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Protein Kinase Bα/Akt1 Regulates Placental Development and Fetal Growth

The Journal of biological chemistry, 2003-08, Vol.278 (34), p.32124-32131 [Peer Reviewed Journal]

2003 © 2003 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology. ;ISSN: 0021-9258 ;EISSN: 1083-351X ;DOI: 10.1074/jbc.M302847200 ;PMID: 12783884

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Title:
Protein Kinase Bα/Akt1 Regulates Placental Development and Fetal Growth
Author: Yang, Zhong-Zhou ; Tschopp, Oliver ; Hemmings-Mieszczak, Maja ; Feng, Jianhua ; Brodbeck, Daniela ; Perentes, Elias ; Hemmings, Brian A.
Subjects: Amino Acid Sequence ; Animals ; Base Sequence ; Blotting, Western ; DNA Primers ; Embryonic and Fetal Development - physiology ; Immunohistochemistry ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Placentation ; Protein-Serine-Threonine Kinases - genetics ; Protein-Serine-Threonine Kinases - physiology ; Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-akt
Is Part Of: The Journal of biological chemistry, 2003-08, Vol.278 (34), p.32124-32131
Description: Protein kinase Bα (PKBα/Akt1) is implicated in the regulation of metabolism, transcription, cell survival, angiogenesis, cell migration, growth, and tumorigenesis. Previously, it was reported that PKBα-deficient mice are small with increased neonatal mortality (Cho, H., Thorvaldsen, J. L., Chu, Q., Feng, F., and Birnbaum, M. J. (2001) J. Biol. Chem. 276, 38349–38352 and Chen, W. S., Xu, P. Z., Gottlob, K., Chen, M. L., Sokol, K., Shiyanova, T., Roninson, I., Wenig, W., Suzuki, R., Tobe, K., Kadowaki, T., and Hay, N. (2001) Genes Dev. 15, 2203–2208). Here we show that PKBα is widely expressed in placenta including all types of trophoblast and vascular endothelial cells. Pkbα–/– placentae display significant hypotrophy, with marked reduction of the decidual basalis and nearly complete loss of glycogen-containing cells in the spongiotrophoblast, and exhibit decreased vascularization. Pkbα–/– placentae also show significant reduction of phosphorylation of PKB and endothelial nitric-oxide synthase. These defects may cause placental insufficiency, fetal growth impairment, and neonatal mortality. These data represent the first evidence for the role of PKBα and endothelial nitricoxide synthase in regulating placental development and provide an animal model for intrauterine growth retardation.
Publisher: United States: Elsevier Inc
Language: English
Identifier: ISSN: 0021-9258
EISSN: 1083-351X
DOI: 10.1074/jbc.M302847200
PMID: 12783884
Source: MEDLINE
Alma/SFX Local Collection

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Protein Kinase Bα/Akt1 Regulates Placental Development and Fetal Growth

2003 © 2003 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology. ;ISSN: 0021-9258 ;EISSN: 1083-351X ;DOI: 10.1074/jbc.M302847200 ;PMID: 12783884

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