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10.1073/pnas.1515076112 http://scihub22266oqcxt.onion/10.1073/pnas.1515076112 26655736!4702983!26655736     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26655736.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Proc+Natl+Acad+Sci+U+S+A 2015 ; 112 (52): 15928-33 Nephropedia Template TP {{tp|p=26655736|t=2015. Interleukin-11 alters placentation and causes preeclampsia features in mice |pdf=|usr=}}{{26655736}} gab.com Text Interleukin-11 alters placentation and causes preeclampsia features in mice JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=26655736 #FOAvip Preeclampsia (PE) is a pregnancy-specific disorder characterized by hypertension and proteinuria after 20 wk gestation. Abnormal extravillous trophoblast (EVT) invasion and remodeling of uterine spiral arterioles is thought to contribute to PE development. Interleukin-11 (IL11) impedes human EVT invasion in vitro and is elevated in PE decidua in women. We demonstrate that IL11 administered to mice causes development of PE features. Immunohistochemistry shows IL11 compromises trophoblast invasion, spiral artery remodeling, and placentation, leading to increased systolic blood pressure (SBP), proteinuria, and intrauterine growth restriction, although nonpregnant mice were unaffected. Real-time PCR array analysis identified pregnancy-associated plasma protein A2 (PAPPA2), associated with PE in women, as an IL11 regulated target. IL11 increased PAPPA2 serum and placental tissue levels in mice. In vitro, IL11 compromised primary human EVT invasion, whereas siRNA knockdown of PAPPA2 alleviated the effect. Genes regulating uterine natural killer (uNK) recruitment and differentiation were down-regulated and uNK cells were reduced after IL11 treatment in mice. IL11 withdrawal in mice at onset of PE features reduced SBP and proteinuria to control levels and alleviated placental labyrinth defects. In women, placental IL11 immunostaining levels increased in PE pregnancies and in serum collected from women before development of early-onset PE, shown by ELISA. These results indicate that elevated IL11 levels result in physiological changes at the maternal-fetal interface, contribute to abnormal placentation, and lead to the development of PE. Targeting placental IL11 may provide a new treatment option for PE. Twit Text FOAVip Interleukin-11 alters placentation and causes preeclampsia features in mice ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=26655736 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26655736 #FOAvip English Wikipedia <ref>{{Cite pmid|26655736}}</ref> Interleukin-11 alters placentation and causes preeclampsia features in mice #MMPMID26655736 Winship AL; Koga K; Menkhorst E; Van Sinderen M; Rainczuk K; Nagai M; Cuman C; Yap J; Zhang JG; Simmons D; Young MJ; Dimitriadis E Proc Natl Acad Sci U S A 2015[Dec]; 112 (52): 15928-33 PMID26655736show ga Preeclampsia (PE) is a pregnancy-specific disorder characterized by hypertension and proteinuria after 20 wk gestation. Abnormal extravillous trophoblast (EVT) invasion and remodeling of uterine spiral arterioles is thought to contribute to PE development. Interleukin-11 (IL11) impedes human EVT invasion in vitro and is elevated in PE decidua in women. We demonstrate that IL11 administered to mice causes development of PE features. Immunohistochemistry shows IL11 compromises trophoblast invasion, spiral artery remodeling, and placentation, leading to increased systolic blood pressure (SBP), proteinuria, and intrauterine growth restriction, although nonpregnant mice were unaffected. Real-time PCR array analysis identified pregnancy-associated plasma protein A2 (PAPPA2), associated with PE in women, as an IL11 regulated target. IL11 increased PAPPA2 serum and placental tissue levels in mice. In vitro, IL11 compromised primary human EVT invasion, whereas siRNA knockdown of PAPPA2 alleviated the effect. Genes regulating uterine natural killer (uNK) recruitment and differentiation were down-regulated and uNK cells were reduced after IL11 treatment in mice. IL11 withdrawal in mice at onset of PE features reduced SBP and proteinuria to control levels and alleviated placental labyrinth defects. In women, placental IL11 immunostaining levels increased in PE pregnancies and in serum collected from women before development of early-onset PE, shown by ELISA. These results indicate that elevated IL11 levels result in physiological changes at the maternal-fetal interface, contribute to abnormal placentation, and lead to the development of PE. Targeting placental IL11 may provide a new treatment option for PE. |Animals[MESH] |Blotting, Western[MESH] |Decidua/drug effects/metabolism[MESH] |Enzyme-Linked Immunosorbent Assay[MESH] |Female[MESH] |Gene Expression Regulation, Developmental/drug effects[MESH] |Humans[MESH] |Immunohistochemistry[MESH] |Interleukin-11/genetics/*metabolism/pharmacology[MESH] |Male[MESH] |Mice, Inbred C57BL[MESH] |Placenta/drug effects/*metabolism[MESH] |Placentation/drug effects/genetics/*physiology[MESH] |Pre-Eclampsia/genetics/*metabolism[MESH] |Pregnancy[MESH] |Pregnancy-Associated Plasma Protein-A/genetics/metabolism[MESH] |RNA Interference[MESH] |Receptors, Interleukin-11/genetics/metabolism[MESH] |Recombinant Proteins/pharmacology[MESH]Interleukin-11 alters placentation and causes preeclampsia features in(epmc).pdf DeepDyve Pubget Overpricing