Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 234, Issue 12, Pages 23448-23460Publisher
WILEY
DOI: 10.1002/jcp.28914
Keywords
angiogenesis; endothelial progenitor cells; ischemic stroke; migration; NF-kappa B signaling pathway; proliferation; PTGS2
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Funding
- Guangzhou Science and Technology Project [201604020003]
- National Natural Science Foundation of China [81760413, 81760902]
- TCM Science and Technology in Guangdong Provincial Hospital of Chinese Medicine [YN2016ZD04]
- Tackling Key Problems in Science and Technology and Trial Production of New Products in Liuzhou [2014J030407, 2016G020213]
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The objective of the current study is to investigate the effect of PTGS2 on proliferation, migration, angiogenesis and apoptosis of endothelial progenitor cells (EPCs) in mice with ischemic stroke through the NF-kappa B signaling pathway. Middle cerebral artery occlusion (MCAO) model was established in mice. EPCs were identified, in which ectopic expression and depletion experiments were conducted. The mRNA and protein expression of related factors in tissues and cells were measured. Besides, proliferation, migration, angiogenesis, and apoptosis, as well as cell cycle distribution, of cells were determined. MCAO mice showed overexpression of interleukin-6 (IL-6), IL-17, and IL-23, and increased positive protein expression of PTGS2, as well as expression of PTGS2, nuclear factor-kappa B (NF-kappa B), tumor suppressor region 1 (TSP-1) and Bcl-2-associated X protein (Bax), but underexpression of vascular endothelial growth factor (VEGF), S-phase kinase associated protein 2 (Skp2), and B-cell lymphoma 2 (Bcl-2). Moreover, ectopic expression of tumor necrosis factor-alpha significantly elevated the expression of PTGS2, NF-kappa B, TSP-1, and Bax, as well as cell apoptosis and cell cycle arrest, but decreased the expression of VEGF, Skp2, and Bcl-2, as well as proliferation, migration and angiogenesis of EPCs, and the PTGS2-siRNA group showed an opposite trend. Taken together, we conclude that the specific knockdown of PTGS2 expression could repress the NF-kappa B signaling pathway, thereby inhibits apoptosis and promotes proliferation, migration and angiogenesis of EPCs, providing protective effect on mice with ischemic stroke.
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