title: Changes in the distribution of tenascin and fibronectin in the mouse ovary during folliculogenesis, atresia, corpus luteum formation and luteolysis.
abstract: Tenascin and fibronectin are components of the extracellular matrices that oppose and promote adhesion, respectively. Using immunohistochemical techniques, we studied the distribution of tenascin and fibronectin in the mouse ovary, in which dynamic reconstruction and degeneration occur during folliculogenesis, atresia, ovulation, corpus luteum formation and luteolysis. In growing follicles, tenascin was only detected in the theca externa layer, while fibronectin was detected in the theca externa layer, theca interna layer and basement membrane. During follicular atresia, granulosa cells, which are surrounded by the basement membrane, began to die through apoptosis. In atretic follicles, tenascin was detected in the basement membrane and theca externa layer. Distribution of fibronectin in atretic follicles was similar to that in healthy growing follicles, except that granulosa cells were slightly immunopositive for fibronectin. In young corpus luteum, luteal cells exhibit high 3 beta -hydroxysteroid dehydrogenase (3 beta -HSD) activity, an enzyme indispensable for progesterone production. Tenascin was barely detected in young luteal cells. 3 beta -HSD activity in luteal cells declines with corpus luteum age, and in older corpus luteum there is an increase in apoptotic death of luteal cells. Tenascin was intensely immunopositive in old luteal cells.In contrast, fibronectin immunostaining in luteal cells was relatively constant during corpus luteum formation and luteolysis. Our observations suggest that tenascin is critical in controlling the degenerative changes of tissues in mouse ovaries. Moreover, in all circumstances observed in this study, tenascin always co-localized with fibronectin, suggesting fibronectin is indispensable for the function of tenascin.
authors.affiliation: Department of Biological Science, Faculty of Science, Nara Women's University, Japan. ponko@cc.nara-wu.ac.jp
authors.forename: Keiko
authors.initials: K
authors.lastname: Yasuda
authors.forename: Emi
authors.initials: E
authors.lastname: Hagiwara
authors.forename: Akiko
authors.initials: A
authors.lastname: Takeuchi
authors.forename: Chinatsu
authors.initials: C
authors.lastname: Mukai
authors.forename: Chiyuki
authors.initials: C
authors.lastname: Matsui
authors.forename: Atsushi
authors.initials: A
authors.lastname: Sakai
authors.forename: Satoshi
authors.initials: S
authors.lastname: Tamotsu
mesh_terms: D015096:3-Hydroxysteroid Dehydrogenases / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000502:physiology; D003338:Corpus Luteum / Q000254:growth & development / Q000378:metabolism; D005260:Female; D005353:Fibronectins / Q000378:metabolism*; D005496:Follicular Atresia / Q000378:metabolism; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D003341:Luteolysis / Q000378:metabolism; D051379:Mice / Q000254:growth & development* / Q000378:metabolism*; D008813:Mice, Inbred ICR; D006080:Ovarian Follicle / Q000254:growth & development / Q000378:metabolism; D010053:Ovary / Q000378:metabolism*; D019063:Tenascin / Q000378:metabolism*
chemical_list: D005353:Fibronectins; D019063:Tenascin; D015096:3-Hydroxysteroid Dehydrogenases