Influence of mesenchymal stem cells on respiratory distress syndrome in newborn swines via the JAK-STAT signaling pathway.

信号转导 JAK-STAT信号通路 贾纳斯激酶 斯达 车站3 磷酸化 癌症研究 状态4 生物 STAT蛋白 间充质干细胞 细胞生物学 免疫学 医学 酪氨酸激酶
作者
Wang Hz,Chunbo Yang,Zhang By,Li N,Zhiyong Han,F Chen
出处
期刊:PubMed 卷期号:23 (17): 7550-7556 被引量:5
标识
DOI:10.26355/eurrev_201909_18872
摘要

Acute respiratory distress syndrome (ARDS) threatens humans' health worldwide, causing huge labor and economic cost investment. This study aims to explore whether mesenchymal stem cells (MSCs) affect RDS in newborn swines via the Janus kinase-signal transducers and activators of transcription (JAK-STAT) signaling pathway by the establishment of the model of the disease.The phosphorylation of the JAK-STAT signal transduction proteins was first detected via Western blotting to verify the regulatory effect of MSCs on RDS in newborn swines through the JAK-STAT signaling pathway. Then, the Reverse Transcription-Polymerase Chain Reaction (RT-PCR) was utilized to analyze the influences of the injection of MSCs into the blood of newborn model RDS swines on inflammatory factors in vivo. To further demonstrate the signal transduction function put forwarded, the RT-PCR and enzyme-linked immunosorbent assay (ELISA) were adopted to analyze the influences of the JAK-STAT signaling pathway inhibitor on the expression of the signature proteins of RDS in newborn swines and the changes in the inflammatory factors.MSCs induced the phosphorylation of JAK and STAT, and they activated the JAK-STAT signal transduction of RDS in newborn swines. Compared with those in normal saline group, the interleukin (IL)-2, IL-6, IL-8, and tumor necrosis factor-α (TNF-α) expression levels in MSC group were increased, namely, MSCs substantially promoted their expression levels (p<0.05), but those of IL-10 and IL-13 were significantly decreased (p<0.05).The inhibitor of the JAK-STAT signaling pathway can suppress the therapeutic effect of MSCs on RDS in newborn swines.
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