scholarly journals Scavenger receptor class B type I regulates cellular cholesterol metabolism and cell signaling associated with breast cancer development

2013 ◽  
Vol 15 (5) ◽  
Author(s):  
Christiane Danilo ◽  
Jorge L Gutierrez-Pajares ◽  
Maria Antonietta Mainieri ◽  
Isabelle Mercier ◽  
Michael P Lisanti ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Signaling ◽  
Cholesterol Metabolism ◽  
Scavenger Receptor ◽  
Cancer Development ◽  
Type I ◽  
Cellular Cholesterol ◽  
Breast Cancer Development ◽  
Scavenger Receptor Class ◽  
Class B

Cholesterol Metabolism—Impacts on SARS-CoV-2 Infection Prognosis, Entry, and Antiviral Therapies

2020 ◽  
Author(s):  
Congwen Wei ◽  
Luming Wan ◽  
Yanhong Zhang ◽  
Chen Fan ◽  
Qiulin Yan ◽  
...  
Keyword(s):  
Cholesterol Metabolism ◽  
Scavenger Receptor ◽  
Hdl Cholesterol ◽  
Lung Cells ◽  
Type I ◽  
Antiviral Therapies ◽  
Scavenger Receptor Class ◽  
Global Pandemic ◽  
Class B ◽  
Clinically Significant

AbstractThe recently emerged pathogenic SARS-coronavirus 2 (SARS-CoV-2) has spread rapidly, leading to a global pandemic. In this study, we show that SARS-CoV-2 infection was associated with clinically significant lower level of HDL cholesterol (HDL-C), which can be used as indicators of disease severity and poor prognosis. Importantly, we found the spike protein of SARS-CoV-2 (SARS-2-S) bound to HDL. Antagonists of HDL receptor-Scavenger receptor class B type I (SR-B1), strongly inhibited SARS-CoV-2 infection. Notably, the lipids transfer function of SR-B1 was indispensable for this inhibition, offering explanations for the reduced serum HDL level observed in COVID-19 patients. Basing on findings here, we speculate that SR-B1-mediated pulmonary HDL-vitamin E uptake could participate in mediating SARS-CoV-2 infection of lung cells, and the unique expression profile of SR-B1 may also affect SARS-CoV-2 cell and tissue tropism. These findings might help to provide further insights into viral transmission, pathological characteristics and reveal therapeutic targets.Graphical Abstract

scholarly journals Scavenger Receptor Class B Type I as a Mediator of Cellular Cholesterol Efflux to Lipoproteins and Phospholipid Acceptors

1998 ◽  
Vol 273 (10) ◽  
pp. 5599-5606 ◽  
Author(s):  
Bo Jian ◽  
Margarita de la Llera-Moya ◽  
Yong Ji ◽  
Nan Wang ◽  
Michael C. Phillips ◽  
...  
Keyword(s):  
Cholesterol Efflux ◽  
Scavenger Receptor ◽  
Type I ◽  
Cellular Cholesterol ◽  
Scavenger Receptor Class ◽  
Class B ◽  
Cellular Cholesterol Efflux

Stabilization of Caveolin-1 by Cellular Cholesterol and Scavenger Receptor Class B Type I†

Biochemistry ◽  
2002 ◽  
Vol 41 (39) ◽  
pp. 11931-11940 ◽  
Author(s):  
Philippe G. Frank ◽  
Yves L. Marcel ◽  
Margery A. Connelly ◽  
Douglas M. Lublin ◽  
Vivian Franklin ◽  
...  
Keyword(s):  
Scavenger Receptor ◽  
Type I ◽  
Cellular Cholesterol ◽  
Caveolin 1 ◽  
Scavenger Receptor Class ◽  
Class B

High scavenger receptor class B type I expression is related to tumor aggressiveness and poor prognosis in breast cancer

Tumor Biology ◽  
2015 ◽  
Vol 37 (3) ◽  
pp. 3581-3588 ◽  
Author(s):  
Baoying Yuan ◽  
Changshun Wu ◽  
Xingwen Wang ◽  
Dan Wang ◽  
Huiling Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Poor Prognosis ◽  
Scavenger Receptor ◽  
Type I ◽  
Tumor Aggressiveness ◽  
Scavenger Receptor Class ◽  
Class B

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

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.

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