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Gene expression and protein distribution of collagen, fibronectin and laminin in bovine follicles and corpora lutea

The aim of this study was to locate sites of expression and deposition of collagen, fibronectin and laminin in the bovine ovary. RNA from the granulosa and basement membrane/theca fractions of maturing follicles and from corpora lutea of the early, middle and late luteal phase was probed with cDNAs for collagen types I and IV, fibronectin and laminin. Antisera against collagens I and IV were used in western analysis of protein from follicular fluid, granulosa, basement membrane/theca and corpus luteum. Collagen subunits 1(I) and 2(I) were expressed in the basement membrane/theca but not in the granulosa of the follicle. They were also expressed in all luteal extracts, especially those from the early phase. Collagen 2(IV) was highly expressed in the basement membrane/theca and to a lesser extent in corpora lutea. Collagen 3(IV) was expressed in the granulosa, basement membrane/theca and early corpus luteum. Fibronectin 1 and laminin B2 were expressed in all tissues. Laminin B1 was expressed in all tissues except the granulosa. Collagen IV was immunodetected in all follicle extracts, with the strongest signal in the basement membrane/theca. Collagen I occurred in all luteal extracts and in the basement membrane/theca but not in follicular fluid or the granulosa. These results demonstrate tissue-specific expression of ovarian structural proteins and suggest that changes occur during the progression from follicle to corpus luteum. The production of collagen IV in the follicle wall and of collagen I in the corpus luteum is consistent with previous biochemical studies. Evidence for collagen IV in the follicular antrum suggests that the follicle wall originates from granulosa as well as theca cells. The expression of laminin and fibronectin in luteal as well as follicular tissues suggests a complex postovulatory extracellular matrix and provides a possible mechanism for the regulation of the endocrine cell phenotype by extracellular proteins.