ArticleJournal of cell science2010
Angiotensin-II-induced apoptosis requires regulation of nucleolin and Bcl-xL by SHP-2 in primary lung endothelial cells.
Article in Journal of cell science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 64 citations in OpenAlex.
- BAK and BAX: Therapeutic Targets for Acute Myocardial Infarction and Myocardial Ischemia-Reperfusion Injury.Biology · 2025Review
- Apoptosis in post-streptococcal glomerulonephritis and mechanisms for failed of inflammation resolution.Pediatric nephrology (Berlin, Germany) · 2024Review
- Review
- Relationship Between D-Dimer Levels and Neutrophil-to-Lymphocyte Ratio (NLR) in Preeclamptic Pregnant Women with COVID-19: A Cohort Study.Medical science monitor : international medical journal of experimental and clinical research · 2023Observational
- Acute Lung Injury in aortic dissection : new insights in anesthetic management strategies.Journal of cardiothoracic surgery · 2023Review
- In Vitro Characterization of a Tissue Renin-Angiotensin System in Human Nucleus Pulposus Cells.Cells · 2022Article
- A comprehensive review of SHP2 and its role in cancer.Cellular oncology (Dordrecht, Netherlands) · 2022Review
- Captopril reduces lung inflammation and accelerated senescence in response to thoracic radiation in mice.Journal of radiation research · 2021Article
- A hypothesis for pathobiology and treatment of COVID-19: The centrality of ACE1/ACE2 imbalance.British journal of pharmacology · 2020Review
- Activation of angiotensin II type-2 receptor protects against cigarette smoke-induced COPD.Pharmacological research · 2020Article
- Integrated analysis of patient samples identifies biomarkers for venetoclax efficacy and combination strategies in acute myeloid leukemia.Nature cancer · 2020Article
- Role of Renin-Angiotensin System in Acute Lung Injury Caused by Viral Infection.Infection and drug resistance · 2020Review
- The tyrosine phosphatase SHP2 controls TGFβ-induced STAT3 signaling to regulate fibroblast activation and fibrosis.Nature communications · 2018Article
- GPCRs in pulmonary arterial hypertension: tipping the balance.British journal of pharmacology · 2018Review
- Post-Transcriptional Regulation of Anti-Apoptotic BCL2 Family Members.International journal of molecular sciences · 2018Review
- Vascular mechanotransduction data in a rodent model of diabetes: Pressure-induced regulation of SHP2 and associated signaling in the rat inferior vena cava.Data in brief · 2017Article
- Endothelial cell apoptosis in angiogenesis and vessel regression.Cellular and molecular life sciences : CMLS · 2017Review
- Bindarit reduces the incidence of acute aortic dissection complicated lung injury via modulating NF-κB pathway.Experimental and therapeutic medicine · 2017Article
- Mitochondrial-dependent mechanisms are involved in angiotensin II-induced apoptosis in dopaminergic neurons.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2016Article
- The hepatocyte growth factor isoform NK2 activates motogenesis and survival but not proliferation due to lack of Akt activation.Cellular signalling · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Angiotensin II (Ang II) is a key proapoptotic factor in fibrotic tissue diseases. However, the mechanism of Ang-II-induced cell death in endothelial cells has not been previously elucidated. Using the neutral comet assay and specific receptor antagonists and agonists, we found that Ang-II-mediated apoptosis in primary pulmonary endothelial cells required the AT2 receptor. Ang II caused cytochrome c release from the mitochondria concurrent with caspase-3 activation and DNA fragmentation, and apoptosis was suppressed by an inhibitor of Bax-protein channel formation, implicating mitochondrial-mediated apoptosis. There was no evidence that the extrinsic apoptotic pathway was involved, because caspase-9, but not caspase-8, was activated by Ang-II treatment. Apoptosis required phosphoprotein phosphatase activation, and inhibition of the SHP-2 phosphatase (encoded by Ptpn11) blocked cell death. Reduced levels of anti-apoptotic Bcl-2-family members can initiate intrinsic apoptosis, and we found that Ang-II treatment lowered cytosolic Bcl-x(L) protein levels. Because the protein nucleolin has been demonstrated to bind Bcl-x(L) mRNA and prevent its degradation, we investigated the role of nucleolin in Ang-II-induced loss of Bcl-x(L). RNA-immunoprecipitation experiments revealed that Ang II reduced the binding of nucleolin to Bcl-x(L) mRNA in an AU-rich region implicated in instability of Bcl-x(L) mRNA. Inhibition of SHP-2 prevented Ang-II-induced degradation of Bcl-x(L) mRNA. Taken together, our findings suggest that nucleolin is a primary target of Ang-II signaling, and that Ang-II-activated SHP-2 inhibits nucleolin binding to Bcl-x(L) mRNA, thus affecting the equilibrium between pro- and anti-apoptotic members of the Bcl-2 family.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.