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Am J Physiol Lung Cell Mol Physiol 277: L1165-L1171, 1999;
1040-0605/99 $5.00
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Vol. 277, Issue 6, L1165-L1171, December 1999

Regulation of connective tissue growth factor expression by prostaglandin E2

Dennis A. Ricupero, David C. Rishikof, Ping-Ping Kuang, Christine F. Poliks, and Ronald H. Goldstein

Pulmonary Center and Department of Biochemistry, Boston University School of Medicine, Boston 02118-2394; and Boston Veterans Affairs Medical Center, Boston, Massachusetts 02130

Transforming growth factor-beta (TGF-beta ) stimulates alpha 1(I) collagen mRNA synthesis in human lung fibroblasts through a mechanism that is partially sensitive to cycloheximide and that may involve synthesis of connective tissue growth factor (CTGF). Northern blot analyses indicate that TGF-beta stimulates time- and dose-dependent increases in CTGF mRNA. In TGF-beta -stimulated fibroblasts, maximal levels of CTGF mRNA (3.7-fold above baseline) occur at 6 h. The TGF-beta -stimulated increase in CTGF mRNA was not blocked by cycloheximide. Nuclear run-on analysis indicates that TGF-beta increases the CTGF transcription rate. The TGF-beta -stimulated increases in CTGF transcription and steady-state levels of CTGF mRNA are attenuated in prostaglandin E2 (PGE2)-treated fibroblasts. PGE2 fails to attenuate luciferase activity induced by TGF-beta in fibroblasts transfected with the TGF-beta -responsive luciferase reporter construct p3TP-LUX. In amino acid-deprived fibroblasts, PGE2 and insulin regulate alpha 1(I) collagen mRNA levels without affecting CTGF mRNA levels. The data suggest that the regulation of alpha 1(I) collagen mRNA levels by TGF-beta and PGE2 may function through both CTGF-dependent and CTGF-independent mechanisms.

transforming growth factor-beta ; insulin; amino acid deficiency; type I collagen; human lung fibroblast


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