Potential involvement of S1PR1/STAT3 signaling pathway in cardiac valve damage due to rheumatic heart disease
作者： X.-D. Wu , Z.-Y. Zeng , D.-P. Gong , J.-L. Wen , F. Huang
DOI: 10.1080/10520295.2019.1574028
关键词: Western blot 、 STAT3 、 S1PR1 、 STAT protein 、 Immunology 、 Stat3 Signaling Pathway 、 Pathogenesis 、 Fibrosis 、 Heart disease 、 Medicine
摘要: Rheumatic heart disease (RHD) is a public health burden in developing countries. Th17 cell-associated cytokines might play role the pathogenesis and development of RHD, but specific molecular mechanism not completely understood. We investigated potential sphingosine-1-phosphate receptor 1 (S1PR1)/signal transducer activator transcription 3 (STAT3) signaling pathway cardiac valve damage rat model RHD. used 20 Lewis rats divided randomly into control RHD groups. The was constructed by injecting inactivated group A Streptococci complete Freund's adjuvant (CFA). were injected with normal saline CFA. cell-related measured ELISA. Fibrosis assessed histological examination. RT-qPCR western blot to detect expression S1PR1 STAT3/phosphorylated STAT3 (p-STAT3). S1PR1/STAT3 activated model. Compared group, serum levels IL-17 IL-21 associated cells increased significantly group; collagen volume fraction also substantially increased. be involved induced regulating cells.
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