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Elevated placental adenosine signaling contributes to the pathogenesis of preeclampsia.
Iriyama, Takayuki; Sun, Kaiqi; Parchim, Nicholas F; Li, Jessica; Zhao, Cheng; Song, Anren; Hart, Laura A; Blackwell, Sean C; Sibai, Baha M; Chan, Lee-Nien L; Chan, Teh-Sheng; Hicks, M John; Blackburn, Michael R; Kellems, Rodney E; Xia, Yang.
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  • Iriyama T; From Departments of Biochemistry and Molecular Biology (T.I., K.S., N.F.P., J.L., C.Z., A.S., M.R.B., R.E.K., Y.X.) and Department of Obstetrics, Gynecology, and Reproductive Sciences (L.A.H., S.C.B., B.M.S.), University of Texas Medical School at Houston: Department of Obstetrics and Gynecology, Fa
  • Sun K; From Departments of Biochemistry and Molecular Biology (T.I., K.S., N.F.P., J.L., C.Z., A.S., M.R.B., R.E.K., Y.X.) and Department of Obstetrics, Gynecology, and Reproductive Sciences (L.A.H., S.C.B., B.M.S.), University of Texas Medical School at Houston: Department of Obstetrics and Gynecology, Fa
  • Parchim NF; From Departments of Biochemistry and Molecular Biology (T.I., K.S., N.F.P., J.L., C.Z., A.S., M.R.B., R.E.K., Y.X.) and Department of Obstetrics, Gynecology, and Reproductive Sciences (L.A.H., S.C.B., B.M.S.), University of Texas Medical School at Houston: Department of Obstetrics and Gynecology, Fa
  • Li J; From Departments of Biochemistry and Molecular Biology (T.I., K.S., N.F.P., J.L., C.Z., A.S., M.R.B., R.E.K., Y.X.) and Department of Obstetrics, Gynecology, and Reproductive Sciences (L.A.H., S.C.B., B.M.S.), University of Texas Medical School at Houston: Department of Obstetrics and Gynecology, Fa
  • Zhao C; From Departments of Biochemistry and Molecular Biology (T.I., K.S., N.F.P., J.L., C.Z., A.S., M.R.B., R.E.K., Y.X.) and Department of Obstetrics, Gynecology, and Reproductive Sciences (L.A.H., S.C.B., B.M.S.), University of Texas Medical School at Houston: Department of Obstetrics and Gynecology, Fa
  • Song A; From Departments of Biochemistry and Molecular Biology (T.I., K.S., N.F.P., J.L., C.Z., A.S., M.R.B., R.E.K., Y.X.) and Department of Obstetrics, Gynecology, and Reproductive Sciences (L.A.H., S.C.B., B.M.S.), University of Texas Medical School at Houston: Department of Obstetrics and Gynecology, Fa
  • Hart LA; From Departments of Biochemistry and Molecular Biology (T.I., K.S., N.F.P., J.L., C.Z., A.S., M.R.B., R.E.K., Y.X.) and Department of Obstetrics, Gynecology, and Reproductive Sciences (L.A.H., S.C.B., B.M.S.), University of Texas Medical School at Houston: Department of Obstetrics and Gynecology, Fa
  • Blackwell SC; From Departments of Biochemistry and Molecular Biology (T.I., K.S., N.F.P., J.L., C.Z., A.S., M.R.B., R.E.K., Y.X.) and Department of Obstetrics, Gynecology, and Reproductive Sciences (L.A.H., S.C.B., B.M.S.), University of Texas Medical School at Houston: Department of Obstetrics and Gynecology, Fa
  • Sibai BM; From Departments of Biochemistry and Molecular Biology (T.I., K.S., N.F.P., J.L., C.Z., A.S., M.R.B., R.E.K., Y.X.) and Department of Obstetrics, Gynecology, and Reproductive Sciences (L.A.H., S.C.B., B.M.S.), University of Texas Medical School at Houston: Department of Obstetrics and Gynecology, Fa
  • Chan LN; From Departments of Biochemistry and Molecular Biology (T.I., K.S., N.F.P., J.L., C.Z., A.S., M.R.B., R.E.K., Y.X.) and Department of Obstetrics, Gynecology, and Reproductive Sciences (L.A.H., S.C.B., B.M.S.), University of Texas Medical School at Houston: Department of Obstetrics and Gynecology, Fa
  • Chan TS; From Departments of Biochemistry and Molecular Biology (T.I., K.S., N.F.P., J.L., C.Z., A.S., M.R.B., R.E.K., Y.X.) and Department of Obstetrics, Gynecology, and Reproductive Sciences (L.A.H., S.C.B., B.M.S.), University of Texas Medical School at Houston: Department of Obstetrics and Gynecology, Fa
  • Hicks MJ; From Departments of Biochemistry and Molecular Biology (T.I., K.S., N.F.P., J.L., C.Z., A.S., M.R.B., R.E.K., Y.X.) and Department of Obstetrics, Gynecology, and Reproductive Sciences (L.A.H., S.C.B., B.M.S.), University of Texas Medical School at Houston: Department of Obstetrics and Gynecology, Fa
  • Blackburn MR; From Departments of Biochemistry and Molecular Biology (T.I., K.S., N.F.P., J.L., C.Z., A.S., M.R.B., R.E.K., Y.X.) and Department of Obstetrics, Gynecology, and Reproductive Sciences (L.A.H., S.C.B., B.M.S.), University of Texas Medical School at Houston: Department of Obstetrics and Gynecology, Fa
  • Kellems RE; From Departments of Biochemistry and Molecular Biology (T.I., K.S., N.F.P., J.L., C.Z., A.S., M.R.B., R.E.K., Y.X.) and Department of Obstetrics, Gynecology, and Reproductive Sciences (L.A.H., S.C.B., B.M.S.), University of Texas Medical School at Houston: Department of Obstetrics and Gynecology, Fa
  • Xia Y; From Departments of Biochemistry and Molecular Biology (T.I., K.S., N.F.P., J.L., C.Z., A.S., M.R.B., R.E.K., Y.X.) and Department of Obstetrics, Gynecology, and Reproductive Sciences (L.A.H., S.C.B., B.M.S.), University of Texas Medical School at Houston: Department of Obstetrics and Gynecology, Fa
Circulation ; 131(8): 730-41, 2015 Feb 24.
Article en En | MEDLINE | ID: mdl-25538227
BACKGROUND: Preeclampsia is a prevalent hypertensive disorder of pregnancy and a leading cause of maternal and neonatal morbidity and mortality worldwide. This pathogenic condition is speculated to be caused by placental abnormalities that contribute to the maternal syndrome. However, the specific factors and signaling pathways that lead to impaired placentas and maternal disease development remain elusive. METHODS AND RESULTS: Using 2 independent animal models of preeclampsia (genetically engineered pregnant mice with elevated adenosine exclusively in placentas and a pathogenic autoantibody-induced preeclampsia mouse model), we demonstrated that chronically elevated placental adenosine was sufficient to induce hallmark features of preeclampsia, including hypertension, proteinuria, small fetuses, and impaired placental vasculature. Genetic and pharmacological approaches revealed that elevated placental adenosine coupled with excessive A2B adenosine receptor (ADORA2B) signaling contributed to the development of these features of preeclampsia. Mechanistically, we provided both human and mouse evidence that elevated placental CD73 is a key enzyme causing increased placental adenosine, thereby contributing to preeclampsia. CONCLUSIONS: We determined that elevated placental adenosine signaling is a previously unrecognized pathogenic factor for preeclampsia. Moreover, our findings revealed the molecular basis underlying the elevation of placental adenosine and the detrimental role of excess placental adenosine in the pathophysiology of preeclampsia, and thereby, we highlight novel therapeutic targets.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Placenta / Preeclampsia / Transducción de Señal / Adenosina / Regulación hacia Arriba Tipo de estudio: Etiology_studies / Prognostic_studies Límite: Adult / Animals / Female / Humans / Pregnancy Idioma: En Revista: Circulation Año: 2015 Tipo del documento: Article Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Placenta / Preeclampsia / Transducción de Señal / Adenosina / Regulación hacia Arriba Tipo de estudio: Etiology_studies / Prognostic_studies Límite: Adult / Animals / Female / Humans / Pregnancy Idioma: En Revista: Circulation Año: 2015 Tipo del documento: Article Pais de publicación: Estados Unidos