ArticleScientific reports2016
Identification of Cofilin-1 Induces G0/G1 Arrest and Autophagy in Angiotensin-(1-7)-treated Human Aortic Endothelial Cells from iTRAQ Quantitative Proteomics.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Omentum-Derived Mesenchymal Stem Cells Promote Antibacterial Effects and Protect Endothelial Functions via PAI-1.Stem cell reviews and reports · 2026Article
- LIM kinases in cardiovascular health and disease.Frontiers in physiology · 2024Review
- Cerebral Ischemia-Reperfusion Is Associated With Upregulation of Cofilin-1 in the Motor Cortex.Frontiers in cell and developmental biology · 2021Article
- Up-regulation of cofilin-1 in cell senescence associates with morphological change and p27Aging cell · 2021Article
- The GABARAP Co-Secretome Identified by APEX2-GABARAP Proximity Labelling of Extracellular Vesicles.Cells · 2020Article
- Autophagy in metabolic syndrome: breaking the wheel by targeting the renin-angiotensin system.Cell death & disease · 2020Review
- Markers of Endothelial Cells in Normal and Pathological Conditions.Biochemistry (Moscow) Supplement. Series A, Membrane and cell biology · 2020Article
- Pre-treatment with angiotensin-(1-7) inhibits tumor growth via autophagy by downregulating PI3K/Akt/mTOR signaling in human nasopharyngeal carcinoma xenografts.Journal of molecular medicine (Berlin, Germany) · 2018Article
- Utilizing proteomics to understand and define hypertension: where are we and where do we go?Expert review of proteomics · 2018Review
- MicroRNA-200a/200b Modulate High Glucose-Induced Endothelial Inflammation by TargetingFrontiers in physiology · 2018Article
- MicroRNA-146a-5p Mediates High Glucose-Induced Endothelial Inflammation via Targeting Interleukin-1 Receptor-Associated Kinase 1 Expression.Frontiers in physiology · 2017Article
- Markers and Biomarkers of Endothelium: When Something Is Rotten in the State.Oxidative medicine and cellular longevity · 2017Review
- Morphological and proteomic analysis of biofilms from the Antarctic archaeon, Halorubrum lacusprofundi.Scientific reports · 2016Article
- Inhibiting Autophagy in Renal Cell Cancer and the Associated Tumor Endothelium.Cancer journal (Sudbury, Mass.)Review
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The angiotensin-converting enzyme 2/angiotensin-(1-7)/Mas axis is a pathway that acts against the detrimental effects of the renin-angiotensin system. However, the effects of angiotensin-(1-7) on endothelial protein expression and the related phenotypes are unclear. We performed a duplicate of iTRAQ quantitative proteomic analysis on human aortic endothelial cells (HAECs) treated with angiotensin-(1-7) for 6 hours. Cofilin-1 was identified as a highly abundant candidate with consistent >30% coverage and >1.2-fold overexpression in the angiotensin-(1-7)-treated group. Gene ontology analysis showed that the "regulation_of_mitosis" was significantly altered, and cell cycle analysis indicated that the 6-hour angiotensin-(1-7) treatment significantly induced G0/G1 arrest. Knockdown of the cofilin-1 (CFL1) gene suggested the G0/G1 phase arrest was mediated by the modulation of p27 and the p21/Cyclin/CDK complex by Cofilin-1. Interestingly, quiescent HAECs escaped G0/G1 arrest upon angiotensin-(1-7) treatment for 24 hours, and angiotensin-(1-7) induced autophagy by upregulating Beclin-1 and microtubule-associated protein 1 light chain 3b-II expression, which was also attenuated by A779 pre-treatment and CFL1 knockdown. After pre-treatment with 3-methyladenine (3MA), treatment with angiotensin-(1-7) for 24 h induced significant G0/G1 phase arrest and apoptosis, suggesting a pro-survival role of autophagy in this context. In conclusion, Cofilin-1 plays a dominant role in angiotensin-(1-7)-induced G0/G1 arrest and autophagy to maintain cellular homeostasis in HAECs.
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