LOCALIZATION OF THE EXPRESSION OF TYPE-I, TYPE-II AND TYPE-III COLLAGEN GENES IN HUMAN NORMAL AND HYPOCHONDROGENESIS CARTILAGE CANALS

Citation
D. Leguellec et al., LOCALIZATION OF THE EXPRESSION OF TYPE-I, TYPE-II AND TYPE-III COLLAGEN GENES IN HUMAN NORMAL AND HYPOCHONDROGENESIS CARTILAGE CANALS, Histochemical Journal, 26(9), 1994, pp. 695-704
Citations number
28
Categorie Soggetti
Cytology & Histology
Journal title
ISSN journal
00182214
Volume
26
Issue
9
Year of publication
1994
Pages
695 - 704
Database
ISI
SICI code
0018-2214(1994)26:9<695:LOTEOT>2.0.ZU;2-C
Abstract
The expression of type I, II and III collagens genes was examined in h uman normal and hypochondrogenesis cartilage canals employing electrop horetic analysis, immunohistochemistry and in sih hybridization techni ques. In normal cartilage, collagens type I and III were present in pe richondrium, in the connective tissue surrounding the vessels of carti lage canals and in the dense fibrous tissue. However, types I and III procollagen mRNAs were detected only in fibroblasts of the perichondri um and of the canals, but not in the polymorphic cells. Type II collag en was present in the cartilage matrix and in the dense fibrous tissue , in good accordance with the localization of type II procollagen mRNA s detected in the chondrocytes and in the polymorphic cells. These dat a suggest that there are no transitional cells expressing type I, II a nd III collagen genes and that polymorphic cells are of chondrocytic o rigin. In the case of hypochondrogenesis, type II collagen was less ab undant than in normal cartilage, whereas the corresponding mRNA level was equivalent. That suggests that a postranscriptional regulation of this protein is involved in the decrease of type II collagen productio n. Type I collagen, unexpectedly detected in the cartilage matrix, was synthesized by chondrocytes and polymorphic cells, suggesting a repla cement of type II by type I collagen. The canal hypertrophy observed i n this pathological case could thus be due to a modification in the re gulation of the growth of cartilage canals caused by a defective carti lage matrix.