Vasohibin is thought to be an important negative feedback regulator of angiogenesis that is selectively induced in endothelial cells by VEGF. Here, we assessed the role of vasohibin on HIF-1α expression under oxidative stress induced by hydrogen peroxide (H₂O₂) in HUVEC. VEGF induced significant cell growth that was associated with an increase in vasohibin expression. Following H₂O₂-pretreatment, VEGF further increased cell growth but this was contrastingly associated with a decrease in vasohibin expression when compared with VEGF alone. Interestingly, vasohibin inhibited cell proliferation through degradation of HIF-1α expression during H₂O₂-pretreatment. Furthermore, vasohibin elevated the expression of prolyl hydroxylase (PHD). These results suggest that vasohibin plays crucial roles as a negative feedback regulator of angiogenesis through HIF-1α degradation via PHD.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.febslet.2012.03.007 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Tubulin detyrosination shapes cytoskeletal architecture and virulence.
Proc Natl Acad Sci U S A
January 2025
Maladies infectieuses et Vecteurs: Ecologie, Génétique, Evolution et Contrôle, University of Montpellier, CNRS, Institut de Recherche pour le Développement, Montpellier 34095, France.
Tubulin detyrosination has been implicated in various human disorders and is important for regulating microtubule dynamics. While in most organisms this modification is restricted to α-tubulin, in trypanosomatid parasites, it occurs on both α- and β-tubulin. Here, we show that in , a single vasohibin (LmVASH) enzyme is responsible for differential kinetics of α- and β-tubulin detyrosination.
View Article and Find Full Text PDFcircSIRT2/miR-542-3p/VASH1 axis regulates endothelial-to-mesenchymal transition (EndMT) in subretinal fibrosis in age-related macular degeneration models.
Aging Cell
January 2025
Department of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China.
Neovascular age-related macular degeneration (nAMD), characterized by choroidal neovascularization (CNV), is one of the leading causes of severe visual impairment and irreversible vision loss around the world. Subretinal fibrosis (SRF) contributes to the incomplete response to anti-vascular endothelial growth factor (VEGF) treatment and is one of the main reasons for long-term poor visual outcomes in nAMD. Reducing SRF is urgently needed in the anti-VEGF era.
View Article and Find Full Text PDFForced Vasohibin-1 Expression Increases Paclitaxel Sensitivity of Ovarian Cancer by Inhibiting Microtubule Activity.
Cancer Rep (Hoboken)
December 2024
Department of Obstetrics and Gynecology, School of Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Background: Vasohibin-1 (VASH1), an angiogenic inhibitor, exhibits tubulin carboxypeptidase activity, which is involved in microtubule functions. Paclitaxel, the core chemotherapeutic agent for ovarian cancer chemotherapy, has a point of action on microtubules and may interact with VASH1.
Aims: To examine the influence of VASH1 on intracellular tubulin detyrosination status, cyclin B1 expression, and paclitaxel chemosensitivity using VASH1-overexpressing ovarian cancer cell lines.
VASH2 enhances KIF3C-mediated EGFR-endosomal recycling to promote aggression and chemoresistance of lung squamous cell carcinoma by increasing tubulin detyrosination.
Cell Death Dis
October 2024
Cancer Molecular Diagnostics Core, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, 300202, Tianjin, China.
Article Synopsis
- Lung squamous cell carcinoma (LUSC) has a high mortality rate and limited treatment options, primarily relying on chemotherapy, which faces challenges due to multi-drug resistance.
- Researchers identified vasohibin-2 (VASH2) as a key prognostic biomarker that promotes tumor growth and chemoresistance by affecting the detyrosination of α-tubulin, negatively impacting patient outcomes.
- Targeting VASH2's TCP activity could enhance chemotherapy efficacy, suggesting that combining standard treatments with EpoY, a TCP inhibitor, may improve outcomes for LUSC patients.
Chronic Activation of Tubulin Tyrosination Improves Heart Function.
Circ Res
October 2024
Department of Experimental Pharmacology and Toxicology (N.P., B.G., E.K., G.M., S.S., L.C.), University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Article Synopsis
- - Hypertrophic cardiomyopathy (HCM) is a common genetic heart disorder linked to sarcomere gene mutations, resulting in left ventricular thickening and diastolic dysfunction; new research emphasizes the importance of microtubule alterations in heart failure.
- - The study explored the effects of increasing tubulin tyrosination via adeno-associated virus transfer in various models, including HCM human cardiomyocytes and specific mouse models, revealing that this approach improved heart function by reducing harmful microtubule modifications and enhancing contractility.
- - Results indicated that enhancing tubulin tyrosination led to better heart function metrics such as contractility and cardiac output in both human and mouse models, while also suggesting potential benefits of targeting the micro
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!