scholarly journals Peroxisome Proliferator-activated Receptor-γ Activation Inhibits Interleukin-1β-mediated Platelet-derived Growth Factor-α Receptor Gene Expression via CCAAT/Enhancer-binding Protein-δ in Vascular Smooth Muscle Cells

2001 ◽  
Vol 276 (16) ◽  
pp. 12893-12897 ◽  
Author(s):  
Yasunori Takata ◽  
Yutaka Kitami ◽  
Takafumi Okura ◽  
Kunio Hiwada
Keyword(s):  
Gene Expression ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Receptor Gene ◽  
Platelet Derived Growth Factor ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Enhancer Binding Protein ◽  
Factor Α ◽  
Receptor Gene Expression

Platelet-derived growth factor and growth-related genes in rat lung. II. Effect of exposure to 85% O2

1992 ◽  
Vol 262 (2) ◽  
pp. L140-L146 ◽  
Author(s):  
R. N. Han ◽  
S. Buch ◽  
B. A. Freeman ◽  
M. Post ◽  
A. K. Tanswell
Keyword(s):  
Gene Expression ◽  
Cell Division ◽  
Growth Factor ◽  
Receptor Gene ◽  
Platelet Derived Growth Factor ◽  
Chain Gene ◽  
Transcription Analysis ◽  
A Chain ◽  
Type Receptor ◽  
Receptor Gene Expression

The expression of platelet-derived growth factor (PDGF), its receptor, and related genes was studied in the lung tissue of rats exposed to air or 85% O2. PDGF-B chain mRNA was increased by 6 days and PDGF B-type receptor mRNA was increased by 4 and 6 days of exposure to 85% O2. Despite a continued increase of cell division, both PDGF-B chain and B-type receptor mRNAs had returned to control values by 14 days of exposure to 85% O2. PDGF-A chain mRNA was unaffected by exposure to 85% O2. Nuclear runoff transcription analysis confirmed increased transcription of PDGF-B chain mRNA, whereas Western blot analysis of lung homogenates suggested consequent increased translation of PDGF-B chain mRNA to PDGF-BB at 7 days of exposure to 85% O2. Combined immunocytochemistry and autoradiography localized PDGF-BB to the major site of cell division, the pulmonary interstitium. We speculate that the early pulmonary fibroblast hyperplasia observed following exposure to 85% O2 is mediated by increased PDGF-B chain gene expression and may also be mediated by changes in PDGF B-type receptor gene expression.

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