Wanninger, Josef and Neumeier, Markus and Weigert, Johanna and Bauer, Sabrina and Weiss, Thomas S. and Schaeffler, Andreas and Krempl, Corinna and Bleyl, Cornelia and Aslanidis, Charalampos and Schoelmerich, Juergen and Buechler, Christa (2009) Adiponectin-stimulated CXCL8 release in primary human hepatocytes is regulated by ERK1/ERK2, p38 MAPK, NF-kappa B, and STAT3 signaling pathways. AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 297 (3). G611-G618. ISSN 0193-1857, 1522-1547
Full text not available from this repository. (Request a copy)Abstract
Wanninger J, Neumeier M, Weigert J, Bauer S, Weiss TS, Schaffler A, Krempl C, Bleyl C, Aslanidis C, Scholmerich J, Buechler C. Adiponectin-stimulated CXCL8 release in primary human hepatocytes is regulated by ERK1/ERK2, p38 MAPK, NF-kappa B, and STAT3 signaling pathways. Am J Physiol Gastrointest Liver Physiol 297: G611-G618, 2009. First published July 16, 2009; doi: 10.1152/ajpgi.90644.2008.-Adiponectin is believed to exert hepatoprotective effects and induces CXCL8, a chemokine that functions as a survival factor, in vascular cells. In the current study, it is demonstrated that adiponectin also induces CXCL8 expression in primary human hepatocytes but not in hepatocellular carcinoma cell lines. Knock down of the adiponectin receptor (AdipoR) 1 or AdipoR2 by small-interfering RNA indicates that AdipoR1 is involved in adiponectin-stimulated CXCL8 release. Adiponectin activates nuclear factor (NF)-kappa B in primary hepatocytes and pharmacological inhibition of NF-kappa B, the p38 mitogen-activated protein kinase, and extracellular signal-regulated kinase (ERK) 1/ERK2 reduces adiponectin-mediated CXCL8 secretion. Furthermore, adiponectin also activates STAT3 involved in interleukin (IL)-6 and leptin-mediated CXCL8 induction in primary hepatocytes. Inhibition of JAK2 by AG-490 does not abolish adiponectin-stimulated CXCL8, indicating that this kinase is not involved. Pretreatment of primary cells with "STAT3 Inhibitor VI," however, elevates hepatocytic CXCL8 secretion, demonstrating that STAT3 is a negative regulator of CXCL8 in these cells. In accordance with this assumption, IL-6, a well-characterized activator of STAT3, reduces hepatocytic CXCL8. Therefore, adiponectin-stimulated induction of CXCL8 seems to be tightly controlled in primary human hepatocytes, whereas neither NF-kappa B, STAT3, nor CXCL8 are influenced in hepatocytic cell lines. CXCL8 is a survival factor, and its upregulation by adiponectin may contribute to the hepatoprotective effects of this adipokine.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | FATTY LIVER-DISEASE; INTERLEUKIN-8 PRODUCTION; IL-8 PRODUCTION; IN-VITRO; CELLS; RECEPTORS; PROTEIN; TRANSCRIPTION; ACTIVATION; EXPRESSION; adiponectin; hepatocyte; nuclear factor-kappa B; adiponectin receptor 1; STAT3; extracellular signal-regulated kinase; mitogen-activated protein kinase |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Chirurgie Medicine > Lehrstuhl für Innere Medizin I Medicine > Lehrstuhl für Kinder- und Jugendmedizin Medicine > Lehrstuhl für Klinische Chemie und Laboratoriumsmedizin |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 07 Sep 2020 09:41 |
| Last Modified: | 07 Sep 2020 09:41 |
| URI: | https://pred.uni-regensburg.de/id/eprint/28423 |
Actions (login required)
 |
View Item |
