scholarly journals Endothelial Expression of Scavenger Receptor Class B, Type I Protects against Development of Atherosclerosis in Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Boris L. Vaisman ◽  
Tatyana G. Vishnyakova ◽  
Lita A. Freeman ◽  
Marcelo J. Amar ◽  
Stephen J. Demosky ◽  
...  
Keyword(s):  
Plasma Cholesterol ◽  
Scavenger Receptor ◽  
Fold Increase ◽  
Chow Diet ◽  
Type I ◽  
Scavenger Receptor Class ◽  
Class B ◽  
Normal Chow ◽  
Apoe Ko ◽  
Normal Chow Diet

The role of scavenger receptor class B, type I (SR-BI) in endothelial cells (EC) was examined in several novel transgenic mouse models expressing SR-BI in endothelium of mice with normal C57Bl6/N, apoE-KO, orScarb1-KO backgrounds. Mice were also created expressing SR-BI exclusively in endothelium and liver. Endothelial expression of the Tie2-Scarb1transgene had no significant effect on plasma lipoprotein levels in mice on a normal chow diet but on an atherogenic diet, significantly decreased plasma cholesterol levels, increased plasma HDL cholesterol (HDL-C) levels, and protected mice against atherosclerosis. In 8-month-old apoE-KO mice fed a normal chow diet, the Tie2-Scarb1transgene decreased aortic lesions by 24%. Mice expressing SR-BI only in EC and liver had a 1.5 ± 0.1-fold increase in plasma cholesterol compared to mice synthesizing SR-BI only in liver. This elevation was due mostly to increased HDL-C. In EC culture studies, SR-BI was found to be present in both basolateral and apical membranes but greater cellular uptake of cholesterol from HDL was found in the basolateral compartment. In summary, enhanced expression of SR-BI in EC resulted in a less atherogenic lipoprotein profile and decreased atherosclerosis, suggesting a possible role for endothelial SR-BI in the flux of cholesterol across EC.

scholarly journals HDL modification by secretory phospholipase A2 promotes scavenger receptor class B type I interaction and accelerates HDL catabolism

2000 ◽  
Vol 41 (11) ◽  
pp. 1849-1857 ◽  
Author(s):  
Frederick C. de Beer ◽  
Patrice M. Connell ◽  
J. Yu ◽  
Maria C. de Beer ◽  
Nancy R. Webb ◽  
...  
Keyword(s):  
Phospholipase A2 ◽  
Scavenger Receptor ◽  
Type I ◽  
Secretory Phospholipase A2 ◽  
Secretory Phospholipase ◽  
Scavenger Receptor Class ◽  
Class B

Browning of White Adipocytes in Fat Grafts Associated with Higher Level of Necrosis and Type 2 Macrophages Recruitment

2021 ◽  
Author(s):  
Tong Liu ◽  
Su Fu ◽  
Qian Wang ◽  
Hao Cheng ◽  
Dali Mu ◽  
...  
Keyword(s):  
Fold Increase ◽  
Chow Diet ◽  
Sham Operation ◽  
Type I ◽  
Electronic Microscopy ◽  
Fat Transfer ◽  
Fat Grafts ◽  
Female Nude ◽  
Normal Chow

Abstract Background Induced browning adipocytes were assumed less viable and more prone to necrosis for their hypermetabolic property. Our previous study showed that browning of adipocytes was more evident in fat grafts with necrosis in humans. Objectives We aimed to estimate whether fat-transfer-induced browning biogenesis was associated with necrosis and its potential inflammation mechanisms in murine models. Methods Human subcutaneous adipose from thigh or abdomen of 5 patients via liposuction were injected in 100µl or 500µl (n=20 per group) into the dorsal flank of 6-8-week female nude mice fed with normal chow diet, and harvested after 2, 4, 8 and 12 weeks. Control groups did not receive any grafting procedures (sham operation), where lipoaspirates were analyzed immediately after harvest. Histology and electronic microscopy, immunological analyses of browning markers, necrosis marker, and type I/II macrophages markers in mice were performed. Results Histology and electronic microscopy showed browning adipocytes in in fat grafts with higher level of necrosis (0.435±0.017pg/ml for cleaved caspase-3, **p<0.01), IL-6(749.0±134.1pg/ml,***p<0.001) and infiltration of type 2 macrophage profiles in mice(2-fold increase, *p<0.05). Conclusions Browning of adipocytes induced by fat transfer in mice is in parallel with post-grafting necrotic levels, associated with elevated IL-6 and activated M2 macrophages profiles which promote browning development.

MS81 LIVER-SPECIFIC LIPOPLEXES FOR THE KNOCKDOWN OF SCAVENGER RECEPTOR CLASS B TYPE I

2010 ◽  
Vol 11 (2) ◽  
pp. 126
Author(s):  
K. Duwensee ◽  
I. Tancevski ◽  
E. Demetz ◽  
P. Eller ◽  
C. Heim ◽  
...  
Keyword(s):  
Scavenger Receptor ◽  
Type I ◽  
Scavenger Receptor Class ◽  
Class B

scholarly journals Feedback Inhibition of Human Scavenger Receptor Class B Type I Gene Expression by Glucocorticoid in Adrenal and Ovarian Cells

Endocrinology ◽  
2010 ◽  
Vol 151 (7) ◽  
pp. 3214-3224 ◽  
Author(s):  
Sofia Mavridou ◽  
Maria Venihaki ◽  
Olga Rassouli ◽  
Christos Tsatsanis ◽  
Dimitris Kardassis
Keyword(s):  
Gene Expression ◽  
Gene Transcription ◽  
Feedback Inhibition ◽  
Steroid Hormone ◽  
Scavenger Receptor ◽  
Type I ◽  
Mrna Levels ◽  
Ovarian Cells ◽  
Scavenger Receptor Class ◽  
Class B

Scavenger receptor class B type I (SR-BI) facilitates the reverse transport of excess cholesterol from peripheral tissues to the liver via high-density lipoproteins. In steroidogenic tissues, SR-BI supplies cholesterol for steroid hormone production. We show here that the transcription of the human SR-BI gene is subject to feedback inhibition by glucocorticoid in adrenal and ovarian cells. SR-BI mRNA levels were increased in adrenals from corticosterone-insufficient Crh−/− mice, whereas corticosterone replacement by oral administration inhibited SR-BI gene expression in these mice. SR-BI mRNA levels were increased in adrenals from wild-type mice treated with metyrapone, a drug that blocks corticosterone synthesis. Experiments in adrenocortical H295R and ovarian SKOV-3 cells using cycloheximide and siRNA-mediated gene silencing revealed that glucocorticoid-mediated inhibition of SR-BI gene transcription requires de novo protein synthesis and the glucocorticoid receptor (GR). No direct binding of GR to the SR-BI promoter could be demonstrated in vitro and in vivo, suggesting an indirect mechanism of repression of SR-BI gene transcription by GR in adrenal cells. Deletion analysis established that the region of the human SR-BI promoter between nucleotides −201 and −62 is sufficient to mediate repression by glucocorticoid. This region contains putative binding sites for transcriptional repressors that could play a role in SR-BI gene regulation in response to glucocorticoid. In summary, this is the first report showing that glucocorticoid suppress SR-BI expression suggesting that steroidogenic tissues maintain steroid hormone homeostasis by prohibiting SR-BI-mediated high-density lipoprotein cholesterol uptake when the endogenous levels of glucocorticoid are elevated.

scholarly journals Inhibition of hepatic scavenger receptor-class B type I by RNA interference decreases atherosclerosis in rabbits

2012 ◽  
Vol 222 (2) ◽  
pp. 360-366 ◽  
Author(s):  
Egon Demetz ◽  
Ivan Tancevski ◽  
Kristina Duwensee ◽  
Ursula Stanzl ◽  
Eva Huber ◽  
...  
Keyword(s):  
Rna Interference ◽  
Scavenger Receptor ◽  
Type I ◽  
Scavenger Receptor Class ◽  
Class B
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