Autophagy protein 5 enhances the function of rat EPCs and promotes EPCs homing and thrombus recanalization via activating AKT

Hu, Nan; Kong, Lingshang; Chen, Hong; Li, Wendong; Qian, Aimin; Wang, Xiaoyun; Du, Xiaolong; Li, Chenglong; Yu, Xiaobin; Li, Xiaoqiang

doi:10.1016/j.thromres.2015.06.038

Cited by 21 publications

(19 citation statements)

References 46 publications

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“…found that transient hypoxia-induced autophagy promoted ECs survival and growth, and this autophagy was regulated by hypoxia-inducible factor-1α (HIF-1α); but if the stress was prolonged (24 to 72 hr), autophagy overactivation became mTOR-dependent and caused EC death 7 . Brief hypoxia (2 hr)-induced autophagy could increase EPCs migration and tubule formation 23 . But under normal condition, EPCs or other cells without autophagy with ATG5 knockdown showed an increased migratory ability 24, 25 and this finding was also observed in our studies.…”

Section: Discussionmentioning

confidence: 99%

Recombinant Thrombomodulin Exerts Anti-autophagic Action in Endothelial Cells and Provides Anti-atherosclerosis Effect in Apolipoprotein E Deficient Mice

Chen

Wang

Chao

et al. 2017

Sci Rep

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Stress-induced alteration in endothelial cells (ECs) integrity precedes the development of atherosclerosis. Previous studies showed that the soluble recombinant thrombomodulin (rTM) not only increases ECs proliferation but also exerts anti-apoptotic activity in ECs. However, the functional significance of soluble rTM on autophagy-related apoptosis in ECs is still undetermined. Implicating a cytoprotective role for rTM in persistent serum starvation (SS)-induced autophagy in cultured ECs, we found that treatment of rTM decreased the expression of SS-induced autophagy-related proteins, ATG5 and LC3, and the formation of autophagosomes through activation of AKT/mTOR pathway. In addition, treatment of rTM decreased SS-induced EC apoptosis, but this effect of rTM could not be recapitulated by co-treatment with a potent autophagy inducer, rapamycin and in ECs with ATG5 knockdown. In human atherosclerosis specimens, expression of autophagy markers, ATG13 and LC3, were more abundant in aortic intimal ECs with severe atherosclerosis than those without atherosclerosis. Moreover, compared to saline treatment group, administration of rTM reduced LC3 and ATG13 expression, intimal EC apoptosis, and atherosclerotic lesion severity in the aorta of apolipoprotein E deficient mice. In conclusion, treatment with rTM suppressed stress-induced autophagy overactivation in ECs, provided ECs protective effects, and decreased atherosclerosis in apolipoprotein E deficient mice.

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Section: Discussionmentioning

confidence: 99%

Recombinant Thrombomodulin Exerts Anti-autophagic Action in Endothelial Cells and Provides Anti-atherosclerosis Effect in Apolipoprotein E Deficient Mice

Chen

Wang

Chao

et al. 2017

Sci Rep

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“…In the most common PVD, deep venous thrombosis (DVT), ATG5 plays a critical role in the progression of the pathology since it mediates thrombus recanalization, acting mainly on endothelial cells. In this context, ATG5 activates Akt phosphorylation, which is counteracted by the use of 3-methyladenine (3-MA); 3-MA inhibits autophagy by lowering ATG5 levels and concomitantly inhibiting endothelial cell migration and tube formation [168]. Strong evidence of the role of autophagy in promoting angiogenesis has also been derived from other studies on pathologies requiring considerable tissue-remodeling programs, such as cancers, and from findings following the pharmacological inhibition of this pathway.…”

Section: Peripheral Vascular Diseasementioning

confidence: 99%

Mitophagy in Cardiovascular Diseases

Morciano

Patergnani

Bonora

et al. 2020

JCM

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Cardiovascular diseases are one of the leading causes of death. Increasing evidence has shown that pharmacological or genetic targeting of mitochondria can ameliorate each stage of these pathologies, which are strongly associated with mitochondrial dysfunction. Removal of inefficient and dysfunctional mitochondria through the process of mitophagy has been reported to be essential for meeting the energetic requirements and maintaining the biochemical homeostasis of cells. This process is useful for counteracting the negative phenotypic changes that occur during cardiovascular diseases, and understanding the molecular players involved might be crucial for the development of potential therapies. Here, we summarize the current knowledge on mitophagy (and autophagy) mechanisms in the context of heart disease with an important focus on atherosclerosis, ischemic heart disease, cardiomyopathies, heart failure, hypertension, arrhythmia, congenital heart disease and peripheral vascular disease. We aim to provide a complete background on the mechanisms of action of this mitochondrial quality control process in cardiology and in cardiac surgery by also reviewing studies on the use of known compounds able to modulate mitophagy for cardioprotective purposes.

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“…However, currently, there are no specific therapeutic strategies to avoid its complications, especially post‐thrombotic syndrome (PTS) . Endothelial progenitor cells (EPCs), which can accelerate thrombus recanalization by restoring damaged or lost endothelium, enhancing neovascularization and prompting thrombi resolution, have been described as a potential therapeutic application for thrombosis . But the low numbers of EPCs in peripheral blood and the features of fragility to detrimental homeostasis limit their role in the resolution of thrombi.…”

Section: Introductionmentioning

confidence: 99%

MiR‐9 promotes angiogenesis of endothelial progenitor cell to facilitate thrombi recanalization via targeting TRPM7 through PI3K/Akt/autophagy pathway

Zhou

Sun

Zhu

et al. 2020

J Cellular Molecular Medi

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Endothelial progenitor cells (EPCs) have emerged as a promising therapeutic choice for thrombi recanalization. However, this role of EPCs is confined by some detrimental factors. The aim of this study was to explore the role of the miR-9-5p in regulation of the proliferation, migration and angiogenesis of EPCs and the subsequent therapeutic role in thrombosis event. Wound healing, transwell assay, tube formation assay and in vivo angiogenesis assay were carried out to measure cell migration, invasion and angiogenic abilities, respectively. Western blot was performed to elucidate the relationship between miR-9-5p and TRPM7 in the autophagy pathway. It was found that miR-9-5p could promote migration, invasion and angiogenesis of EPCs by attenuating TRPM7 expression via activating PI3K/Akt/autophagy pathway. In conclusion, miR-9-5p, targets TRPM7 via the PI3K/Ak/autophagy pathway, thereby mediating cell proliferation, migration and angiogenesis in EPCs. Acting as a potential therapeutic target, miR-9-5p may play an important role in the prognosis of DVT.

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Autophagy protein 5 enhances the function of rat EPCs and promotes EPCs homing and thrombus recanalization via activating AKT

Cited by 21 publications

References 46 publications

Recombinant Thrombomodulin Exerts Anti-autophagic Action in Endothelial Cells and Provides Anti-atherosclerosis Effect in Apolipoprotein E Deficient Mice

Recombinant Thrombomodulin Exerts Anti-autophagic Action in Endothelial Cells and Provides Anti-atherosclerosis Effect in Apolipoprotein E Deficient Mice

Mitophagy in Cardiovascular Diseases

MiR‐9 promotes angiogenesis of endothelial progenitor cell to facilitate thrombi recanalization via targeting TRPM7 through PI3K/Akt/autophagy pathway

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