Phosphorylation of STAT proteins by recombinant human IL-6 in immortalized human chondrocyte cell lines, T/C28a2 and C28/I2

Evan C Meszaros,1 Charles J Malemud1,2 1Department of Medicine, Division of Rheumatic Diseases, 2Department of Anatomy, Case Western Reserve University School of Medicine and University Hospitals Cleveland Medical Center, Cleveland, OH, USA Abstract: Two immortalized human juvenile chondrocyte cell...

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Autores principales:	Meszaros EC, Malemud CJ
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2017
Materias:	Chondrocyte Cell Lines Cytokine Human Signal Transduction Pathology RB1-214 Therapeutics. Pharmacology RM1-950
Acceso en línea:	https://doaj.org/article/2d08aec397ed4538b3e49289b9a93875
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spelling	oai:doaj.org-article:2d08aec397ed4538b3e49289b9a938752021-12-02T00:04:07ZPhosphorylation of STAT proteins by recombinant human IL-6 in immortalized human chondrocyte cell lines, T/C28a2 and C28/I21178-7031https://doaj.org/article/2d08aec397ed4538b3e49289b9a938752017-09-01T00:00:00Zhttps://www.dovepress.com/phosphorylation-of-stat-proteins-by-recombinant-human-il-6-in-immortal-peer-reviewed-article-JIRhttps://doaj.org/toc/1178-7031Evan C Meszaros,1 Charles J Malemud1,2 1Department of Medicine, Division of Rheumatic Diseases, 2Department of Anatomy, Case Western Reserve University School of Medicine and University Hospitals Cleveland Medical Center, Cleveland, OH, USA Abstract: Two immortalized human juvenile chondrocyte cell lines, T/C28a2 and C28/I2, were employed to determine the extent to which recombinant human (rh) IL-6, a known cytokine activator of the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway in many cell types, caused STAT proteins to be phosphorylated. The results showed that STAT3 was constitutively phosphorylated in the absence of rhIL-6 in T/C28a2 chondrocytes. However, C28/I2 chondrocytes treated with rhIL-6 caused STAT1, STAT3, and STAT5 to be phosphorylated without altering total unphosphorylated STAT proteins. STAT3 phosphorylation in response to rhIL-6 in T/C28a and C28/I2 chondrocytes was efficiently blocked by the JAK3-selective inhibitor WHI-P131 (Janex-1) and by soluble IL-6 receptor-α (sIL-6R). However, the combination of rhIL-6 and ruxolitinib, a JAK1/JAK2-selective inhibitor, was a less effective inhibitor of STAT protein activation. These findings showed that rhIL-6 activated STAT proteins in the C28/I2 chondrocyte cell line. STAT protein phosphorylation could be blocked by a JAK3-selective inhibitor or by the combination of rhIL-6 and sIL-6R. Keywords: chondrocyte cell lines, cytokine, human, signal transductionMeszaros ECMalemud CJDove Medical PressarticleChondrocyte Cell LinesCytokineHumanSignal TransductionPathologyRB1-214Therapeutics. PharmacologyRM1-950ENJournal of Inflammation Research, Vol Volume 10, Pp 143-150 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Chondrocyte Cell Lines Cytokine Human Signal Transduction Pathology RB1-214 Therapeutics. Pharmacology RM1-950
spellingShingle	Chondrocyte Cell Lines Cytokine Human Signal Transduction Pathology RB1-214 Therapeutics. Pharmacology RM1-950 Meszaros EC Malemud CJ Phosphorylation of STAT proteins by recombinant human IL-6 in immortalized human chondrocyte cell lines, T/C28a2 and C28/I2
description	Evan C Meszaros,1 Charles J Malemud1,2 1Department of Medicine, Division of Rheumatic Diseases, 2Department of Anatomy, Case Western Reserve University School of Medicine and University Hospitals Cleveland Medical Center, Cleveland, OH, USA Abstract: Two immortalized human juvenile chondrocyte cell lines, T/C28a2 and C28/I2, were employed to determine the extent to which recombinant human (rh) IL-6, a known cytokine activator of the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway in many cell types, caused STAT proteins to be phosphorylated. The results showed that STAT3 was constitutively phosphorylated in the absence of rhIL-6 in T/C28a2 chondrocytes. However, C28/I2 chondrocytes treated with rhIL-6 caused STAT1, STAT3, and STAT5 to be phosphorylated without altering total unphosphorylated STAT proteins. STAT3 phosphorylation in response to rhIL-6 in T/C28a and C28/I2 chondrocytes was efficiently blocked by the JAK3-selective inhibitor WHI-P131 (Janex-1) and by soluble IL-6 receptor-α (sIL-6R). However, the combination of rhIL-6 and ruxolitinib, a JAK1/JAK2-selective inhibitor, was a less effective inhibitor of STAT protein activation. These findings showed that rhIL-6 activated STAT proteins in the C28/I2 chondrocyte cell line. STAT protein phosphorylation could be blocked by a JAK3-selective inhibitor or by the combination of rhIL-6 and sIL-6R. Keywords: chondrocyte cell lines, cytokine, human, signal transduction
format	article
author	Meszaros EC Malemud CJ
author_facet	Meszaros EC Malemud CJ
author_sort	Meszaros EC
title	Phosphorylation of STAT proteins by recombinant human IL-6 in immortalized human chondrocyte cell lines, T/C28a2 and C28/I2
title_short	Phosphorylation of STAT proteins by recombinant human IL-6 in immortalized human chondrocyte cell lines, T/C28a2 and C28/I2
title_full	Phosphorylation of STAT proteins by recombinant human IL-6 in immortalized human chondrocyte cell lines, T/C28a2 and C28/I2
title_fullStr	Phosphorylation of STAT proteins by recombinant human IL-6 in immortalized human chondrocyte cell lines, T/C28a2 and C28/I2
title_full_unstemmed	Phosphorylation of STAT proteins by recombinant human IL-6 in immortalized human chondrocyte cell lines, T/C28a2 and C28/I2
title_sort	phosphorylation of stat proteins by recombinant human il-6 in immortalized human chondrocyte cell lines, t/c28a2 and c28/i2
publisher	Dove Medical Press
publishDate	2017
url	https://doaj.org/article/2d08aec397ed4538b3e49289b9a93875
work_keys_str_mv	AT meszarosec phosphorylationofstatproteinsbyrecombinanthumanil6inimmortalizedhumanchondrocytecelllinestc28a2andc28i2 AT malemudcj phosphorylationofstatproteinsbyrecombinanthumanil6inimmortalizedhumanchondrocytecelllinestc28a2andc28i2
_version_	1718403916865994752

Phosphorylation of STAT proteins by recombinant human IL-6 in immortalized human chondrocyte cell lines, T/C28a2 and C28/I2

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