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UCP2 protects hypothalamic cells from TNF‐α‐induced damage
Author(s) -
Degasperi Giovanna R.,
Romanatto Talita,
Denis Raphael G.P.,
Araújo Eliana P.,
Moraes Juliana C.,
Inada Natália M.,
Vercesi Aníbal E.,
Velloso Lício A.
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.08.006
Subject(s) - tumor necrosis factor alpha , hypothalamus , oxidative stress , endocrinology , apoptosis , medicine , cytokine , chemistry , biology , microbiology and biotechnology , biochemistry
Uncoupling protein 2 (UCP2) is highly expressed in the hypothalamus; however, little is known about the functions it exerts in this part of the brain. Here, we hypothesized that UCP2 protects hypothalamic cells from oxidative and pro‐apoptotic damage generated by inflammatory stimuli. Intracerebroventricular injection of tumor necrosis factor alpha (TNF‐α)‐induced an increase of UCP2 expression in the hypothalamus, which was accompanied by increased expression of markers of oxidative stress and pro‐apoptotic proteins. The inhibition of UCP2 expression by an antisense oligonucleotide enhanced the damaging effects of TNF‐α. Conversely, increasing the hypothalamic expression of UCP2 by cold exposure reversed most of the effects of the cytokine. Thus, UCP2 acts as a protective factor against cellular damage induced by an inflammatory stimulus in the hypothalamus.