%0 Journal Article
%A Sattler, Katherine
%A El-Battrawy, Ibrahim
%A Cyganek, Lukas
%A Lang, Siegfried
%A Lan, Huan
%A Li, Xin
%A Zhao, Zhihan
%A Utikal, Jochen
%A Wieland, Thomas
%A Borggrefe, Martin
%A Zhou, Xiaobo
%A Akin, Ibrahim
%T TRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes.
%J Scientific reports
%V 11
%N 1
%@ 2045-2322
%C [London]
%I Macmillan Publishers Limited, part of Springer Nature
%M DKFZ-2021-01631
%P 14689
%D 2021
%X 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.
%F PUB:(DE-HGF)16
%9 Journal Article
%$ pmid:34282193
%R 10.1038/s41598-021-93958-3
%U https://inrepo02.dkfz.de/record/169897