Publication Date:
2003-12-04
Description:
Cells undergoing apoptosis during development are removed by phagocytes, but the underlying mechanisms of this process are not fully understood. Phagocytes lacking the phosphatidylserine receptor (PSR) were defective in removing apoptotic cells. Consequently, in PSR-deficient mice, dead cells accumulated in the lung and brain, causing abnormal development and leading to neonatal lethality. A fraction of PSR knockout mice manifested a hyperplasic brain phenotype resembling that of mice deficient in the cell death-associated genes encoding Apaf-1, caspase-3, and caspase-9, which suggests that phagocytes may also be involved in promoting apoptosis. These data demonstrate a critical role for PSR in early stages of mammalian organogenesis and suggest that this receptor may be involved in respiratory distress syndromes and congenital brain malformations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Ming O -- Sarkisian, Matthew R -- Mehal, Wajahat Z -- Rakic, Pasko -- Flavell, Richard A -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1560-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14645847" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
*Apoptosis
;
Brain/abnormalities/cytology/*embryology
;
Cell Division
;
Cell Nucleus/ultrastructure
;
Epithelial Cells/physiology/ultrastructure
;
Eye/embryology
;
Eye Abnormalities/etiology
;
Hematopoietic Stem Cell Transplantation
;
In Situ Nick-End Labeling
;
Inflammation
;
Lung/cytology/*embryology/physiology
;
Macrophages/*physiology
;
Mesoderm/ultrastructure
;
Mice
;
Mice, Knockout
;
Necrosis
;
Neurons/cytology
;
Phagocytosis
;
Phenotype
;
Phosphatidylserines/metabolism
;
Pulmonary Surfactants/metabolism
;
Receptors, Cell Surface/genetics/*metabolism
;
Respiratory Insufficiency/etiology
;
Reverse Transcriptase Polymerase Chain Reaction
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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