Kinetics of expression of connective tissue growth factor gene during liver regeneration after partial hepatectomy and D-galactosamine-induced liver injury in rats

Connective tissue growth factor (CTGF) is up-regulated by TGF-beta1 during wound healing. The present study examined the expression of CTGF during regeneration after 70% partial hepatectomy (PH) or d-galactosamine (GalN)-injured liver in rats. CTGF, TGF-beta1, and type I collagen mRNAs were semiquan...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2000-10, Vol.277 (2), p.448-454
Main Authors: Ujike, K, Shinji, T, Hirasaki, S, Shiraha, H, Nakamura, M, Tsuji, T, Koide, N
Format: Article
Language:English
Subjects:
Animals
Cells, Cultured
Collagen - biosynthesis
Connective Tissue Growth Factor
Extracellular Matrix - metabolism
Galactosamine - metabolism
Growth Substances - biosynthesis
Growth Substances - genetics
Immediate-Early Proteins - biosynthesis
Immediate-Early Proteins - genetics
In Situ Hybridization
Intercellular Signaling Peptides and Proteins
Kinetics
Liver - drug effects
Liver - injuries
Liver - physiology
Liver - surgery
Plasmids - metabolism
Proto-Oncogene Proteins c-fos - biosynthesis
Rats
Rats, Sprague-Dawley
Regeneration
Ribonucleases - metabolism
RNA - metabolism
Time Factors
Transforming Growth Factor beta - biosynthesis
Transforming Growth Factor beta1
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Summary:Connective tissue growth factor (CTGF) is up-regulated by TGF-beta1 during wound healing. The present study examined the expression of CTGF during regeneration after 70% partial hepatectomy (PH) or d-galactosamine (GalN)-injured liver in rats. CTGF, TGF-beta1, and type I collagen mRNAs were semiquantified by a ribonuclease protection assay. After PH, TGF-beta1 and type I collagen were increased at 2-6 h and at 12-48 h. CTGF increased at 6 h and returned to the control level thereafter. The ribonuclease protection assay of cultured hepatic stellate cells (HSC) and in situ hybridization suggest that the cells express CTGF along sinusoid might be HSCs. After GalN administration, CTGF increased at 2-96 h with a shoulder peak at 6-12 h followed by a main peak at 24 h. TGF-beta1 and type I collagen were up-regulated with kinetics similar to those of CTGF. The different kinetics between PH and GalN regenerations indicate that regulation of CTGF in the two processes is different. Higher TGF-beta1 expression after inflammatory/necrotic process in the GalN regeneration may caused the prolonged CTGF expression.
ISSN:0006-291X
DOI:10.1006/bbrc.2000.3693