title: Stromelysin-3 is induced in mouse ovarian follicles undergoing hormonally controlled apoptosis, but this metalloproteinase is not required for follicular atresia.
abstract: Apoptotic processes are often associated with an intense proteolytic remodeling of the extracellular matrix (ECM). Proteolytic degradation of the ECM can also be a signal that induces apoptosis. Here, we have investigated the expression pattern and functional role of the matrix metalloproteinase stromelysin-3 in follicular atresia. Twenty-four hours after the treatment of immature female mice with a low dose of eCG, both apoptosis and the stromelysin-3 mRNA expression were suppressed approximately threefold. However, the initial suppression of apoptosis and stromelysin-3 expression was followed by a time-dependent increase, and 96 h after eCG treatment, the levels were similar to those of untreated control mice. In 15- to 16-day-old juvenile mice, the ovary consisted of relatively undeveloped follicles, and almost no apoptosis and only low stromelysin-3 mRNA expression were observed. However, at the age of 21 days, when several antral follicles were present, a fivefold induction in both apoptosis and stromelysin-3 mRNA expression was detected. For both models, in situ analysis revealed that the expression of stromelysin-3 mRNA was localized to the granulosa cells of atretic follicles. To address the functional role of stromelysin-3 in follicular atresia, stromelysin-3-deficient mice were studied. However, no difference in the pattern of apoptotic DNA fragmentation and no apparent morphological differences were observed when ovaries from wild-type and stromelysin-3-deficient mice were compared. Taken together, our data indicate that stromelysin-3 is induced during follicular atresia, but that this protease is not obligatory for initiation or completion of the atretic process.
authors.affiliation: Department of Medical Biosciences, Medical Biochemistry, Umeå University, S-90187 Umeå, Sweden.
authors.forename: A C
authors.initials: AC
authors.lastname: Hägglund
authors.forename: P
authors.initials: P
authors.lastname: Basset
authors.forename: T
authors.initials: T
authors.lastname: Ny
mesh_terms: D000375:Aging / Q000502:physiology; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D053938:DNA Fragmentation; D005109:Extracellular Matrix / Q000378:metabolism; D005260:Female; D005496:Follicular Atresia / Q000502:physiology*; D006062:Gonadotropins / Q000494:pharmacology; D006728:Hormones / Q000502:physiology*; D017403:In Situ Hybridization; D053507:Matrix Metalloproteinase 11; D008666:Metalloendopeptidases / Q000096:biosynthesis* / Q000172:deficiency / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D006080:Ovarian Follicle / Q000378:metabolism*; D015347:RNA Probes; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis
chemical_list: D006062:Gonadotropins; D006728:Hormones; D015347:RNA Probes; D012333:RNA, Messenger; D053507:Matrix Metalloproteinase 11; D008666:Metalloendopeptidases