Identification of Cardiac Expression Pattern of Transient Receptor Potential Vanilloid Type 1 (TRPV1) Receptor using a Transgenic Reporter Mouse Model

Hong, Juan; Lisco, Amanda M.; Rudebush, Tara; Yu, Li; Gao, Lie; Kitzerow, Oliver; Zucker, Irving H.; Wang, Hanjun

doi:10.1016/j.neulet.2020.135320

Cited by 15 publications

(19 citation statements)

References 22 publications

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“…This conflicts with our lack of functional responses to capsaicin in primary cardiomyocytes as well as in cardiac cell lines, also backed up by positive controls using sensory neurons and cells expressing mouse TRPV1. More importantly, a TRPV1‐Cre Td‐tomato reporter mouse model also found no evidence for TRPV1 in cardiomyocytes 28 …”

Section: Discussionmentioning

confidence: 98%

“…More importantly, a TRPV1-Cre Td-tomato reporter mouse model also found no evidence for TRPV1 in cardiomyocytes. 28…”

Section: Functional Findings Indicating the Absence Of Trpa1 And Trpv1 In Cardiomyocytesmentioning

confidence: 99%

“…This was shown by western blots, immunohistochemistry, and functional assays, using AITC and capsaicin as agonists 21 . However, in a transgenic reporter mouse model for TRPV1, the ion channel was not expressed in cardiomyocytes, but in nerve endings 28 . Given that there has been discrepancy regarding the expression pattern within the myocardium, the aim of this study was to clarify the presence of functional TRPA1 and TRPV1 in cardiomyocytes.…”

Section: Introductionmentioning

confidence: 95%

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No functional TRPA1 in cardiomyocytes

et al. 2021

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Section: Discussionmentioning

confidence: 98%

“…More importantly, a TRPV1-Cre Td-tomato reporter mouse model also found no evidence for TRPV1 in cardiomyocytes. 28…”

Section: Functional Findings Indicating the Absence Of Trpa1 And Trpv1 In Cardiomyocytesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

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No functional TRPA1 in cardiomyocytes

et al. 2021

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“…Hong et al did whole murine heart staining by GFP-marked TRPV1. They did not detect any trace of the channel in atrial or ventricular cardiomyocytes, but found instead expression in nerve endings and endothelial cells 33 . However, Pei et al and Hurt et al found TRPV1 by western blotting and by immunostaining in primary mouse and rat cardiomyocytes 6 , 34 .…”

Section: Discussionmentioning

confidence: 91%

TRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes

Sattler

El‐Battrawy

Cyganek

et al. 2021

Sci Rep

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The non-selective cation channel transient receptor potential vanilloid 1 (TRPV1) is expressed throughout the cardiovascular system. Recent evidence shows a role for TRPV1 in inflammatory processes. The role of TRPV1 for myocardial inflammation has not been established yet. Human induced pluripotent stem cell (iPSC)-derived cardiomyocytes (hiPSC-CM) from 4 healthy donors were incubated with lipopolysaccharides (LPS, 6 h), TRPV1 agonist capsaicin (CAP, 20 min) or the antagonist capsazepine (CPZ, 20 min). TRPV1 expression was studied by PCR and western blotting. TRPV1 internalization was analyzed by immunofluorescence. Interleukin-6 (IL-6) secretion and phosphorylation of JNK, p38 and ERK were determined by ELISA. TRPV1-associated ion channel current was measured by patch clamp. TRPV1-mRNA and -protein were expressed in hiPSC-CM. TRPV1 was localized in the plasma membrane. LPS significantly increased secretion of IL-6 by 2.3-fold, which was prevented by pre-incubation with CPZ. LPS induced TRPV1 internalization. Phosphorylation levels of ERK, p38 or JNK were not altered by TRPV1 stimulation or inhibition. LPS and IL-6 significantly lowered TRPV1-mediated ion channel current. TRPV1 mediates the LPS-induced inflammation in cardiomyocytes, associated with changes of cellular electrophysiology. LPS-induced inflammation results in TRPV1 internalization. Further studies have to examine the underlying pathways and the clinical relevance of these findings.

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“…Moreover, the mechanistic link between TRPCs and Ca 2+ mishandling has been reported in multiple experimental models of cardiac disease including myocardial infarction [ 66 , 81 , 82 , 83 , 84 , 85 , 86 , 87 ], atrial fibrillation [ 88 , 89 , 90 , 91 ], and iron overload cardiomyopathy [ 92 ]. In addition to TRPCs, other members of the TRP superfamily [ 93 , 94 , 95 ], e.g., melastatin (TRPM) [ 96 , 97 , 98 , 99 , 100 , 101 , 102 , 103 , 104 ] and vanilloid (TRPV) subtypes [ 105 , 106 , 107 , 108 , 109 , 110 , 111 , 112 , 113 , 114 , 115 , 116 ], are also potential candidates mediating the non-canonical Ca 2+ entry into cardiomyocytes.…”

Section: Calcium Cycling In Pressure Overload Hypertrophy Dysthyroidism and Human Heart Failurementioning

confidence: 99%

Calcium and Heart Failure: How Did We Get Here and Where Are We Going?

Siri‐Angkul

Dadfar

Jaleel

et al. 2021

IJMS

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The occurrence and prevalence of heart failure remain high in the United States as well as globally. One person dies every 30 seconds from heart disease. Recognizing the importance of heart failure, clinicians and scientists have sought better therapeutic strategies and even cures for end-stage heart failure. This exploration has resulted in many failed clinical trials testing novel classes of pharmaceutical drugs and even gene therapy. As a result, along the way, there have been paradigm shifts toward and away from differing therapeutic approaches. The continued prevalence of death from heart failure, however, clearly demonstrates that the heart is not simply a pump and instead forces us to consider the complexity of simplicity in the pathophysiology of heart failure and reinforces the need to discover new therapeutic approaches.

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Identification of Cardiac Expression Pattern of Transient Receptor Potential Vanilloid Type 1 (TRPV1) Receptor using a Transgenic Reporter Mouse Model

Cited by 15 publications

References 22 publications

No functional TRPA1 in cardiomyocytes

No functional TRPA1 in cardiomyocytes

TRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes

Calcium and Heart Failure: How Did We Get Here and Where Are We Going?

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