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In situ hybridization for procollagen types I, III and IV mRNA in normal and fibrotic rat liver: Evidence for predominant expression in nonparenchymal liver cells
Author(s) -
Milani Stefano,
Herbst Hermann,
Schuppan Detlef,
Hahn Eckhart G.,
Stein Harald
Publication year - 1989
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840100117
Subject(s) - procollagen peptidase , in situ hybridization , biology , hepatic stellate cell , messenger rna , stromal cell , gene expression , microbiology and biotechnology , fibrosis , pathology , gene , endocrinology , biochemistry , medicine , cancer research
The expression of α2(I), α1(III) and α1(IV) procollagen mRNA was analyzed in normal and CCl 4 ‐induced fibrotic rat liver by in situ hybridization using RNA probes. In normal liver, moderate amounts of α2(I) and α1(III) procollagen transcripts were found in sinusoidal cells, in stromal cells of the portal tracts and in the vicinity of central veins, whereas a1(IV) procollagen gene expression was below the threshold of detection. After 2 weeks of CCl 4 treatment, increased transcription of α2(I) and α1(III) procollagen genes was observed in sinusoidal cells. At this stage, α1(IV) procollagen mRNA was detectable in the same cell types and localization as α2(I) and α1(III) procollagen transcripts, although with a weaker signal. After 4 weeks, newly formed fibrous septa showed many cells intensely labeled by α2(I), α1(III) and α1(IV) procollagen probes. Neither in normal liver nor at any stage of fibrosis was any hybridization signal above background observed in hepatocytes. These patterns suggest that in the liver Type I, Type III and Type IV procollagen expression takes place predominantly in nonparenchymal cells. Therefore, hepatocytes do not appear to be significantly involved in procollagen production in this experimental model of liver fibrosis.