Retinoic acid and transforming growth factor beta differentially inhibit platelet-derived-growth-factor-induced Ito-cell activation.
作者： B H Davis , U R Rapp , N O Davidson
DOI: 10.1042/BJ2780043
关键词: Endocrinology 、 Transforming growth factor, beta 3 、 Retinoic acid 、 Tretinoin 、 TGF beta receptor 2 、 Transforming growth factor beta 、 Platelet-derived growth factor receptor 、 Internal medicine 、 Endoglin 、 Cell biology 、 Biology 、 Retinoic acid receptor beta
摘要: Sinusoidal Ito cells (stellate or fat-storing cells) undergo excessive cellular proliferation before the establishment and progression of hepatic fibrosis cirrhosis. Retinoic acid transforming growth factor beta (TGF beta) both inhibit Ito-cell [3H]thymidine incorporation in serum-containing media. Serum-induced mitogenicity was dependent on platelet-derived (PDGF). Additionally, pre-treatment with retinoic TGF blocked PDGF-induced cell proliferation. beta, but not acid, diminished PDGF-receptor smooth-muscle alpha-actin abundance.
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