FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3206988238> ?p ?o ?g. }

• W3206988238 endingPage "1367" @default.
• W3206988238 startingPage "1357" @default.
• W3206988238 abstract "As one of the most common endocrine disorders affecting women, polycystic ovary syndrome (PCOS) is associated with serious conditions including anovulation, endometrial cancer, infertility, hyperandrogenemia, and an increased risk for obesity and metabolic derangements. One contributing etiology to the pathophysiology of hyperandrogenemia associated with PCOS is an intrinsic alteration in ovarian steroidogenesis, leading to enhanced synthesis of androgens including testosterone. Studies have suggested that the increased testosterone synthesis seen in PCOS is driven in part by increased activity of CYP17A1, the rate-limiting enzyme for the formation of androgens in the gonads and adrenal cortex, which represents a critical factor driving enhanced testosterone secretion in PCOS. In this work, we evaluated the hypothesis that dysregulation of the noncoding RNA H19 results in aberrant CYP17 and testosterone production. To achieve this, we measured Cyp17 in ovarian tissues of H19 knockout mice, and quantified serum testosterone levels, in comparison with wild-type controls. We also evaluated circulating and ovarian H19 expression and correlated results with the presence or absence of PCOS in a group of women undergoing evaluation and treatment for infertility. We found that the loss of H19 in a mouse model results in decreased ovarian Cyp17, along with decreased serum testosterone in female mice. Moreover, utilizing serum samples and cumulus cells from women with PCOS, we showed that circulating and ovarian levels of H19 are increased in women with PCOS compared to controls. Findings from our multimodal experimental strategy, involving both a mouse model of dysregulated H19 expression and clinical serum and ovarian cellular samples from women with PCOS, suggest that the loss of H19 may disrupt androgen production via a Cyp17-mediated mechanism. Conversely, excess H19 may play a role in the pathogenesis of PCOS-associated hyperandrogenemia." @default.
• W3206988238 created "2021-10-25" @default.
• W3206988238 creator A5004975090 @default.
• W3206988238 creator A5007467853 @default.
• W3206988238 creator A5029185942 @default.
• W3206988238 creator A5034188355 @default.
• W3206988238 creator A5039690976 @default.
• W3206988238 creator A5046189414 @default.
• W3206988238 date "2021-10-15" @default.
• W3206988238 modified "2023-10-18" @default.
• W3206988238 title "Aberrant H19 Expression Disrupts Ovarian Cyp17 and Testosterone Production and Is Associated with Polycystic Ovary Syndrome in Women" @default.
• W3206988238 cites W1134466512 @default.
• W3206988238 cites W1512733937 @default.
• W3206988238 cites W1975847255 @default.
• W3206988238 cites W1976840283 @default.
• W3206988238 cites W1977279728 @default.
• W3206988238 cites W1986197409 @default.
• W3206988238 cites W2004714113 @default.
• W3206988238 cites W2013183819 @default.
• W3206988238 cites W2014046105 @default.
• W3206988238 cites W2019727134 @default.
• W3206988238 cites W2022756254 @default.
• W3206988238 cites W2024582127 @default.
• W3206988238 cites W2036463060 @default.
• W3206988238 cites W2037129295 @default.
• W3206988238 cites W2045892891 @default.
• W3206988238 cites W2059910219 @default.
• W3206988238 cites W2062389660 @default.
• W3206988238 cites W2064538303 @default.
• W3206988238 cites W2068205741 @default.
• W3206988238 cites W2072263996 @default.
• W3206988238 cites W2076169228 @default.
• W3206988238 cites W2082718793 @default.
• W3206988238 cites W2087286513 @default.
• W3206988238 cites W2096887626 @default.
• W3206988238 cites W2105952005 @default.
• W3206988238 cites W2113329249 @default.
• W3206988238 cites W2115086062 @default.
• W3206988238 cites W2118676910 @default.
• W3206988238 cites W2126438731 @default.
• W3206988238 cites W2130006720 @default.
• W3206988238 cites W2135518377 @default.
• W3206988238 cites W2139449175 @default.
• W3206988238 cites W2139915659 @default.
• W3206988238 cites W2167260945 @default.
• W3206988238 cites W2171871916 @default.
• W3206988238 cites W2274119815 @default.
• W3206988238 cites W2282873125 @default.
• W3206988238 cites W2318408074 @default.
• W3206988238 cites W2322245085 @default.
• W3206988238 cites W2333286680 @default.
• W3206988238 cites W2402933887 @default.
• W3206988238 cites W2523733243 @default.
• W3206988238 cites W2528009933 @default.
• W3206988238 cites W2537254995 @default.
• W3206988238 cites W2547256937 @default.
• W3206988238 cites W2618295127 @default.
• W3206988238 cites W2625169067 @default.
• W3206988238 cites W2661470941 @default.
• W3206988238 cites W2744800174 @default.
• W3206988238 cites W2793824550 @default.
• W3206988238 cites W2888366987 @default.
• W3206988238 cites W2906398640 @default.
• W3206988238 cites W2937578293 @default.
• W3206988238 cites W2939459765 @default.
• W3206988238 cites W2942698391 @default.
• W3206988238 cites W2943588752 @default.
• W3206988238 cites W2948443381 @default.
• W3206988238 cites W2968913425 @default.
• W3206988238 cites W3024371706 @default.
• W3206988238 cites W3031160124 @default.
• W3206988238 cites W3031585628 @default.
• W3206988238 cites W3036813420 @default.
• W3206988238 cites W3040790573 @default.
• W3206988238 cites W3087113995 @default.
• W3206988238 cites W4211231448 @default.
• W3206988238 cites W749462386 @default.
• W3206988238 doi "https://doi.org/10.1007/s43032-021-00700-5" @default.
• W3206988238 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34655046" @default.
• W3206988238 hasPublicationYear "2021" @default.
• W3206988238 type Work @default.
• W3206988238 sameAs 3206988238 @default.
• W3206988238 citedByCount "5" @default.
• W3206988238 countsByYear W32069882382022 @default.
• W3206988238 countsByYear W32069882382023 @default.
• W3206988238 crossrefType "journal-article" @default.
• W3206988238 hasAuthorship W3206988238A5004975090 @default.
• W3206988238 hasAuthorship W3206988238A5007467853 @default.
• W3206988238 hasAuthorship W3206988238A5029185942 @default.
• W3206988238 hasAuthorship W3206988238A5034188355 @default.
• W3206988238 hasAuthorship W3206988238A5039690976 @default.
• W3206988238 hasAuthorship W3206988238A5046189414 @default.
• W3206988238 hasBestOaLocation W32069882382 @default.
• W3206988238 hasConcept C126322002 @default.
• W3206988238 hasConcept C134018914 @default.
• W3206988238 hasConcept C142716871 @default.
• W3206988238 hasConcept C181199279 @default.
• W3206988238 hasConcept C2776683971 @default.

• next