiac hypertrophy through inactivation of myocardial cell autophagy via targeting TRPV3 channel in rat hearts

Ren

Mingyao

et al. 2019

J Cellular Molecular Medi

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Cardiac hypertrophy is a common pathological change frequently accompanied by chronic hypertension and myocardial infarction. Nevertheless, the pathophysiological mechanisms of cardiac hypertrophy have never been elucidated. Recent studies indicated that miR‐103 expression was significantly decreased in heart failure patients. However, less is known about the role of miR‐103 in cardiac hypertrophy. The present study was designed to investigate the relationship between miR‐103 and the mechanism of pressure overload‐induced cardiac hypertrophy. TRPV 3 protein, cardiac hypertrophy marker proteins ( BNP and β‐ MHC ) and autophagy associated proteins (Beclin‐1 and LC 3‐ II ) were up‐regulated, as well as, miR‐103 expression and autophagy associated proteins (p62) were down‐regulated in cardiac hypertrophy models in vivo and in vitro respectively. Further results indicated that silencing TRPV 3 or forcing overexpression of miR‐103 could dramatically inhibit cell surface area, relative fluorescence intensity of Ca 2+ signal and the expressions of BNP , β‐ MHC , Beclin‐1 and LC 3‐ II , but promote p62 expression. Moreover, TRPV 3 protein was decreased in neonatal rat ventricular myocyte transfected with miR‐103, but increased by AMO ‐103. Co‐transfection of the miR‐103 with the luciferase reporter vector into HEK 293 cells caused a sharp decrease in luciferase activity compared with transfection of the luciferase vector alone. The miR‐103‐induced depression of luciferase activity was rescued by an AMO ‐103. These findings suggested that TRPV 3 was a direct target of miR‐103. In conclusion, miR‐103 could attenuate cardiomyocyte hypertrophy partly by reducing cardiac autophagy activity through the targeted inhibition of TRPV 3 signalling in the pressure‐overloaded rat hearts.

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Section: Trpv3 Gene Is a Target Of Mir-103supporting

confidence: 63%

“…Fluorescence measurements in cardiomyocytes have been described previously . The neonatal rat cardiomyocytes were incubated with a working solution containing 10 μmol L −1 Fluo‐3/AM (acetoxymethyl ester form, Molecular Probes, St. Louis, MO, USA) and 0.03% Pluronic F‐127 at 37°C for 40 minutes.…”

Section: Methodsmentioning

confidence: 99%

MiR‐103 inhibiting cardiac hypertrophy through inactivation of myocardial cell autophagy via targeting TRPV3 channel in rat hearts

Ren

Mingyao

et al. 2019

J Cellular Molecular Medi

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“…In rats, the TRPV3 activator Carvacrol is capable to increase the fibrosis produced by aortic banding and it potentiates the AngII-induced increase in Ca 2+ concentration as well as the in vitro proliferation of CFs. In contrast, treatment with siRNA directed against TRPV3 reduces the AngII-induced collagen expression [93]. Another TRPV channel, TRPV4, which determines myofibroblast differentiation and fibrosis in the lung [94], was also shown to mediate TGF-β1-induced differentiation of CFs into myofibroblasts [95].…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-II-Evoked Ca2+ Entry in Murine Cardiac Fibroblasts Does Not Depend on TRPC Channels

Londoño

Marx

Kraft

et al. 2020

Cells

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TRPC proteins form cation conducting channels regulated by different stimuli and are regulators of the cellular calcium homeostasis. TRPC are expressed in cardiac cells including cardiac fibroblasts (CFs) and have been implicated in the development of pathological cardiac remodeling including fibrosis. Using Ca2+ imaging and several compound TRPC knockout mouse lines we analyzed the involvement of TRPC proteins for the angiotensin II (AngII)-induced changes in Ca2+ homeostasis in CFs isolated from adult mice. Using qPCR we detected transcripts of all Trpc genes in CFs; Trpc1, Trpc3 and Trpc4 being the most abundant ones. We show that the AngII-induced Ca2+ entry but also Ca2+ release from intracellular stores are critically dependent on the density of CFs in culture and are inversely correlated with the expression of the myofibroblast marker α-smooth muscle actin. Our Ca2+ measurements depict that the AngII- and thrombin-induced Ca2+ transients, and the AngII-induced Ca2+ entry and Ca2+ release are not affected in CFs isolated from mice lacking all seven TRPC proteins (TRPC-hepta KO) compared to control cells. However, pre-incubation with GSK7975A (10 µM), which sufficiently inhibits CRAC channels in other cells, abolished AngII-induced Ca2+ entry. Consequently, we conclude the dispensability of the TRPC channels for the acute neurohumoral Ca2+ signaling evoked by AngII in isolated CFs and suggest the contribution of members of the Orai channel family as molecular constituents responsible for this pathophysiologically important Ca2+ entry pathway.

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“…In rat cardiac fibroblasts, the activation of TRPV3 by Carvacrol increases cell proliferation and upregulates the expression of collagen and TGF-β1. In a pressure-overload hypertrophy rat model, Carvacrol activation of TRPV3 exacerbates heart function and increases fibrosis [182,183]. These results suggest that TRPV3 could be involved in TGF-β1-induced fibroblast proliferation during cardiac fibrosis, but additional experiments with knockout mice are required to conclusively define the channel's role.…”

Section: Trpv3 and Cardiac Fibrosismentioning

confidence: 99%

“…TRPV3 is expressed in the peripheral neurons and various other cell types. It has recently been found that TRPV3 is also expressed in cardiac myocytes [182] and fibroblasts [183], as detected by PCR and western blotting (WB). In rat cardiac fibroblasts, the activation of TRPV3 by Carvacrol increases cell proliferation and upregulates the expression of collagen and TGF-β1.…”

Section: Trpv3 and Cardiac Fibrosismentioning

confidence: 99%

Ca2+ Signaling in Cardiac Fibroblasts and Fibrosis-Associated Heart Diseases

Feng

Armillei

et al. 2019

JCDD

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Cardiac fibrosis is the excessive deposition of extracellular matrix proteins by cardiac fibroblasts and myofibroblasts, and is a hallmark feature of most heart diseases, including arrhythmia, hypertrophy, and heart failure. This maladaptive process occurs in response to a variety of stimuli, including myocardial injury, inflammation, and mechanical overload. There are multiple signaling pathways and various cell types that influence the fibrogenesis cascade. Fibroblasts and myofibroblasts are central effectors. Although it is clear that Ca2+ signaling plays a vital role in this pathological process, what contributes to Ca2+ signaling in fibroblasts and myofibroblasts is still not wholly understood, chiefly because of the large and diverse number of receptors, transporters, and ion channels that influence intracellular Ca2+ signaling. Intracellular Ca2+ signals are generated by Ca2+ release from intracellular Ca2+ stores and by Ca2+ entry through a multitude of Ca2+-permeable ion channels in the plasma membrane. Over the past decade, the transient receptor potential (TRP) channels have emerged as one of the most important families of ion channels mediating Ca2+ signaling in cardiac fibroblasts. TRP channels are a superfamily of non-voltage-gated, Ca2+-permeable non-selective cation channels. Their ability to respond to various stimulating cues makes TRP channels effective sensors of the many different pathophysiological events that stimulate cardiac fibrogenesis. This review focuses on the mechanisms of Ca2+ signaling in fibroblast differentiation and fibrosis-associated heart diseases and will highlight recent advances in the understanding of the roles that TRP and other Ca2+-permeable channels play in cardiac fibrosis.

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Transient receptor potential vanilloid-3 (TRPV3) activation plays a central role in cardiac fibrosis induced by pressure overload in rats via TGF-β1 pathway

Cited by 27 publications

References 31 publications

MiR‐103 inhibiting cardiac hypertrophy through inactivation of myocardial cell autophagy via targeting TRPV3 channel in rat hearts

MiR‐103 inhibiting cardiac hypertrophy through inactivation of myocardial cell autophagy via targeting TRPV3 channel in rat hearts

Angiotensin-II-Evoked Ca2+ Entry in Murine Cardiac Fibroblasts Does Not Depend on TRPC Channels

Ca2+ Signaling in Cardiac Fibroblasts and Fibrosis-Associated Heart Diseases

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