【摘 要】
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Background Angiotensin Ⅱ (Ang Ⅱ)-induced cardiac remodeling with the underlying mechanisms involving inflammation and fibrosis has been well documented.Cytosolic adaptor caspase recruitment domain 9 (
【机 构】
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Beijing An Zhen Hospital, Capital Medical University, Beijing, China;
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Background Angiotensin Ⅱ (Ang Ⅱ)-induced cardiac remodeling with the underlying mechanisms involving inflammation and fibrosis has been well documented.Cytosolic adaptor caspase recruitment domain 9 (CARD9) has been implicated in the innate immune response.We aimed to examine the role of CARD9 in inflammation and cardiac fibrosis induced by Ang Ⅱ.Methods Twomonthold CARD9deficient (CARD9-/-) and wildtype (WT) male mice were infused with Ang Ⅱ (1,500 ng/kg/min) or saline for 7 days.Heart sections were stained with hematoxylin and eosin and Masson trichrome and examined by immunohistochemistry;and activity and protein levels were measured in macrophages obtained from mice.Results:WT mice with Ang Ⅱ infusion showed a marked increase in CARD9+ macrophages in the heart,but CARD9-/-mice showed significantly suppressed macrophage infiltration and expression of proinflammatory cytokines,including interleukin1β (IL1 β) and connective tissue growth factor (CTGF).Importantly,Ang Ⅱ-induced cardiac fibrosis (extracellular matrix and collagen I deposition) was diminished in CARD9-/-hearts,as was the expression of transforming growth factorβ (TGFβ) and level of myofibroblasts positive for αsmooth muscle actin (αSMA).Furthermore,Ang Ⅱ activation of nuclear factor κ B (NF κ B),JNK and p38 mitogenactivated protein kinases (MAPKs) in WT macrophages was reduced in CARD9-/-macrophages.Conclusion CARD9 plays an important role in regulating cardiac inflammation and fibrosis in response to elevated Ang Ⅱ.
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