Roles of Scavenger Receptor Bi and APO A-I in Selective Uptake of Hdl Cholesterol by Adrenal Cells

@article{Williams2000RolesOS,
  title={Roles of Scavenger Receptor Bi and APO A-I in Selective Uptake of Hdl Cholesterol by Adrenal Cells},
  author={D. L. Williams and Ryan E. Temel and Margery A. Connelly},
  journal={Endocrine Research},
  year={2000},
  volume={26},
  pages={639 - 651}
}
Adrenal cells obtain cholesterol for steroid production via the selective uptake of cholesteryl ester (CE) from HDL particles, a process in which CE is transferred to the plasma membrane without degradation of the HDL particle. Although this process has been studied for two decades, only recently have the receptor and the HDL ligand been identified. Scavenger class B, type I, (SR-BI) is regulated by ACTH in adrenocortical cells in parallel with steroid production. Antibody to SR-BI blocks the… 
SR-BI and cholesterol uptake into steroidogenic cells
SR-B1: A Unique Multifunctional Receptor for Cholesterol Influx and Efflux.
TLDR
The regulation and functional significance of SR-B1 in mediating cholesterol movement into and out of cells is focused on.
Acute inflammation increases the selective uptake of HDL-cholesteryl esters into adrenals of mice overexpressing human secretory phospholipase A 2
TLDR
A novel metabolic role is suggested for sPLA 2 : modification of HDL during the APR to promote increased adrenal uptake of HDL cholesteryl ester to serve as source for steroid hormone synthesis.
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TLDR
It will be interesting to follow future research on scavenger receptor BI that will delineate its functions in cholesterol transport as well as its scavenger functions.
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TLDR
The results imply that enhancing CLA-1 expression by human PDZK1 in the liver can modulate HDL cholesterol metabolism and possibly enhance reverse cholesterol transport to prevent the progression of atherosclerosis in human.
Binding and Internalization of Lipopolysaccharide by Cla-1, a Human Orthologue of Rodent Scavenger Receptor B1*
TLDR
Cla-1 was found to bind and internalize monomerized and HDL-associated LPS, indicating that Cla-1 may play important role in septic shock by affecting LPS cellular uptake and clearance.
Acute inflammation increases selective uptake of HDL cholesteryl esters into adrenals of mice overexpressing human sPLA2.
TLDR
A novel metabolic role is suggested for sPLA2: modification of HDL during the APR to promote increased adrenal uptake of HDL cholesteryl ester to serve as source for steroid hormone synthesis.
SR-BI mediates neutral lipid sorting from LDL to lipid droplets and facilitates their formation
TLDR
It is concluded that SR-BI mediates LDL-induced LD formation in vitro and in vivo by directly transporting LDL derived neutral lipids such as CE and TAG into LDs without lipolysis and de novo lipid synthesis.
Apolipoprotein A-I Deficiency Results in Markedly Increased Atherosclerosis in Mice Lacking the LDL Receptor
TLDR
It is demonstrated that despite normal levels of HDL-C, apoA-I deficiency is associated with a significant loss of protection from the formation of atherosclerosis in LDLR−/− mice fed a chow diet.
Attenuated corticosterone response to chronic ACTH stimulation in hepatic lipase-deficient mice: evidence for a role for hepatic lipase in adrenal physiology.
TLDR
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References

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Scavenger receptor class B, type I (SR-BI) is the major route for the delivery of high density lipoprotein cholesterol to the steroidogenic pathway in cultured mouse adrenocortical cells.
The class B, type I scavenger receptor, SR-BI, binds high density lipoprotein (HDL) and mediates the selective uptake of HDL cholesteryl ester (CE) by cultured transfected cells. The high levels of
Apolipoprotein A-I is required for cholesteryl ester accumulation in steroidogenic cells and for normal adrenal steroid production.
TLDR
Results suggest that apo A-I is essential for the selective uptake of HDL-cholesteryl esters, which has a major impact on adrenal gland physiology causing diminished basal corticosteroid production, a blunted steroidogenic response to stress, and increased expression of compensatory pathways to provide cholesterol substrate for steroid production.
Mechanism of Scavenger Receptor Class B Type I-mediated Selective Uptake of Cholesteryl Esters from High Density Lipoprotein to Adrenal Cells*
TLDR
An examination of lipid uptake from reconstituted HDL particles of defined composition and size shows that there is a non-stoichiometric uptake of HDL lipid components, with CE being preferred over the major HDL phospholipids, phosphatidylcholine and sphingomyelin.
Regulation by Adrenocorticotropic Hormone of the in Vivo Expression of Scavenger Receptor Class B Type I (SR-BI), a High Density Lipoprotein Receptor, in Steroidogenic Cells of the Murine Adrenal Gland*
TLDR
This work has used immunoblotting and immunohistochemical methods to show that SR-BI is specifically expressed in a distinctive pattern on the surfaces of steroid-producing cells in the murine adrenal gland's cortex and that its expression in vivo is induced by adrenocorticotropic hormone and suppressed by glucocortioids.
Expression and microvillar localization of scavenger receptor, class B, type I (a high density lipoprotein receptor) in luteinized and hormone-desensitized rat ovarian models.
TLDR
The data argue that SR-BI can be regulated by the cholesterol status of the luteal cell independently of gonadotropic stimulation, and supports the hypothesis that microvilli and microvillar channels represent a cell surface compartment that is specialized for the selective uptake of lipoprotein cholesterol into steroidogenic cells.
Comparison of Class B Scavenger Receptors, CD36 and Scavenger Receptor BI (SR-BI), Shows That Both Receptors Mediate High Density Lipoprotein-Cholesteryl Ester Selective Uptake but SR-BI Exhibits a Unique Enhancement of Cholesteryl Ester Uptake*
TLDR
The results show that the extracellular domain of mSR-BI is essential for efficient HDL CE uptake, but the C-terminal cytoplasmic tail also has a major influence on the selective uptake process.
Apolipoproteins of HDL can directly mediate binding to the scavenger receptor SR-BI, an HDL receptor that mediates selective lipid uptake.
TLDR
The ability of individual human HDL apolipoproteins reconstituted into phospholipid/unesterified cholesterol complexes to bind to murine SR-BI expressed in stably transfected cultured cells is examined, and all three of the HDL apoA-I, apOA-II, and apoC-III tested can directly mediate binding to mSR-BI.
The Class B, Type I Scavenger Receptor Promotes the Selective Uptake of High Density Lipoprotein Cholesterol Ethers into Caveolae*
TLDR
It is concluded that Caveolae are acceptors for HDL-derived cholesterol ethers, and that caveolae constitute a reversible, plasma membrane pool ofolesterol ethers.
Characterization of CLA-1, a Human Homologue of Rodent Scavenger Receptor BI, as a Receptor for High Density Lipoprotein and Apoptotic Thymocytes*
TLDR
The results demonstrate that CLA-1, a close structural homologue of SR-BI, is also functionally related toSR-BI and may play an important role as a “docking receptor” for HDL in connection with selective uptake of cholesterol esters and an additional role in recognition of damaged cells is suggested.
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