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פותח על ידי קלירמאש פתרונות בע"מ -
PTEN overexpression suppresses proliferation and differentiation and enhances apoptosis of the mouse mammary epithelium
Year:
2002
Source of publication :
Journal of Clinical Investigation
Authors :
שני, משה
;
.
Volume :
110
Co-Authors:
Dupont, J., Section on Molecular and Cellular Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, United States, Physiologie de la Reproduction et des Comportements, Université Francois Rabelais de Tours, Nouzilly, France
Renou, J.P., Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, United States
Shani, M., Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, United States
Hennighausen, L., Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, United States
LeRoith, D., Section on Molecular and Cellular Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, United States, Clinical Endocrinology Branch, NIDDK, NIH, Bethesda, MD 20892-1758, United States
Facilitators :
From page:
815
To page:
825
(
Total pages:
11
)
Abstract:
The phosphatase PTEN regulates growth, adhesion, and apoptosis, among many other cell processes. To investigate its role during mouse mammary gland development, we generated MK-PTEN, a transgenic mouse model in which human PTEN is overexpressed in ductal and alveolar mammary epithelium during puberty, pregnancy, lactation, and involution. No obvious phenotype was observed in mammary tissue of pubescent virgin mice. However, MK-PTEN females could not lactate normally, and ∼30% of pups died, with survivors exhibiting growth retardation. Transgenic offspring nursed by wild-type foster mothers, conversely, developed normally. This phenotype is consistent with a reduced number of alveolar epithelial cells due to a decrease in cell proliferation and an increase in apoptosis. Using mammary-enriched cDNA microarrays, we identified several genes that were preferentially expressed in MK-PTEN mammary tissue, including the IGF-binding protein-5 (Igfbp5) gene, and others whose expression was reduced, including the genes for c-Jun amino-terminal kinase. Secretory epithelial cell differentiation was impaired, as measured by the expression of specific milk protein genes. MK-PTEN mice also exhibited a 50% decrease in the phosphorylation state of Akt. Taken together, these results suggest that PTEN controls mammary gland development and, consequently, lactation.
Note:
Related Files :
Animals
apoptosis
Female
gene expression
lactation
mice
phenotype
pregnancy
עוד תגיות
תוכן קשור
More details
DOI :
10.1172/JCI200213829
Article number:
Affiliations:
Database:
סקופוס
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
23382
Last updated date:
02/03/2022 17:27
Creation date:
16/04/2018 23:59
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Scientific Publication
PTEN overexpression suppresses proliferation and differentiation and enhances apoptosis of the mouse mammary epithelium
110
Dupont, J., Section on Molecular and Cellular Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, United States, Physiologie de la Reproduction et des Comportements, Université Francois Rabelais de Tours, Nouzilly, France
Renou, J.P., Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, United States
Shani, M., Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, United States
Hennighausen, L., Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, United States
LeRoith, D., Section on Molecular and Cellular Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, United States, Clinical Endocrinology Branch, NIDDK, NIH, Bethesda, MD 20892-1758, United States
PTEN overexpression suppresses proliferation and differentiation and enhances apoptosis of the mouse mammary epithelium
The phosphatase PTEN regulates growth, adhesion, and apoptosis, among many other cell processes. To investigate its role during mouse mammary gland development, we generated MK-PTEN, a transgenic mouse model in which human PTEN is overexpressed in ductal and alveolar mammary epithelium during puberty, pregnancy, lactation, and involution. No obvious phenotype was observed in mammary tissue of pubescent virgin mice. However, MK-PTEN females could not lactate normally, and ∼30% of pups died, with survivors exhibiting growth retardation. Transgenic offspring nursed by wild-type foster mothers, conversely, developed normally. This phenotype is consistent with a reduced number of alveolar epithelial cells due to a decrease in cell proliferation and an increase in apoptosis. Using mammary-enriched cDNA microarrays, we identified several genes that were preferentially expressed in MK-PTEN mammary tissue, including the IGF-binding protein-5 (Igfbp5) gene, and others whose expression was reduced, including the genes for c-Jun amino-terminal kinase. Secretory epithelial cell differentiation was impaired, as measured by the expression of specific milk protein genes. MK-PTEN mice also exhibited a 50% decrease in the phosphorylation state of Akt. Taken together, these results suggest that PTEN controls mammary gland development and, consequently, lactation.
Scientific Publication
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