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p38 mitogen-activated protein kinase contributes to TNFメ-induced endothelial tube formation of bone-marrow-derived mesenchymal stem cells by activating the JAK/STAT/TIE2 signaling axis
Sukjin Ou 1 (Graduate student), Tae Yoon Kim 1 (Undergraduate student), Euitaek Jung 1 (Graduate student), Soon Young Shin 1,2,* (Professor)
1Biological Sciences and 2Cancer and Metabolism Institute, Konkuk University
Bone marrow-derived mesenchymal stem cells (BM-MSCs) can differentiate into endothelial cells in an inflammatory microenvironment. However, the regulatory mechanisms underlying this process are not entirely understood. Here, we found that TIE2 in BM-MSCs was upregulated at the transcriptional level after stimulation with tumor necrosis factor-alpha (TNFメ), a major pro-inflammatory cytokine. Additionally, the STAT-binding sequence within the proximal region of TIE2 was necessary for TNFメ-induced TIE2 promoter activation. TIE2 and STAT3 knockdown reduced TNFメ-induced endothelial tube formation in BM-MSCs. Among the major TNFメ-activated MAP kinases (ERK1/2, JNK1/2, and p38 MAPK) in BM-MSCs, only inhibition of the p38 kinase abrogated TNFメ-induced TIE2 upregulation by inhibiting the JAK-STAT signaling pathway. These findings suggest that p38 MAP contributes to the endothelial differentiation of BM-MSCs by activating the JAK-STAT-TIE2 signaling axis in the inflammatory microenvironment.
Abstract, Accepted Manuscript [Submitted on August 22, 2023, Accepted on October 28, 2023]
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