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Verfasst von:Sattler, Katherine [VerfasserIn]   i
 El-Battrawy, Ibrahim [VerfasserIn]   i
 Cyganek, Lukas [VerfasserIn]   i
 Lang, Siegfried [VerfasserIn]   i
 Lan, Huan [VerfasserIn]   i
 Li, Xin [VerfasserIn]   i
 Zhao, Zhihan [VerfasserIn]   i
 Utikal, Jochen [VerfasserIn]   i
 Wieland, Thomas [VerfasserIn]   i
 Borggrefe, Martin [VerfasserIn]   i
 Zhou, Xiao-Bo [VerfasserIn]   i
 Akın, Ibrahim [VerfasserIn]   i
Titel:TRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes
Verf.angabe:Katherine Sattler, Ibrahim El-Battrawy, Lukas Cyganek, Siegfried Lang, Huan Lan, Xin Li, Zhihan Zhao, Jochen Utikal, Thomas Wieland, Martin Borggrefe, Xiaobo Zhou and Ibrahim Akin
E-Jahr:2021
Jahr:19 July 2021
Umfang:12 S.
Fussnoten:Published: 19 July 2021 ; Gesehen am 31.05.2022
Titel Quelle:Enthalten in: Scientific reports
Ort Quelle:[London] : Springer Nature, 2011
Jahr Quelle:2021
Band/Heft Quelle:11(2021), Artikel-ID 14689, Seite 1-12
ISSN Quelle:2045-2322
Abstract: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.
DOI:doi:10.1038/s41598-021-93958-3
URL:kostenfrei: Volltext: https://doi.org/10.1038/s41598-021-93958-3
 kostenfrei: Volltext: https://www.nature.com/articles/s41598-021-93958-3
 DOI: https://doi.org/10.1038/s41598-021-93958-3
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Cardiovascular biology
 Mechanisms of disease
K10plus-PPN:180534854X
Verknüpfungen:→ Zeitschrift
 
 
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