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IL-10 attenuates TNF- -induced NF B pathway activation and cardiomyocyte apoptosis
Author(s) -
Sanjiv Dhingra,
Alok Sharma,
Rakesh C. Arora,
Ján Slezák,
Pawan K. Singal
Publication year - 2009
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvp040
Subject(s) - mapk/erk pathway , tumor necrosis factor alpha , p38 mitogen activated protein kinases , phosphorylation , kinase , apoptosis , microbiology and biotechnology , signal transduction , chemistry , protein kinase a , oxidative stress , mitogen activated protein kinase , extracellular , nf κb , cancer research , biology , endocrinology , biochemistry
We have recently reported that tumour necrosis factor-alpha (TNF-alpha) increases oxidative stress and apoptosis in cardiomyocytes by upregulating p38 mitogen-activated protein (MAP) kinase (MAPK) phosphorylation. Interleukin-10 (IL-10) blocked these effects of TNF-alpha by upregulating extracellular signal-regulated kinase 1/2 (ERK 1/2) MAPK phosphorylation. However, the precise site of this IL-10 action is still unknown, and this is investigated in the present study.

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