MiR-143-3p targets ATG2B to inhibit autophagy and promote endothelial progenitor cells tube formation in deep vein thrombosis

<sec> <title>Aim:</title> In this study, we aimed to investigate the effects and mechanisms of miRNA-130a in human endothelial progenitor cells (EPCs) involved in Deep vein thrombosis (DVT). </sec> <sec> <title>Methods:</title> EPCs were isolated and identified by cell morphology and surface marker detection. The effect of miR-130a on the migration, invasion and angiogenesis of EPCs in vitro were also detected. In addition, whether miR-130a is involved in the MMP-1 expression and Akt/PI3K/mTOR signaling pathway was also demonstrated. </sec> <sec> <title>Results:</title> Results suggested that miRNA-130a promotes migration, invasion, and tube formation of EPCs by positively regulating the expression of MMP-1 through Akt/PI3K/mTOR signaling pathway. </sec> <sec> <title>Conclusion:</title> Thus, as a potential therapeutic target, miRNA-130a may play an important role in the treatment of DVT. </sec>

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Batroxobin Mobilizes Circulating Endothelial Progenitor Cells in Patients With Deep Vein Thrombosis

Clinical and Applied Thrombosis/Hemostasis ◽

10.1177/1076029609347903 ◽

2009 ◽

Vol 17 (1) ◽

pp. 75-79 ◽

Cited By ~ 11

Author(s):

Lei Zhang ◽

Shi Hong Lu ◽

Li Li ◽

Yu-Guo Tao ◽

Yong Ling Wan ◽

...

Keyword(s):

Deep Vein Thrombosis ◽

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Endothelial Progenitor ◽

Vein Thrombosis ◽

Circulating Endothelial Progenitor Cells ◽

Deep Vein

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Ox-LDL induced endothelial progenitor cells oxidative stress via p38/Keap1/Nrf2 pathway

10.21203/rs.3.rs-348365/v1 ◽

2021 ◽

Author(s):

Qijun Jiang ◽

Chengpeng Li ◽

Zhigang Gong ◽

Zhigang Li ◽

Shifang Ding

Keyword(s):

Oxidative Stress ◽

Membrane Potential ◽

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Nuclear Translocation ◽

Tube Formation ◽

Ros Generation ◽

Endothelial Progenitor ◽

Migration Ability ◽

Nrf2 Pathway

Abstract Background In many studies, endothelial progenitor cells (EPCs) highly expressing antioxidant protein were induced oxidative stress and apoptosis by Oxidized-low density lipoprotein (ox-LDL). Nrf2 which was resently reported to regulate the antioxidant genes and cellular redox regulators was highly expressed in EPCs. However, its role in ox-LDL induced EPCs oxidative stress and apoptosis has not been fully illustrated. Methods EPCs isolated from human peripheral blood mononuclear cells were treated with different concentration of ox-LDL, Keap1 siRNA and a specific p38 MAPK inhibitor SB203580, then used to assay the whole cellular Nrf2 (total Nrf2, t-Nrf2), cytoplasmic Nrf2 (c-Nrf2), nuclear Nrf2 (n- Nrf2), NAD(P) H:quinone oxidoreductase 1 (NQO1) protein levels and Bax /Bcl-2 with western blot, NQO1 mRNA levels with RT-PCR, ROS level with H2DCF-DA, the loss/disruption of mitochondrial membrane potential (MMP) with JC-1, apoptosis with Annexin-V and PI,migration ability with transwell chambers and tube formation. Results The ox-LDL treatment decreased the n-Nrf2/Histone H3 to c-Nrf2/GAPDH ratio, NQO1 mRNA and protein expression levels. Treatment of ox-LDL enhanced the ROS production, induced loss of membrane potential, increase in cell shrinkage, pyknotic nuclei and apoptosis of EPCs. The Keap1 knockdown with Keap1 siRNA increased the nuclear translocation of Nrf2, the NQO1 mRNA and protein transcription levels, and prevented ox-LDL induced ROS generation and formation of JC-1 monomers. Treatment of ox-LDL increased the activation of p38. Pretreatment with SB203580 significantly eliminated ox-LDL induced the inhibition of Nrf2 nuclear translocation, the depression of the mRNA transcription levels of NQO-1, the ROS generation and the formation of JC-1 monomers in EPCs. The pretreatment of Keap1 siRNA decreased the Bax/Bcl-2 ratio which was increased by the treatment of ox-LDL in EPCs. The ox-LDL treatment decreased EPCs migration activity and tube formation. Whereas the pre-treatment with Keap1 siRNA preserved the migration ability and tube formation of EPCs Conclusion Ox-LDL induced EPCs oxidative stress and apoptosis via p38/Keap1/Nrf2 pathway.

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Corrigendum to “Transplantation of VEGFl65-overexpressing vascular endothelial progenitor cells relieves endothelial injury after deep vein thrombectomy” [Thromb. Res. 137 (2016) 41–45]

Thrombosis Research ◽

10.1016/j.thromres.2017.04.026 ◽

2017 ◽

Vol 154 ◽

pp. 107 ◽

Cited By ~ 1

Author(s):

Jun-jian Tang ◽

Qing-you Meng ◽

Zhi-xin Cai ◽

Xiao-qiang Li

Keyword(s):

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Endothelial Injury ◽

Vascular Endothelial ◽

Endothelial Progenitor ◽

Deep Vein

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Nox2 siRNA Transfection Down Regulates VEGF Induced-Angiogenesis on Endothelial Progenitor Cells Which Are Derived From HCB

Blood ◽

10.1182/blood.v116.21.5188.5188 ◽

2010 ◽

Vol 116 (21) ◽

pp. 5188-5188

Author(s):

Eun-Sun Yoo ◽

Yeung-Chul Mun ◽

Eun Mi Nam ◽

Kyoung Eun Lee ◽

Jung Won Huh ◽

...

Keyword(s):

Nadph Oxidase ◽

Western Blot ◽

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Tube Formation ◽

Sirna Transfection ◽

Endothelial Progenitor ◽

Intracellular Ros ◽

Perk Expression

Abstract Abstract 5188 Background: Reactive oxygen species (ROS) such as superoxide and H2O2 have roles signaling for molecules on angiogenesis. NADPH oxidase Nox2 (gp91phox) is a major source of ROS. Previous, we had found that Nox2-based NADPH oxidase (gp91phox)-induced ROS may play important roles on EPCs migration and proliferation by VEGF (Blood. 2009;114:Abstract 1445). In the present study, we studied the impact of down-regulation of Nox2 on intracellular ROS level, proliferation, transmigration, and in vitro tube formation of HCB derived EPCs via Nox2 siRNA transfection. Methods: Outgrowing endothelial progenitor cells were established from mononuclear cells of human cord blood (Yoo et al, Stem cells. 2003;21:228-235) using EGM-2 media in a fibronectin-coated dish. EPCs were transfected with HiPerFection transfection reagent plus Nox2 siRNA or non-targeting control siRNA and cultured for 5 hours. 100ng/ml of VEGF was added to the transfected cells and cultured for overnight. Expression of Nox2 and pERK in the Nox2 siRNA transfected EPCs were detected by western blot analysis. Intracellular ROS level was analyzed by staining with 2, 7-dichlrodihydro-fluorescein-diacetate (H2DCF-DA) and flow cytometry. Transmigration against VEGF was performed using transwell system (Costar) and in vitro tube formation was assayed using In vitro angiogenesis kit (Chemicon). Results: Intracellular ROS level was increased during endothelial progenitor cell culture which were derived from HCB by VEGF treatment. Proliferation, in vitro tube formation matrigel assay and migration assay on endothelial progenitor cells using VEGF were decreased with Nox2 siRNA transfection when compared with that of control group. In western blot data, Nox2-based NADPH oxidase (gp91phox) was increased by VEGF and decreased by Nox2 siRNA transfection. VEGF induced pERK expression was also decreased by Nox2 siRNA transfection as well. Conclusions: Based on our studies, Nox2-based NADPH oxidase (gp91phox)-induced ROS may have important roles on proliferation in HCB induced EPCs by VEGF stimulation. Furthermore, Nox2 siRNA transfection into HCB derived EPC down-regulated intracellular ROS production and pERK expression. Our data may be useful finding the new therapeutic targets for ischemic heart and ischemic limb diseases by manipulating the level of intracellular ROS via Nox2. Disclosures: No relevant conflicts of interest to declare.

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