Phosphatidylserine receptor is required for clearance of apoptotic cells

Speaker: 吳岳穎

Commentator: 楊倍昌 老師

Time: 03/31/2004 14:00~15:00

Place: Room 601

Abstract:

   During development, the control of cell number between cell proliferation and cell death plays a critical role in our highly integrated systems. Apoptosis, also called programmed cell death, has the ability to limit the inflammatory responses and autoimmune disease through the disposal of apoptotic cells by rapid uptake by phagocytes (1). In the process of cell apoptosis, some “eat me” flags for phagocytes recognition, such as phosphatidylserine (PS), would expose on the outer surface of dying cells. Many receptors are involved in the identification of PS, including b₂-glycoprotein I receptor, a_vb₃ vitronectin receptor, Mer receptor tyrosine kinase, and phosphatidylserine receptor (PSR). In previous in vitro study, PSR is essential for the clearance of apoptotic cells by phagocytes, but the underlying mechanisms of this process need to be elucidated. In this study, the authors found abnormal lung development and accumulation of apoptotic cells in PSR-deficient mice. Furthermore, severe brain malformation, hyperplasia phenotype, and defective engulfment of apoptotic cells were observed in 15% of PSR-deficient mice CNS. Such defects lead to neonatal lethality and indicate that PSR is essential in early stages of mammalian organogenesis and development. Impaired PSR-dependent phagocytosis of cell corpses might provide another possible mechanism, that is different from defects in lung surfactant protein expression, in some forms of respiratory distress syndrome (2).

References:

1.      Pittoni V. and Valesini G. The clearance of apoptotic cells: implications for autoimmunity. Autoimmun. Rev. 1, 154-161 (2002).

2.      Li M. O. et al. Phosphatidylserine receptor is required for clearance of apoptotic cells. Science 302, 1560-1563 (2003).