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Silencing of the angiotensinogen gene in adipocytes decreases markers of inflammation, lipogenesis and adipogenesis
Author(s) -
Xin Wenting,
Kalupahaishan S.,
Booker Suzanne,
Siriwardhalin,
MoustaidMoussa Naima
Publication year - 2011
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.25.1_supplement.775.14
Subject(s) - adipogenesis , gene silencing , lipogenesis , inflammation , medicine , endocrinology , chemistry , gene , adipose tissue , biology , biochemistry
Several studies implicated the renin angiotensin system (RAS) and its precursor, angiotensinogen (Agt), in metabolic/inflammatory disorders associated with obesity. Indeed, genetic inactivation of Agt reduced adiposity, and improved inflammation and insulin sensitivity, while overexpression of Agt in adipose tissue significantly increased adipocytes hypertrophy, insulin resistance and inflammation. We propose that these effects are tightly associated with adipose Agt expression. To test this hypothesis, 3T3‐L1 preadipocytes were transfected with siRNA targeting Agt. Lipid accumulation and adipogenesis were subsequently assessed following differentiation of transfected cells. As expected, gene silencing led to low to undetectable levels of Agt expression in mature adipocytes. Adipocytes lacking Agt accumulated significantly less lipids (p<0.05), expressed lower levels of adipogenic maker PPAR‐gamma (p<0.05) and secreted less IL‐6(P<0.01) and MCP‐1(P<0.01). In summary, these studies indicate an important role for Agt in adipose tissue development and immune functions, and further support a potential role for adipose RAS as a therapeutic target in obesity‐related metabolic and inflammatory disorders.