The low density lipoprotein receptor (LDLR)-related protein (LRP) is a multifunctional receptor which mediates the endocytic uptake of several ligands implicated in Alzheimer's disease pathophysiology. Although LRP, as a member of the LDLR family, is likely to be regulated in response to various cellular stresses, this regulation has not been fully understood yet. In the present study we studied the regulation of LRP expression in primary cultured rat astrocytes in response to serum deprivation as a general cellular stress. A significant increase in LRP expression was detected after serum deprivation and this increase was blocked by treatment of U0126, an inhibitor of MAP kinase. This serum deprivation action was partially reversed by either serum or D-glucose supplementation, but further augmented by glutamine. This result contrasted with a finding that glutamine suppressed gadd153 protein induced by serum deprivation. Taken together, the present data suggest that serum deprivation induces dramatically LRP expression in astrocytes partly by MAPK signaling pathways and by signaling pathways apparently distinct from gadd153 induction.
|Number of pages
|Biochemical and Biophysical Research Communications
|Published - 2002
Bibliographical noteFunding Information:
This work was supported in part by Grants from National Institute of Health, Korea (334-6113-211-207-00) (to Dr. Inho Jo), and by Biomedical Brain Research Center grant from the Ministry of Health and Welfare (to Dr. Sangmee Ahn Jo). We thank Dr. Hong Pyo Kim for preparing rat astrocyte and Dr. Jeong-Eun Park and Ms. Eun-Kyung Kim for preparation of data presentation and statistical analysis.
- Growth arrest and DNA damage-inducible
- Low density lipoprotein receptor-related protein
- MAP kinase
- Serum deprivation