TRP Channels in the Heart

Freichel, Marc; Berlin, Michael; Schürger, Alexander; Mathar, Ilka; Bacmeister, Lucas; Medert, Rebekka; Frede, W.; Marx, André; Segin, Sebastian; Londoño, Juan E. Camacho

doi:10.4324/9781315152837-9

Cited by 42 publications

(63 citation statements)

References 1 publication

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“…Although, the induced stress-stimulated contractility, known as the Anrep effect, is diminished in isolated papillary muscles and cardiomyocytes from TRPC6 KO, but not TRPC3 KO mice [59]. In [13,19,27,34,61]. Here, we will discuss the role of TRPC channels in processes related to cardiac ischemic diseases.…”

Section: Role Of Trpc Channels In Cardiac Physiopathologymentioning

confidence: 97%

“…In the case of cardiac fibroblasts, all TRPC isoforms have been described. In particular, the mRNAs of TRPC1, 3, 4 and 6 are detected in mouse cardiac fibroblast [27]. Meanwhile, isolated rat ventricular fibroblasts have significant mRNA expression of TRPC2, 3…”

Section: Trpc Channels In the Cardiovascular Systemmentioning

confidence: 98%

“…Under physiological conditions, the function of TRPC channels in the heart seems not essential [4,57]. As reviewed recently, hearts from knockout (KO) mice of different TRPC channels do not present any significant contractile abnormalities [27].…”

Section: Role Of Trpc Channels In Cardiac Physiopathologymentioning

confidence: 99%

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TRPC channels: Dysregulation and Ca<sup>2+</sup> Mishandling In Ischemic Heart Disease

Falcón

Galeano-Otero

Martín-Bórnez

et al. 2019

Preprint

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Transient receptor potential canonical (TRPC) channels are ubiquitously expressed in excitable and non-excitable cardiac cells where they sense and respond to a wide variety of physical and chemical stimuli. As other TRP, TRPC may form homo or heterotetrameric ion channel, and they can associate with other membrane receptors and ion channels to regulate intracellular calcium concentration. Dysfunctions of TRPC channels are involved in many types of cardiovascular diseases. Significant increase of the expression of different TRPC isoforms has been observed in different animal model of heart infarcts, and in vitro experimental model of ischemia and reperfusion. TRPC-mediated increase of the intracellular Ca2+ concentration seems required for the activation of signaling pathway that plays minor roles in the healthy heart, but they are more relevant for cardiac responses to ischemia, such as the activation of different factors of transcription and cardiac hypertrophy, fibrosis, and angiogenesis. In this review, we will highlight the current knowledge regarding TRPC implication in different cellular processes related to ischemia and reperfusion, and to heart infarction.

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Section: Role Of Trpc Channels In Cardiac Physiopathologymentioning

confidence: 97%

Section: Trpc Channels In the Cardiovascular Systemmentioning

confidence: 98%

See 1 more Smart Citation

TRPC channels: Dysregulation and Ca<sup>2+</sup> Mishandling In Ischemic Heart Disease

Falcón

Galeano-Otero

Martín-Bórnez

et al. 2019

Preprint

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“…So far, the physiological impact of store-operated Ca 2+ entry (SOCE) in adult cardiomyocytes is still under debate, notably due to low-to-moderate expression of their molecular constituents including the molecular complex of STIM1 with Orai1 channels but also with different isoforms of transient receptor potential canonical channels (TRPCs; notably 1, 4, and 5) [1][2][3][4][5]. However, there is now strong evidence revealing a role for SOCE in developmental and pathologic cardiac growth, in which Ca 2+ handling regulation through Ca 2+ -permeable channels is a cornerstone [6][7][8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Specific Upregulation of TRPC1 and TRPC5 Channels by Mineralocorticoid Pathway in Adult Rat Ventricular Cardiomyocytes

Bartoli

Bachiller

Antigny

et al. 2019

Cells

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Whereas cardiac TRPC (transient receptor potential canonical) channels and the associated store-operated Ca2+ entry (SOCE) are abnormally elevated during cardiac hypertrophy and heart failure, the mechanism of this upregulation is not fully elucidated but might be related to the activation of the mineralocorticoid pathway. Using a combination of biochemical, Ca2+ imaging, and electrophysiological techniques, we determined the effect of 24-h aldosterone treatment on the TRPCs/Orai-dependent SOCE in adult rat ventricular cardiomyocytes (ARVMs). The 24-h aldosterone treatment (from 100 nM to 1 µM) enhanced depletion-induced Ca2+ entry in ARVMs, as assessed by a faster reduction of Fura-2 fluorescence decay upon the addition of Mn2+ and increased Fluo-4/AM fluorescence following Ca2+ store depletion. These effects were prevented by co-treatment with a specific mineralocorticoid receptor (MR) antagonist, RU-28318, and they are associated with the enhanced depletion-induced N-[4-[3,5-Bis(trifluoromethyl)-1H-pyrazol-1-yl]phenyl]-4-methyl-1,2,3-thiadiazole-5-carboxamide (BTP2)-sensitive macroscopic current recorded by patch-clamp experiments. Molecular screening by qRT-PCR and Western blot showed a specific upregulation of TRPC1, TRPC5, and STIM1 expression at the messenger RNA (mRNA) and protein levels upon 24-h aldosterone treatment of ARVMs, corroborated by immunostaining. Our study provides evidence that the mineralocorticoid pathway specifically promotes TRPC1/TRPC5-mediated SOCE in adult rat cardiomyocytes.

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“…The receptor has been identified in peripheral terminals of nociceptors innervating the skin (Tsukagoshi et al, 2006), meningeal tissue (Dux et al, 2003), urinary bladder (Liu et al, 2014), respiratory tract (De Logu et al, 2016;Zhao et al, 2016), cochlea (Vass et al, 2004) and the heart (Freichel et al, 2017). Presence of TRPV1 receptors on structures of the central nervous system such as hypothalamus, hippocampus and substantia nigra has been also documented (Cristino et al, 2006).…”

Section: Functions Of the Transient Receptor Potential Vanilloid 1 (Tmentioning

confidence: 99%

Meningeal trigeminovascular reactions mediated by TRPV1 and TRPA1 receptors: effect of adriamycin treatment

Deák

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TRP Channels in the Heart

Cited by 42 publications

References 1 publication

TRPC channels: Dysregulation and Ca<sup>2+</sup> Mishandling In Ischemic Heart Disease

TRPC channels: Dysregulation and Ca<sup>2+</sup> Mishandling In Ischemic Heart Disease

Specific Upregulation of TRPC1 and TRPC5 Channels by Mineralocorticoid Pathway in Adult Rat Ventricular Cardiomyocytes

Meningeal trigeminovascular reactions mediated by TRPV1 and TRPA1 receptors: effect of adriamycin treatment

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