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In particular, an EDS variant is caused by a genetic mutation resulting in abnormal secretion of biglycan and decorin, two small leucine-rich proteoglycans highly expressed in reproductive tissues. Because biglycan\/decorin null mutant (Bgn\u2212\/\u2212Dcn\u2212\/\u2212) mice demonstrate phenotypic changes similar to EDS, we used this model to test whether either biglycan or decorin or both play a role in the attainment of successful term gestation. Wild-type biglycan null mutant, decorin null mutant, and biglycan\/decorin null mutant pregnancies were assessed for the length of gestation, pup and placenta weight, and litter size. Quantitative real-time PCR was performed to measure biglycan and decorin gene expression, and immunohistochemistry was performed to assess protein expression in placenta and fetal membranes at embryonic days E12, E15, and E18. Bgn\u2212\/\u2212Dcn\u2212\/\u2212 dams displayed preterm birth, whereas the possession of at least two biglycan or decorin wild-type alleles was protective of preterm birth. The number of Bgn\u2212\/\u2212Dcn\u2212\/\u2212 pups was decreased at postnatal day P1 but not at E18. Biglycan and decorin were upregulated in the placenta in the absence of each other and were developmentally regulated in fetal membranes, suggesting that these two proteoglycans demonstrate genetic complementation and contribute to gestational success in a dose-dependent manner. Thus, the biglycan\/decorin null mutant mouse is a model of genetically induced preterm birth and perinatal loss. This model presents novel targets for preventive or therapeutic manipulation of preterm birth.<\/jats:p>","DOI":"10.1530\/rep-10-0387","type":"journal-article","created":{"date-parts":[[2011,4,19]],"date-time":"2011-04-19T00:00:21Z","timestamp":1303171221000},"page":"183-194","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":34,"title":["A mouse model of spontaneous preterm birth based on the genetic ablation of biglycan and decorin"],"prefix":"10.1093","volume":"142","author":[{"given":"Megan L","family":"Calmus","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elyse E","family":"Macksoud","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard","family":"Tucker","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Renato V","family":"Iozzo","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Women and Infants' Hospital of Rhode Island, The Warren Alpert Medical School of Brown University, 101 Dudley Street, Providence, Rhode Island 02905, USA 1Department of Pathology Anatomy and Cell Biology, Thomas Jefferson University, 1020 Locust Street, Philadelphia, Pennsylvania 19107, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Beatrice E","family":"Lechner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2011,7,1]]},"reference":[{"key":"2026010712572747000_bib1","doi-asserted-by":"crossref","first-page":"107R","DOI":"10.1093\/glycob\/cwf065","article-title":"Mice deficient in small leucine-rich proteoglycans: novel in vivo models for osteoporosis, osteoarthritis, Ehlers\u2013Danlos syndrome, muscular dystrophy, and corneal 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