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10.1161/JAHA.117.005506 http://scihub22266oqcxt.onion/10.1161/JAHA.117.005506 C5586418!5586418 !28778941     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28778941 &cmd=llinks): Failed to open stream: HTTP request failed! 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Prenatal Mechanistic Target of Rapamycin Complex 1 (m TORC1) Inhibition by Rapamycin Treatment of Pregnant Mice Causes Intrauterine Growth Restriction and Alters Postnatal Cardiac Growth, Morphology, and Function |pdf=|usr=}}{{28778941 }} gab.com Text Prenatal Mechanistic Target of Rapamycin Complex 1 (m TORC1) Inhibition by Rapamycin Treatment of Pregnant Mice Causes Intrauterine Growth Restriction and Alters Postnatal Cardiac Growth, Morphology, and Function JO: J Am Heart Assoc http://www.kidney.de/pget.php?&tw=1&pmid=28778941 #FOAvip BACKGROUND: Fetal growth impacts cardiovascular health throughout postnatal life in humans. Various animal models of intrauterine growth restriction exhibit reduced heart size at birth, which negatively influences cardiac function in adulthood. The mechanistic target of rapamycin complex 1 (mTORC1) integrates nutrient and growth factor availability with cell growth, thereby regulating organ size. This study aimed at elucidating a possible involvement of mTORC1 in intrauterine growth restriction and prenatal heart growth. METHODS AND RESULTS: We inhibited mTORC1 in fetal mice by rapamycin treatment of pregnant dams in late gestation. Prenatal rapamycin treatment reduces mTORC1 activity in various organs at birth, which is fully restored by postnatal day 3. Rapamycin-treated neonates exhibit a 16% reduction in body weight compared with vehicle-treated controls. Heart weight decreases by 35%, resulting in a significantly reduced heart weight/body weight ratio, smaller left ventricular dimensions, and reduced cardiac output in rapamycin- versus vehicle-treated mice at birth. Although proliferation rates in neonatal rapamycin-treated hearts are unaffected, cardiomyocyte size is reduced, and apoptosis increased compared with vehicle-treated neonates. Rapamycin-treated mice exhibit postnatal catch-up growth, but body weight and left ventricular mass remain reduced in adulthood. Prenatal mTORC1 inhibition causes a reduction in cardiomyocyte number in adult hearts compared with controls, which is partially compensated for by an increased cardiomyocyte volume, resulting in normal cardiac function without maladaptive left ventricular remodeling. CONCLUSIONS: Prenatal rapamycin treatment of pregnant dams represents a new mouse model of intrauterine growth restriction and identifies an important role of mTORC1 in perinatal cardiac growth. Twit Text FOAVip Prenatal Mechanistic Target of Rapamycin Complex 1 (m TORC1) Inhibition by Rapamycin Treatment of Pregnant Mice Causes Intrauterine Growth Restriction and Alters Postnatal Cardiac Growth, Morphology, and Function ????J Am Heart Assoc http://www.kidney.de/pget.php?&tw=1&pmid=28778941 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28778941 #FOAvip English Wikipedia <ref>{{Cite pmid|28778941 }}</ref> Prenatal Mechanistic Target of Rapamycin Complex 1 (m TORC1) Inhibition by Rapamycin Treatment of Pregnant Mice Causes Intrauterine Growth Restriction and Alters Postnatal Cardiac Growth, Morphology, and Function #MMPMID28778941 Hennig M ; Fiedler S ; Jux C ; Thierfelder L ; Drenckhahn JD J Am Heart Assoc 2017[Aug]; 6 (8 ): ä PMID28778941 show ga BACKGROUND: Fetal growth impacts cardiovascular health throughout postnatal life in humans. Various animal models of intrauterine growth restriction exhibit reduced heart size at birth, which negatively influences cardiac function in adulthood. The mechanistic target of rapamycin complex 1 (mTORC1) integrates nutrient and growth factor availability with cell growth, thereby regulating organ size. This study aimed at elucidating a possible involvement of mTORC1 in intrauterine growth restriction and prenatal heart growth. METHODS AND RESULTS: We inhibited mTORC1 in fetal mice by rapamycin treatment of pregnant dams in late gestation. Prenatal rapamycin treatment reduces mTORC1 activity in various organs at birth, which is fully restored by postnatal day 3. Rapamycin-treated neonates exhibit a 16% reduction in body weight compared with vehicle-treated controls. Heart weight decreases by 35%, resulting in a significantly reduced heart weight/body weight ratio, smaller left ventricular dimensions, and reduced cardiac output in rapamycin- versus vehicle-treated mice at birth. Although proliferation rates in neonatal rapamycin-treated hearts are unaffected, cardiomyocyte size is reduced, and apoptosis increased compared with vehicle-treated neonates. Rapamycin-treated mice exhibit postnatal catch-up growth, but body weight and left ventricular mass remain reduced in adulthood. Prenatal mTORC1 inhibition causes a reduction in cardiomyocyte number in adult hearts compared with controls, which is partially compensated for by an increased cardiomyocyte volume, resulting in normal cardiac function without maladaptive left ventricular remodeling. CONCLUSIONS: Prenatal rapamycin treatment of pregnant dams represents a new mouse model of intrauterine growth restriction and identifies an important role of mTORC1 in perinatal cardiac growth. |*Prenatal Exposure Delayed Effects [MESH] |Animals [MESH] |Animals, Newborn [MESH] |Apoptosis/drug effects [MESH] |Cardiac Output/drug effects [MESH] |Cell Size/drug effects [MESH] |Female [MESH] |Fetal Growth Retardation/*chemically induced/metabolism/pathology/physiopathology [MESH] |Fetal Heart/*drug effects/growth & development/pathology [MESH] |Gestational Age [MESH] |Homeobox Protein Nkx-2.5/genetics [MESH] |Lyases/deficiency/genetics [MESH] |Mechanistic Target of Rapamycin Complex 1/*antagonists & inhibitors/metabolism [MESH] |Mice, 129 Strain [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Myocardial Contraction/drug effects [MESH] |Myocytes, Cardiac/drug effects/metabolism/pathology [MESH] |Organ Size [MESH] |Organogenesis/drug effects [MESH] |Pregnancy [MESH] |Promoter Regions, Genetic [MESH] |Sirolimus/*pharmacology [MESH] |Ventricular Function, Left/drug effects [MESH]Prenatal Mechanistic Target of Rapamycin Complex 1 (m TORC1) Inhibitio(epmc).pdf DeepDyve Pubget Overpricing