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  • 1
    Online Resource
    Online Resource
    Physiological Concentrations of Estrogen Decrease LDL Transcytosis by Coronary Artery Endothelial Cells – Elucidation of Molecular Mechanisms
    Elsevier BV ; 2018
    In:  Atherosclerosis Supplements Vol. 32 ( 2018-06), p. 7-8
    Details
    In: Atherosclerosis Supplements, Elsevier BV, Vol. 32 ( 2018-06), p. 7-8
    Type of Medium: Online Resource
    ISSN: 1567-5688
    URL: Article
    DOI: 10.1016/j.atherosclerosissup.2018.04.023
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2018
    detail.hit.zdb_id: 1499887-7
    detail.hit.zdb_id: 2098677-4
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  • 2
    Online Resource
    Online Resource
    Endothelial HMGB1 Is a Critical Regulator of LDL Transcytosis via an SREBP2–SR-BI Axis
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health)
    Abstract: LDL (low-density lipoprotein) transcytosis across the endothelium is performed by the SR-BI (scavenger receptor class B type 1) receptor and contributes to atherosclerosis. HMGB1 (high mobility group box 1) is a structural protein in the nucleus that is released by cells during inflammation; extracellular HMGB1 has been implicated in advanced disease. Whether intracellular HMGB1 regulates LDL transcytosis through its nuclear functions is unknown. Approach and Results: HMGB1 was depleted by siRNA in human coronary artery endothelial cells, and transcytosis of LDL was measured by total internal reflection fluorescence microscopy. Knockdown of HMGB1 attenuated LDL transcytosis without affecting albumin transcytosis. Loss of HMGB1 resulted in reduction in SR-BI levels and depletion of SREBP2 (sterol regulatory element-binding protein 2)—a transcription factor upstream of SR-BI. The effect of HMGB1 depletion on LDL transcytosis required SR-BI and SREBP2. Overexpression of HMGB1 caused an increase in LDL transcytosis that was unaffected by inhibition of extracellular HMGB1 or depletion of RAGE (receptor for advanced glycation endproducts)—a cell surface receptor for HMGB1. The effect of HMGB1 overexpression on LDL transcytosis was prevented by knockdown of SREBP2. Loss of HMGB1 caused a reduction in the half-life of SREBP2; incubation with LDL caused a significant increase in nuclear localization of HMGB1 that was dependent on SR-BI. Animals lacking endothelial HMGB1 exhibited less acute accumulation of LDL in the aorta 30 minutes after injection and when fed a high-fat diet developed fewer fatty streaks and less atherosclerosis. Conclusions: Endothelial HMGB1 regulates LDL transcytosis by prolonging the half-life of SREBP2, enhancing SR-BI expression. Translocation of HMGB1 to the nucleus in response to LDL requires SR-BI.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.120.314557
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 1494427-3
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  • 3
    Online Resource
    Online Resource
    Estrogen Inhibits LDL (Low-Density Lipoprotein) Transcytosis by Human Coronary Artery Endothelial Cells via GPER (G-Protein–Coupled Estrogen Receptor) and SR-BI (Scavenger Receptor Class B Type 1)
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 38, No. 10 ( 2018-10), p. 2283-2294
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 38, No. 10 ( 2018-10), p. 2283-2294
    Abstract: The atheroprotective effects of estrogen are independent of circulating lipid levels. Whether estrogen regulates transcytosis of LDL (low-density lipoprotein) across the coronary endothelium is unknown. Approach and Results— Using total internal reflection fluorescence microscopy, we quantified transcytosis of LDL across human coronary artery endothelial cells from multiple donors. LDL transcytosis was significantly higher in cells from men compared with premenopausal women. Estrogen significantly attenuated LDL transcytosis by endothelial cells from male but not female donors; transcytosis of albumin was not affected. Estrogen caused downregulation of endothelial SR-BI (scavenger receptor class B type 1), and overexpression of SR-BI was sufficient to restore LDL transcytosis. Similarly, depletion of SR-BI by siRNA attenuated endothelial LDL transcytosis and prevented any further effect of estrogen. In contrast, treatment with estrogen had no effect on SR-BI expression by liver cells. Inhibition of estrogen receptors α and β had no effect on estrogen-mediated attenuation of LDL transcytosis. However, estrogen’s effect on LDL transcytosis was blocked by depletion of the GPER (G-protein–coupled estrogen receptor). GPER was found to be enriched in endothelial cells compared with hepatocytes and is reported to signal via transactivation of the EGFR (epidermal growth factor receptor); inhibition of EGFR prevented the effect of estrogen on LDL transcytosis and SR-BI mRNA. Last, SR-BI expression was significantly higher in human coronary artery endothelial cells from male compared with premenopausal female donors. Conclusions— Estrogen significantly inhibits LDL transcytosis by downregulating endothelial SR-BI; this effect requires GPER.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.118.310792
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 1494427-3
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  • 4
    Online Resource
    Online Resource
    Abstract 452: Estrogen Inhibits LDL Transcytosis by Coronary Artery Endothelial Cells via GPER and SR-BI
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 38, No. Suppl_1 ( 2018-05)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 38, No. Suppl_1 ( 2018-05)
    Abstract: Objectives: Premenopausal women have a significantly lower rate of atherosclerosis than men, an effect attributed to estrogen. The atheroprotective effects of estrogen are independent of circulating lipid levels and may be due to an effect on the vessel wall. Early on in atherosclerosis, circulating LDL is able to cross an intact endothelial monolayer by transcytosis and accumulate in the intima. Little is known about the mechanisms of transcytosis but using novel assays we recently discovered a role for the SR-BI and ALK1 receptors. We hypothesized that estrogen can attenuate LDL transcytosis by coronary artery endothelial cells. Approach and Results: Using a recently described assay based on total internal reflection fluorescence microscopy, we quantified transcytosis of LDL across human coronary artery endothelial cells treated with physiological concentrations of estrogen. Estrogen significantly attenuated LDL transcytosis by endothelial cells from male donors; the effect was ligand-specific as transcytosis of albumin was not affected. Estrogen caused down-regulation of endothelial SR-BI but not ALK1 and over-expression of SR-BI was sufficient to restore LDL transcytosis. Similarly, depletion of SR-BI by siRNA attenuated endothelial LDL transcytosis and prevented any further effect of estrogen. In contrast, treatment with estrogen had no effect on SR-BI expression by liver cells from a male donor. Inhibition of estrogen receptors α and β had no effect on estrogen-mediated attenuation of LDL transcytosis. However, estrogen’s effect was blocked by depletion of the G-protein coupled estrogen receptor (GPER) by siRNA. GPER was found to be enriched in endothelial cells compared to hepatocytes and is known to signal via transactivation of the epidermal growth factor receptor (EGFR); we observed that inhibition of EGFR also prevented the effect of estrogen on LDL transcytosis. Lastly, male mice demonstrated more vascular deposition of LDL than age-matched female mice after acute injection. Conclusions: Physiological concentrations of estrogen significantly inhibit LDL transcytosis by down-regulating endothelial SR-BI; this effect requires GPER. This may contribute to the lower rates of atherosclerosis in premenopausal women.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/atvb.38.suppl_1.452
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 1494427-3
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