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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2024.5
- 수록면
- 238 - 243 (6page)
- DOI
- https://doi.org/10.5483/BMBRep.2023-0152
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초록· 키워드
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Bone marrow-derived mesenchymal stem cells (BM-MSCs) candifferentiate into endothelial cells in an inflammatory microenvironment. However, the regulatory mechanisms underlyingthis process are not entirely understood. Here, we found thatTIE2 in BM-MSCs was upregulated at the transcriptional levelafter stimulation with tumor necrosis factor-alpha (TNFα), a majorpro-inflammatory cytokine. Additionally, the STAT-binding sequence within the proximal region of TIE2 was necessary forTNFα-induced TIE2 promoter activation. TIE2 and STAT3 knockdown reduced TNFα-induced endothelial tube formation in BM-MSCs. Among the major TNFα-activated MAP kinases (ERK1/2,JNK1/2, and p38 MAPK) in BM-MSCs, only inhibition of the p38kinase abrogated TNFα-induced TIE2 upregulation by inhibitingthe JAK-STAT signaling pathway. These findings suggest that p38MAP contributes to the endothelial differentiation of BM-MSCsby activating the JAK-STAT-TIE2 signaling axis in the inflammatory microenvironment.
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