title: Changes in the localization of type I, III and IV collagen mRNAs in the kidneys of hereditary nephritic (ICGN) mice with renal fibrosis.
abstract: Renal fibrotic change, extreme accumulation of extracellular matrix (ECM) components in glomeruli and tubulointerstitum, is one of the characteristic features of ICR-derived glomerulonephritis (ICGN) mice. Decreased degradation of ECMs by matrixmetalloproteinases was demonstrated in kidneys of ICGN mice. To determine the balance between production and degradation of ECMs in kidneys of ICGN mice, we examined expression of mRNAs of ECMs in those. To demonstrate the localization of type I, III and IV collagen mRNAs in kidney sections of ICGN and control ICR mice, in situ hybridization using digoxigenin-labeled oligonucleotide antisense probes for procollagen-alpha(1) (I), -alpha(1) (III) and -alpha(1) (IV) mRNAs, respectively, was performed. Negative or trace expressions of type I and III collagen mRNAs were observed in the kidneys of control mice, but stronger expressions of those were seen in glomeruli and injured renal tubules of the kidneys of ICGN mice. Moderate expression of type IV collagen mRNA was demonstrated in a part of glomeruli and renal tubules of both control and ICGN mice, and no remarkable difference was seen between them. Severe renal fibrosis, extreme accumulation of interstitial type I and III collagens is caused by increased production and decreased degradation in the kidneys of ICGN mice. Thus, the profiles of metabolism between interstitial and membranous collagens may be different in the kidneys of ICGN mice, and excessive production of interstitial collagens may be the dominant cause of renal disease in them.
authors.affiliation: Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University, Japan.
authors.forename: Kozue
authors.initials: K
authors.lastname: Uchio
authors.forename: Noboru
authors.initials: N
authors.lastname: Manabe
authors.forename: Misuzu
authors.initials: M
authors.lastname: Yamaguchi-Yamada
authors.forename: Yasufumi
authors.initials: Y
authors.lastname: Goto
authors.forename: Yoshie
authors.initials: Y
authors.lastname: Yamamoto
authors.forename: Atsuo
authors.initials: A
authors.lastname: Ogura
authors.forename: Hajime
authors.initials: H
authors.lastname: Miyamoto
mesh_terms: D000818:Animals; D003094:Collagen / Q000235:genetics / Q000378:metabolism*; D017931:DNA Primers; D004195:Disease Models, Animal; D005109:Extracellular Matrix / Q000378:metabolism*; D005355:Fibrosis; D015870:Gene Expression; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D007668:Kidney / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D008813:Mice, Inbred ICR; D009404:Nephrotic Syndrome / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics
chemical_list: D017931:DNA Primers; D012333:RNA, Messenger; D003094:Collagen