2008
DOI: 10.1210/me.2007-0257
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Placenta Defects and Embryonic Lethality Resulting from Disruption of Mouse Hydroxysteroid (17-β) Dehydrogenase 2 Gene

Abstract: Hydroxysteroid (17-beta) dehydrogenase 2 (HSD17B2) is a member of aldo-keto reductase superfamily, known to catalyze the inactivation of 17beta-hydroxysteroids to less active 17-keto forms and catalyze the conversion of 20alpha-hydroxyprogesterone to progesterone in vitro. To examine the role of HSD17B2 in vivo, we generated mice deficient in Hsd17b2 [HSD17B2 knockout (KO)] by a targeted gene disruption in embryonic stem cells. From the homozygous mice carrying the disrupted Hsd17b2, 70% showed embryonic letha… Show more

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Cited by 26 publications
(21 citation statements)
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“…Enlargement of the spongiotrophoblast layer in mouse placentae has been observed in several mouse models with decreased fetal survival, including over-expression of epidermal growth factor receptor [32], trisomy 15 syndrome [33] and hydroxysteroid 17β dehydrogenase 2 null mice [34]. This is relevant to the enlarged spongiotrophoblast layer in placentae from pregnant Nas1 -/-mice, which have enhanced mid-gestational fetal loss.…”
Section: Discussionmentioning
confidence: 96%
See 1 more Smart Citation
“…Enlargement of the spongiotrophoblast layer in mouse placentae has been observed in several mouse models with decreased fetal survival, including over-expression of epidermal growth factor receptor [32], trisomy 15 syndrome [33] and hydroxysteroid 17β dehydrogenase 2 null mice [34]. This is relevant to the enlarged spongiotrophoblast layer in placentae from pregnant Nas1 -/-mice, which have enhanced mid-gestational fetal loss.…”
Section: Discussionmentioning
confidence: 96%
“…In addition, since impaired IGF1 expression can reduce fecundity and placental nutrient exchange [31], it is possible that low levels of IGF1 in Nas1 -/-mice [15] may be a contributing factor to the reduced fecundity and/or altered placental morphometry in pregnant Nas1 -/-mice. To our knowledge, this is the first study to show increased fetal reabsorption and altered placental morphology in a model of maternal hyposulfataemia.Enlargement of the spongiotrophoblast layer in mouse placentae has been observed in several mouse models with decreased fetal survival, including over-expression of epidermal growth factor receptor [32], trisomy 15 syndrome [33] and hydroxysteroid 17β dehydrogenase 2 null mice [34]. This is relevant to the enlarged spongiotrophoblast layer in placentae from pregnant Nas1 -/-mice, which have enhanced mid-gestational fetal loss.…”
mentioning
confidence: 96%
“…However, the placentas of HSD17B2KO mice displayed histological malformations, while no signs of thrombosis were observed. Furthermore, the treatment of pregnant female mice with an anti-estrogen or with progesterone did not prevent the foetal loss of the HSD17B2KO mice (Rantakari et al 2008). Thus, the cause of embryonic deaths in the HSD17B2KO mice is likely not due to the lack of progesterone or due to an increased action of estrogens.…”
Section: Hsd17b2ko Mice In Addition To Several Other Tissuesmentioning
confidence: 94%
“…Transgenic mice expressing human 17␤-HSD2 (HSD17B2TG) [31,123] showed growth retardation, delayed eye opening and disrupted spermatogenesis. Since part of these effects could be rescued by a synthetic retinoic acid receptor agonist, it can be speculated that 17␤-HSD2 plays a role in the action of retinoids.…”
Section: ˇ-Hsd2mentioning
confidence: 99%