First Author | Murao K | Year | 2006 |
Journal | Biochem Biophys Res Commun | Volume | 344 |
Issue | 1 | Pages | 226-32 |
PubMed ID | 16600185 | Mgi Jnum | J:108186 |
Mgi Id | MGI:3623187 | Doi | 10.1016/j.bbrc.2006.03.131 |
Citation | Murao K, et al. (2006) High-density lipoprotein is a potential growth factor for adrenocortical cells. Biochem Biophys Res Commun 344(1):226-32 |
abstractText | The entry of cholesterol contained within high-density lipoprotein (HDL) into adrenocortical cells is mediated by a human homologue of SR-BI, CD36, and LIMPII Analogous-1 (CLA-1) and thus augmenting their growth. To address the role of CLA-1, we created a mutant mCLA that lacked the C-terminal tail. HDL CE selective uptake by cells carrying the mCLA-1 receptor was fully active and equivalent to those transfected with full-length CLA-1 (fCLA-1). Expression of mCLA inhibited the proliferation of an adrenocortical cell line and the incorporation of [(3)H]thymidine into the cells. This effect was sensitive to wortmannin, an inhibitor of phosphoinositide 3-kinase (PI3K). Our transcriptional studies revealed that the inhibitory action of mCLA required the transcriptional factor AP-1 and the effect of HDL on AP-1 activation was also abrogated by wortmannin. These findings raise the possibility that the inhibitors of the effects of HDL may be of therapeutic value for adrenocortical tumor. |