Abstract

Adiponectin is one of the few peptides secreted by fat known to have anti-inflammatory properties. Obesity in humans is associated with low levels of circulating adiponectin. Adiponectin deficiency could potentially lead to a proinflammatory milieu, increasing susceptibility to progression of cardiovascular diseases and other inflammatory conditions. Previous studies from our lab have shown that adiponectin deficiency in mice did not lead to statistically significant increases in circulating levels of proinflammatory cytokines under basal conditions or in response to low dose infusion of Angiotensin II (ANGII). The present study evaluates the effect of chronic ANGII infusion on expression of cytokines in the livers of female C57BL/6J and adiponectin deficient mice (Adipo -/-). Female mice (24-28wks), were implanted with osmotic pump containing either ANG II (800 ng/Kg /min) or saline. Blood samples and tissue were collected at the end of 14 days. Liver tissue expression of the cytokines were quantified using real-time PCR (BioRad CFX 96 thermocycler) and SYBR Green mastermix. Data was normalized to the expression of GAPDH. Expression of cytokines IL6, IL8, IL17a was undetectable in the liver tissue of C57BL/6J and Adiponectin deficient mice. Angiotensin II infusion did not produce detectable changes in cytokine expression in either group. Expression of TNFα, TGF β , and adhesion molecules such as E-Selectin, VCAM1, Collagen1a1 in Adipo-/- mice were comparable to that of C57BL/6J mice. ANGII infusion did not produce statistically significant changes in these biomarkers either. Finally, expression of ANGII signaling components such as Angiotensin type 1 receptor (AT 1 ), NFκB and PPARγ were robustly expressed in both C57BL/6J and adiponectin deficient mice. In conclusion, chronic infusion of ANGII in Adiponectin deficiency did not result in a significant increases in expression of markers of proinflammatory milieu in the liver tissue.

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