No functional TRPA1 in cardiomyocytes

Hoebart, Clara; Rojas-Galvan, Natalia S; Ciotu, Cosmin I; Aykaç, İbrahim; Reissig, Lukas F.; Weninger, Wolfgang J.; Kiss, Attila; Podesser, Bruno K.; Fischer, Michael J.M.; Heber, Stefan

doi:10.1111/apha.13659

Cited by 16 publications

(23 citation statements)

References 53 publications

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“…Considering these publications altogether, the scales seem to be in favour of an absence rather than of a presence of TRPA1 and TRPV1 in ventricular myocytes. Hoebart et al 1 nicely confirmed the efficiency of their proceedings by providing positive controls on DRG neurons which strongly support their conclusions. Others who observed the channels also used several approaches to strengthen their findings.…”

Section: E D I T O R I a L Trpa1 And Trpv1 Do We Hold You In Our Heart?supporting

confidence: 55%

“…Despite these reports, in the study presented in this issue, Hoebart et al 1 were unable to unmask any TRPA1 signature. In freshly isolated mouse cardiomyocytes, they did not find significant Ca 2+ level variations neither after application of AITC nor after application of two other TRPA1 agonists whilst the molecules were efficient on dorsal root ganglion (DRG) neurons known to functionally express TRPA1 9 .…”

mentioning

confidence: 81%

“…It is even harder to prove its absence. In the present study, Hoebart et al 1 searched for the existence of the previously reported TRPA1 in cardiomyocytes, to determine whether it can constitute an interesting target for analgesic treatment. Indeed, similar to bathing in Loch Ness lake could have disastrous consequence in case of previously reported presence of the Monster, targeting TRPA1 for analgesic purpose could have dramatic consequences in case of TRPA1 expression in cardiomyocytes.…”

mentioning

confidence: 98%

“…Negative results contribute to the advancement of knowledge, at least as an argument of debate. A good example is given in this issue of Acta Physiologica by Hoebart et al 1 who found no sign of life of the Transient Receptor Potential Ankyrin 1 (TRPA1) ion channel on cardiomyocytes despite a wide range of experimental approaches. Going fishing is always an exciting adventure, but coming home with the empty net is a bitter experience, especially since you have to convince your entourage that you did your best, but that the sought‐after fish was really absent from this lake, even if others have already reported traces of it.…”

mentioning

confidence: 99%

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TRPA1 and TRPV1, do we hold you in our heart?

Guinamard

Hof

2021

Acta Physiologica

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Section: E D I T O R I a L Trpa1 And Trpv1 Do We Hold You In Our Heart?supporting

confidence: 55%

mentioning

confidence: 81%

mentioning

confidence: 98%

mentioning

confidence: 99%

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TRPA1 and TRPV1, do we hold you in our heart?

Guinamard

Hof

2021

Acta Physiologica

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“…For fluorescent imaging plate reader calcium assays, non-transfected and transfected HEK293T cells (which are widely used for establishing detailed pharmacological and biophysical profiles for drugs and their targets, including experiments involving TRPA1 function [81][82][83]) were seeded at a density of 30,000 cells/well in a black flat-bottom 96-well cell culture plate (Greiner Bio-One, Kremsmünster, Austria) coated with poly-D-lysine (100 mg•mL −1 , Sigma-Aldrich, St. Louis, MO, USA). Then they were loaded with the Calcium 6 dye for two hours (Calcium 6 Kit by Molecular Devices, San Jose, CA, USA) in an extracellular solution.…”

Section: Trpa1 Activity Assaymentioning

confidence: 99%

Effects of Venlafaxine, Risperidone and Febuxostat on Cuprizone-Induced Demyelination, Behavioral Deficits and Oxidative Stress

Mihai

Ungurianu

Ciotu

et al. 2021

IJMS

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Multiple sclerosis (MS) is a demyelinating, autoimmune disease that affects a large number of young adults. Novel therapies for MS are needed considering the efficiency and safety limitations of current treatments. In our study, we investigated the effects of venlafaxine (antidepressant, serotonin-norepinephrine reuptake inhibitor), risperidone (atypical antipsychotic) and febuxostat (gout medication, xanthine oxidase inhibitor) in the cuprizone mouse model of acute demyelination, hypothesizing an antagonistic effect on TRPA1 calcium channels. Cuprizone and drugs were administered to C57BL6/J mice for five weeks and locomotor activity, motor performance and cold sensitivity were assessed. Mice brains were harvested for histological staining and assessment of oxidative stress markers. Febuxostat and metabolites of venlafaxine (desvenlafaxine) and risperidone (paliperidone) were tested for TRPA1 antagonistic activity. Following treatment, venlafaxine and risperidone significantly improved motor performance and sensitivity to a cold stimulus. All administered drugs ameliorated the cuprizone-induced deficit of superoxide dismutase activity. Desvenlafaxine and paliperidone showed no activity on TRPA1, while febuxostat exhibited agonistic activity at high concentrations. Our findings indicated that all three drugs offered some protection against the effects of cuprizone-induced demyelination. The agonistic activity of febuxostat can be of potential use for discovering novel TRPA1 ligands.

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Transient receptor potential vanilloid type 1: cardioprotective effects in diabetic models

Bao,

Gao,

et al. 2023

Channels

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Cardiovascular disease, especially heart failure (HF) is the leading cause of death in patients with diabetes. Individuals with diabetes are prone to a special type of cardiomyopathy called diabetic cardiomyopathy (DCM), which cannot be explained by heart diseases such as hypertension or coronary artery disease, and can contribute to HF. Unfortunately, the current treatment strategy for diabetes-related cardiovascular complications is mainly to control blood glucose levels; nonetheless, the improvement of cardiac structure and function is not ideal. The transient receptor potential cation channel subfamily V member 1 (TRPV1), a nonselective cation channel, has been shown to be universally expressed in the cardiovascular system. Increasing evidence has shown that the activation of TRPV1 channel has a potential protective influence on the cardiovascular system. Numerous studies show that activating TRPV1 channels can improve the occurrence and progression of diabetes-related complications, including cardiomyopathy; however, the specific mechanisms and effects are unclear. In this review, we summarize that TRPV1 channel activation plays a protective role in the heart of diabetic models from oxidation/nitrification stress, mitochondrial function, endothelial function, inflammation, and cardiac energy metabolism to inhibit the occurrence and progression of DCM. Therefore, TRPV1 may become a latent target for the prevention and treatment of diabetes-induced cardiovascular complications.

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No functional TRPA1 in cardiomyocytes

Cited by 16 publications

References 53 publications

TRPA1 and TRPV1, do we hold you in our heart?

TRPA1 and TRPV1, do we hold you in our heart?

Effects of Venlafaxine, Risperidone and Febuxostat on Cuprizone-Induced Demyelination, Behavioral Deficits and Oxidative Stress

Transient receptor potential vanilloid type 1: cardioprotective effects in diabetic models

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