We previously described that pervanadate, a potent tyrosine phosphatase inhibitor, induced contraction of rat myometrium via phospholipase (PL) C-gamma1 activation [Biol Reprod 54 (1996) 1383]. In this study, we found that pervanadate induced tyrosine phosphorylation of the platelet-derived growth factor (PDGF)-beta receptor, interaction of the phosphorylated PDGF receptor with the phosphorylated PLC-gamma1, production of inositol phosphates (InsPs), extracellular signal-regulated kinase (ERK) activation and DNA synthesis. All these responses were insensitive to PDGF receptor kinase inhibition or PDGF receptor down-regulation. We showed that Src family kinases were activated by pervanadate, and that InsPs production and phosphorylation of both PLC-gamma1 and the PDGF receptor were blocked by PP1, an Src inhibitor. In contrast, the stimulation of ERK by pervanadate was totally refractory to PP1. These results demonstrated that the activation of Src by pervanadate is involved in PLC-gamma1/InsPs signalling but does not play a major role in ERK activation.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/s0898-6568(01)00269-8 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Local Inflammation Precedes Diaphragm Wasting and Fibrotic Remodelling in a Mouse Model of Pancreatic Cancer.
J Cachexia Sarcopenia Muscle
February 2025
Department of Physical Therapy, University of Florida Health Cancer Center, Gainesville, Florida, USA.
Background: Cancer cachexia represents a debilitating muscle wasting condition that is highly prevalent in gastrointestinal cancers, including pancreatic ductal adenocarcinoma (PDAC). Cachexia is estimated to contribute to ~30% of cancer-related deaths, with deterioration of respiratory muscles suspected to be a key contributor to cachexia-associated morbidity and mortality. In recent studies, we identified fibrotic remodelling of respiratory accessory muscles as a key feature of human PDAC cachexia.
View Article and Find Full Text PDFDynamics of resistance to immunotherapy and TKI in patients with advanced renal cell carcinoma.
Cancer Treat Rev
January 2025
Medical Oncology, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy; Department of Medical and Surgical Sciences (DIMEC), University of Bologna, Bologna, Italy. Electronic address:
Immune-based combinations are the cornerstone of the first-line treatment of metastatic renal cell carcinoma patients, leading to outstanding outcomes. Nevertheless, primary resistance and disease progression is a critical clinical challenge. To properly address this issue, it is pivotal to understand the mechanisms of resistance to immunotherapy and tyrosine kinase inhibitors, that tumor eventually develop under treatment.
View Article and Find Full Text PDFEndothelial-secreted Endocan activates PDGFRA and regulates vascularity and spatial phenotype in glioblastoma.
Nat Commun
January 2025
The Intellectual and Developmental Disabilities Research Center, The Semel Institute for Neuroscience and Human Behavior, and The Broad Stem Cell Research Center, The Jonsson Comprehensive Cancer Center, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Extensive neovascularization is a hallmark of glioblastoma (GBM). In addition to supplying oxygen and nutrients, vascular endothelial cells provide trophic support to GBM cells via paracrine signaling. Here we report that Endocan (ESM1), an endothelial-secreted proteoglycan, confers enhanced proliferative, migratory, and angiogenic properties to GBM cells and regulates their spatial identity.
View Article and Find Full Text PDFAnandamide Inhibits Vascular Smooth Muscle Migration, Endothelial Adhesion Protein Expression and Monocyte Adhesion of Human Coronary Artery Cells.
Cells
December 2024
Institute of Pharmacology and Toxicology, Rostock University Medical Center, Schillingallee 70, 18057 Rostock, Germany.
Endocannabinoids have been shown to play a complex role in the pathophysiology of a number of cardiovascular disorders. In the present study, the effects of the two major endocannabinoids anandamide (AEA) and 2-arachidonoylglycerol (2-AG) were investigated in human coronary artery smooth muscle cells (HCASMC) and human coronary artery endothelial cells (HCAEC) with regard to potential atheroprotective and anti-inflammatory effects. In HCASMC, AEA showed an inhibitory effect on platelet-derived growth factor-induced migration, but not proliferation, independent of major cannabinoid-activatable receptors (CB, CB, TRPV1), while 2-AG left both responses unaffected.
View Article and Find Full Text PDFHigh glucose couples DJ-1 with PTEN to activate PDGFRβ for renal proximal tubular cell injury.
PLoS One
January 2025
VA Research, Education and Clinical Center, South Texas Veterans Health Care System, San Antonio, Texas, United States of America.
Article Synopsis
- The study investigates how high glucose levels in diabetes lead to kidney cell damage through the activation of a signaling pathway involving DJ-1 and PTEN.
- DJ-1 is found to be upregulated in kidney cells under high glucose conditions, which triggers the Akt/mTORC1 signaling pathway, resulting in cell growth and fibrosis.
- The research indicates that inhibiting DJ-1 can prevent glucose-induced cell growth and damage, while overexpressing DJ-1 replicates the harmful effects, highlighting its role in renal injury related to diabetes.
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!