Fibronectin Promotes Cell Cycle Entry in Smooth Muscle Cells in Primary Culture
| Autor: | Bimma Henderson, Ulf Hedin, Piotr Religa, Monsur Kazi, Joy Roy, Karin Lundmark, Phan Kiet Tran |
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| Rok vydání: | 2002 |
| Předmět: |
Male
Cyclin A Hyperphosphorylation Cell Cycle Proteins Resting Phase Cell Cycle Retinoblastoma Protein Muscle Smooth Vascular Rats Sprague-Dawley Extracellular matrix Cyclin D1 Animals Enzyme Inhibitors Phosphorylation Cyclin D3 Aorta Cells Cultured biology Cell growth Tumor Suppressor Proteins Cell Cycle G1 Phase Cell Biology Cell cycle Genistein Fibronectins Rats Cell biology Fibronectin Carotid Arteries biology.protein Carotid Artery Injuries Cyclin-Dependent Kinase Inhibitor p27 |
| Zdroj: | Experimental Cell Research. 273:169-177 |
| ISSN: | 0014-4827 |
| Popis: | Smooth muscle cell proliferation after arterial injury is regulated by growth factors and components of the extracellular matrix. We have previously demonstrated that fibronectin promotes a phenotypic modulation of freshly isolated rat smooth muscle cells from a contractile to a synthetic phenotype in primary culture and supports the ability of the cells to respond to growth factors. Here, we analyzed if fibronectin promotes cell cycle entry in freshly isolated rat aortic smooth muscle cells during primary culture. Cell cycle analysis showed that cells seeded on fibronectin remained in the G 0 /G 1 phase of the cell cycle during the first 6 days of culture. During this period, there was an increased expression of cyclin D1 and p27 KIP1 in the absence of exogenous growth factors. Addition of serum was followed by enhanced cyclin D1 expression, decreased p27 KIP1 levels, hyperphosphorylation of Rb protein, induction of cyclin A and cyclin D3 expression, and cell cycle progression into S phase. The results indicate that fibronectin initiates cell cycle entry in freshly isolated smooth muscle cells by promoting the induction of cyclin D1 and thereby facilitates further cell cycle progression together with growth factors. |
| Databáze: | OpenAIRE |
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