| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
Papers In Press, published online ahead of print November 16, 2002
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Pharmacological Sciences, University Medical Center, Stony Brook, NY 11794-8651
Corresponding Author: Connelly{at}pharm.sunysb.edu
This study was designed to examine the metabolic fate of HDL cholesteryl ester (CE) delivered to cells expressing SR-BI via transient or stable transfection or in adrenal and hepatoma cells naturally expressing SR-BI. Comparison of SR-BI with its related class B scavenger receptor, CD36, showed not only a greater uptake of HDL CE but also a more rapid and extensive hydrolysis of HDL CE when delivered by SR-BI. Hydrolysis of HDL CE delivered by both receptors was via a neutral CE hydrolase as judged by inhibitor sensitivity. Analysis of chimeric receptors formed by domain swapping between SR-BI and CD36 showed that efficient HDL CE hydrolysis was due to the SR-BI extracellular domain but not the transmembrane domains or cytoplasmic tails. These data indicate that SR-BI, but not CD36, can efficiently direct HDL CE to a neutral CE hydrolytic pathway. In contrast, LDL CE was delivered to the cell and hydrolyzed equally well by SR-BI and CD36. Hydrolysis of LDL CE delivered by SR-BI was via a neutral CE hydrolase but that delivered by CD36 occurred via an acidic CE hydrolase, indicating that SR-BI and CD36 deliver LDL CE to different metabolic pathways. Comparison of inhibitor sensitivities in Y1-BS1 adrenal cells, Fu5AH hepatoma cells, and transfected cells suggests that hydrolysis of HDL CE delivered by SR-BI occurs via cell type-specific neutral CE hydrolases. In Y1-BS1 cells, HDL CE hydrolysis was sensitive to diethylumbelliferyl phosphate (UBP) or diisopropylfluorophosphate (DFP) whereas the uptake of HDL CE was not. Diethylumbelliferyl phosphate-sensitive HDL CE hydrolytic activity was recovered in a membrane fraction of Y1-BS1 cells. These findings suggest that SR-BI efficiently delivers HDL CE to a metabolically active membrane compartment where CE is hydrolyzed by a neutral CE hydrolase.
Revised on October 17, 2002
Accepted on October 29, 2002
Scavenger receptor, class B, Type I (SR-BI)-directed HDL-cholesteryl ester hydrolysis
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  M. Febbraio CD36 Goes Native Arterioscler. Thromb. Vasc. Biol., July 1, 2008; 28(7): 1209 - 1210. [Full Text] [PDF]
|
|
|
|
|
|
V. Luangrath, M. R. Brodeur, D. Rhainds, and L. Brissette Mouse CD36 Has Opposite Effects on LDL and Oxidized LDL Metabolism In Vivo Arterioscler. Thromb. Vasc. Biol., July 1, 2008; 28(7): 1290 - 1295. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Parathath, Y. F. Darlington, M. de la Llera Moya, D. Drazul-Schrader, D. L. Williams, M. C. Phillips, G. H. Rothblat, and M. A. Connelly Effects of amino acid substitutions at glycine 420 on SR-BI cholesterol transport function J. Lipid Res., June 1, 2007; 48(6): 1386 - 1395. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. B. Kraemer, W.-J. Shen, S. Patel, J.-i. Osuga, S. Ishibashi, and S. Azhar The LDL receptor is not necessary for acute adrenal steroidogenesis in mouse adrenocortical cells Am J Physiol Endocrinol Metab, February 1, 2007; 292(2): E408 - E412. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Xie, J. A. Richardson, S. D. Turley, and J. M. Dietschy Cholesterol substrate pools and steroid hormone levels are normal in the face of mutational inactivation of NPC1 protein J. Lipid Res., May 1, 2006; 47(5): 953 - 963. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Parathath, M. A. Connelly, R. A. Rieger, S. M. Klein, N. A. Abumrad, M. de la Llera-Moya, C. R. Iden, G. H. Rothblat, and D. L. Williams Changes in Plasma Membrane Properties and Phosphatidylcholine Subspecies of Insect Sf9 Cells Due to Expression of Scavenger Receptor Class B, Type I, and CD36 J. Biol. Chem., October 1, 2004; 279(40): 41310 - 41318. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. C. Bastie, T. Hajri, V. A. Drover, P. A. Grimaldi, and N. A. Abumrad CD36 in Myocytes Channels Fatty Acids to a Lipase-Accessible Triglyceride Pool That Is Related to Cell Lipid and Insulin Responsiveness Diabetes, September 1, 2004; 53(9): 2209 - 2216. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. M. Camarota, J. M. Chapman, D. Y. Hui, and P. N. Howles Carboxyl Ester Lipase Cofractionates with Scavenger Receptor BI in Hepatocyte Lipid Rafts and Enhances Selective Uptake and Hydrolysis of Cholesteryl Esters from HDL3 J. Biol. Chem., June 25, 2004; 279(26): 27599 - 27606. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Parathath, D. Sahoo, Y. F. Darlington, Y. Peng, H. L. Collins, G. H. Rothblat, D. L. Williams, and M. A. Connelly Glycine 420 Near the C-terminal Transmembrane Domain of SR-BI Is Critical for Proper Delivery and Metabolism of High Density Lipoprotein Cholesteryl Ester J. Biol. Chem., June 11, 2004; 279(24): 24976 - 24985. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. A. Connelly, M. de la Llera-Moya, Y. Peng, D. Drazul-Schrader, G. H. Rothblat, and D. L. Williams Separation of Lipid Transport Functions by Mutations in the Extracellular Domain of Scavenger Receptor Class B, Type I J. Biol. Chem., July 3, 2003; 278(28): 25773 - 25782. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Rigotti, H. E. Miettinen, and M. Krieger The Role of the High-Density Lipoprotein Receptor SR-BI in the Lipid Metabolism of Endocrine and Other Tissues Endocr. Rev., June 1, 2003; 24(3): 357 - 387. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| All ASBMB Journals | Journal of Biological Chemistry |
| Molecular and Cellular Proteomics | ASBMB Today |
