Scavenger receptor class B,type 1 facilitates cellular fatty acid uptake |
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| Institution: | 1. University of Michigan, Department of Surgery, Ann Arbor, MI;2. University of Michigan, College of Pharmacy, Ann Arbor, MI;3. Brigham and Women’s Hospital, Department of Medicine, Boston, MA;4. University of Michigan, Department of Pharmacology, Ann Arbor, MI;5. University of Michigan, Department of Biomedical Engineering, Ann Arbor, MI;6. University of Kansas, Department of Medicinal Chemistry, Lawrence, KS;1. Department of Endocrinology, University of Groningen, University Medical Center Groningen, The Netherlands;2. Department of Gastroenterology and Hepatology, University of Groningen, University Medical Center Groningen, The Netherlands;3. Department of Nephrology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713GZ, Groningen, The Netherlands;4. Department of Pediatrics, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713GZ, Groningen, The Netherlands;1. Department of Cardiothoracic Surgery, The Third Affiliated Hospital of Soochow University, Changzhou, 213003, China;2. Comprehensive Laboratory, The Third Affiliated Hospital of Soochow University, Changzhou, 213003, China;1. Cancer Research Lab, Department of Clinical Biochemistry, Faculty of Medical Sciences, Tarbiat Modares University, P.O. Box 14115-331, Tehran, Iran;2. Department of Surgery, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran |
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| Abstract: | SR-B1 belongs to the class B scavenger receptor, or CD36 super family. SR-B1 and CD36 share an affinity for a wide array of ligands. Although they exhibit similar ligand binding specificity, SR-B1 and CD36 have some very specific lipid transport functions. Whereas SR-B1 primarily facilitates the selective delivery of cholesteryl esters (CEs) and cholesterol from HDL particles to the liver and non-placental steroidogenic tissues, as well as participating in cholesterol efflux from cells, CD36 primarily mediates the uptake of long-chain fatty acids in high fatty acid-requiring organs such as the heart, skeletal muscle and adipose tissue. However, CD36 also mediates cholesterol efflux and facilitates selective lipoprotein-CE delivery, although less efficiently than SR-B1. Interestingly, the ability or efficiency of SR-B1 to mediate fatty acid uptake has not been reported. In this paper, using overexpression and siRNA-mediated knockdown of SR-B1, we show that SR-B1 possesses the ability to facilitate fatty acid uptake. Moreover, this function is not blocked by BLT-1, a specific chemical inhibitor of HDL-CE uptake activity of SR-B1, nor by sulfo-N-succinimidyl oleate, which inhibits fatty acid uptake by CD36. Attenuated fatty acid uptake was also observed in primary adipocytes isolated from SR-B1 knockout mice. In conclusion, facilitation of fatty acid uptake is an additional function that is mediated by SR-B1. |
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