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Time‐course expression of PGC‐1 in acute inflammation
Author(s) -
Llimona Flávia,
LimaSalgado Thais Martins,
Souza Heraldo Possolo
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1016.1
Subject(s) - inflammation , medicine , endocrinology , mitochondrial biogenesis , biology , chemistry , mitochondrion , microbiology and biotechnology
Peroxisomal proliferator‐activated receptor coactivator 1 (PGC1) controls expression of several genes involved in cell energy homeostasis. PGC1 isoforms (α and β) are present in tissues with high oxidative metabolism and enhance mitochondrial biogenesis, β‐oxidation of fatty acids and gluconeogenesis in response to exposure to cold, fasting and exercise. We hypothesized that PGC1 expression may also be modulated during inflammatory response. Systemic inflammation was induced in male Wistar rats by acute pancreatitis (AP), caused by retrograde perfusion of sodium taurocholate into biliopancreatic duct. Animals were sacrificed after 2, 24 and 48h and PGC1 α and β expression were measured by quantitative PCR. Systemic inflammation was confirmed by increased white blood cell count and circulating cytokines. PGC1α expression was increased in liver and spleen (2.0±0.1 and 4.3±0.5 fold vs sham, respectively), 48h after AP. At same time, lungs and leukocytes presented enhanced PGC1β expression (2.2±0.3 and 6.2±1.3 fold vs sham, respectively). On the other hand, PGC1β expression was decreased in lymph nodes 2h after AP induction (0.5±0,1 vs sham). Thus, we conclude that during systemic inflammation there is increased expression of PGC1α and β especially in the later stages of the disease, which may be related to the increasing demand of energy in different tissues. Financial Support: CAPES, FAPESP# 09/1141‐1