Your browser doesn't support javascript.
loading
Upregulation of DAPK2 ameliorates oxidative damage and apoptosis of placental cells in hypertensive disorder complicating pregnancy by suppressing human placental microvascular endothelial cell autophagy through the mTOR signaling pathway.
Wang, Yan; Liu, Lian-Lian; Tian, Yuan; Chen, Yang; Zha, Wen-Hui; Li, Yang; Wu, Fu-Ju.
Afiliación
  • Wang Y; Department of Obstetrics and Gynecology, The Second Hospital of Jilin University, Changchun 130041, PR China.
  • Liu LL; Department of Obstetrics and Gynecology, The Second Hospital of Jilin University, Changchun 130041, PR China.
  • Tian Y; Department of Obstetrics and Gynecology, The Second Hospital of Jilin University, Changchun 130041, PR China.
  • Chen Y; Department of Obstetrics and Gynecology, The Second Hospital of Jilin University, Changchun 130041, PR China.
  • Zha WH; Department of Obstetrics and Gynecology, The Second Hospital of Jilin University, Changchun 130041, PR China.
  • Li Y; Department of Obstetrics and Gynecology, The Second Hospital of Jilin University, Changchun 130041, PR China.
  • Wu FJ; Department of Obstetrics and Gynecology, The Second Hospital of Jilin University, Changchun 130041, PR China. Electronic address: Drwu_fuju@126.com.
Int J Biol Macromol ; 121: 488-497, 2019 Jan.
Article en En | MEDLINE | ID: mdl-30243997
Death-associated protein kinase 2 (DAPK2) has indicated functional roles in cellular processes, including survival, apoptosis, and autophagy. This study is aimed to identify the effect of DAPK2 on oxidative damage and apoptosis of placental cells in hypertensive disorder complicating pregnancy (HDCP) through mTOR pathway. Microarray-based gene expression analysis was performed to predict the differentially expressed genes related to HDCP. To investigate the specific mechanism of DAPK2 in HDCP cells, placental microvascular endothelial cells were treated with mimic or siRNA of DAPK2 and mTOR to detect the expression of related genes, cell autophagy and apoptosis and oxidative damage. Finally, rats were modeled with HDCP to verify the cell experiment results. DAPK2 was downregulated in HDCP, and could activate mTOR. Besides, DAPK2 overexpression led to decreases in autophagy in HPVECs as well as apoptosis and oxidative damage in placental cells indicated by a substantial decrease in Beclin-1, LC3 II/LC3 I and Bax along with an increase in Bcl-2, 4EBP1 and p70S6K. It also ameliorates blood pressure elevation in HDCP rats. The study defined remission effect of DAPK2 on placental cell oxidative damage and apoptosis in HDCP via mTOR activation. Together, DAPK2 regulating mTOR pathway presents a promising therapy for HDCP treatment.
Asunto(s)
Palabras clave

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Transducción de Señal / Regulación hacia Arriba / Estrés Oxidativo / Células Endoteliales / Hipertensión Inducida en el Embarazo / Serina-Treonina Quinasas TOR / Proteínas Quinasas Asociadas a Muerte Celular Tipo de estudio: Prognostic_studies Límite: Female / Humans / Pregnancy Idioma: En Revista: Int J Biol Macromol Año: 2019 Tipo del documento: Article

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Transducción de Señal / Regulación hacia Arriba / Estrés Oxidativo / Células Endoteliales / Hipertensión Inducida en el Embarazo / Serina-Treonina Quinasas TOR / Proteínas Quinasas Asociadas a Muerte Celular Tipo de estudio: Prognostic_studies Límite: Female / Humans / Pregnancy Idioma: En Revista: Int J Biol Macromol Año: 2019 Tipo del documento: Article