Pericyte‐specific expression ofRgs5:implications for PDGF and EDG receptor signaling during vascular maturation
Autor: | Cecilia Bondjers, Hyeseon Cho, Tohru Kozasa, John H. Kehrl, Christer Betsholtz |
---|---|
Rok vydání: | 2003 |
Předmět: |
Transcription
Genetic GTPase-activating protein medicine.medical_treatment Receptors Cell Surface Models Biological Biochemistry Immediate-Early Proteins Receptors G-Protein-Coupled Receptor Platelet-Derived Growth Factor beta Mice Growth factor receptor Sphingosine Genetics medicine Animals Receptors Platelet-Derived Growth Factor RNA Messenger Phosphorylation Molecular Biology In Situ Hybridization Mitogen-Activated Protein Kinase 1 Platelet-Derived Growth Factor Endothelin-1 biology Chemistry Angiotensin II Growth factor 3T3 Cells Arteries Cell biology medicine.anatomical_structure Receptors Lysophospholipid embryonic structures biology.protein Pericyte Lysophospholipids Signal transduction Pericytes RGS Proteins Platelet-derived growth factor receptor Signal Transduction Biotechnology |
Zdroj: | The FASEB Journal. 17:1-17 |
ISSN: | 1530-6860 0892-6638 |
DOI: | 10.1096/fj.02-0340fje |
Popis: | RGS proteins finely tune heterotrimeric G-protein signaling. Implying the need for such fine-tuning in the developing vascular system, in situ hybridization revealed a striking and extensive expression pattern of Rgs5 in the arterial walls of E12.5-E17.5 mouse embryos. The distribution and location of the Rgs5-positive cells typified that of pericytes and strikingly overlapped the known expression pattern of platelet-derived growth factor receptor (PDGFR)-beta. Both E14.5 PDGFR-beta- and platelet-derived growth factor (PDGF)-B-deficient mice exhibited markedly reduced levels of Rgs5 in their vascular plexa and small arteries. This likely reflects the loss of pericytes in the mutant mice. RGS5 acts as a potent GTPase activating protein for Gi(alpha) and Gq(alpha) and it attenuated angiotensin II-, endothelin-1-, sphingosine-1-phosphate-, and PDGF-induced ERK-2 phosphorylation. Together these results indicate that RGS5 exerts control over PDGFR-beta and GPCR-mediated signaling pathways active during fetal vascular maturation. |
Databáze: | OpenAIRE |
Externí odkaz: |