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Sattler, Katherine [VerfasserIn]; El-Battrawy, Ibrahim [VerfasserIn]; Cyganek, Lukas [VerfasserIn]; Lang, Siegfried [VerfasserIn]; Lan, Huan [VerfasserIn]; Li, Xin [VerfasserIn]; Zhao, Zhihan [VerfasserIn]; Utikal, Jochen [VerfasserIn]; Wieland, Thomas [VerfasserIn]; Borggrefe, Martin [VerfasserIn]; Zhou, Xiao-Bo [VerfasserIn]; Akın, Ibrahim [VerfasserIn]

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

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  • Medientyp: E-Artikel
  • Titel: TRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes
  • Beteiligte: Sattler, Katherine [VerfasserIn]; El-Battrawy, Ibrahim [VerfasserIn]; Cyganek, Lukas [VerfasserIn]; Lang, Siegfried [VerfasserIn]; Lan, Huan [VerfasserIn]; Li, Xin [VerfasserIn]; Zhao, Zhihan [VerfasserIn]; Utikal, Jochen [VerfasserIn]; Wieland, Thomas [VerfasserIn]; Borggrefe, Martin [VerfasserIn]; Zhou, Xiao-Bo [VerfasserIn]; Akın, Ibrahim [VerfasserIn]
  • Erschienen: 19 July 2021
  • Erschienen in: Scientific reports ; 11(2021), Artikel-ID 14689, Seite 1-12
  • Sprache: Englisch
  • DOI: 10.1038/s41598-021-93958-3
  • ISSN: 2045-2322
  • Identifikator:
  • Schlagwörter: Cardiovascular biology ; Mechanisms of disease
  • Entstehung:
  • Anmerkungen: Published: 19 July 2021
  • Beschreibung: 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.
  • Zugangsstatus: Freier Zugang