Role of High-Density Lipoprotein and Scavenger Receptor B Type I in the Promotion of Endothelial Repair

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Abstract

There is considerable experimental evidence that high-density lipoprotein (HDL) cholesterol and the principal high-affinity HDL receptor scavenger receptor B type I (SR-BI) afford cardiovascular protection. However, the fundamental mechanisms underlying the protection remain complex and not well understood. Recent work in cell culture indicates that the HDL-SR-BI tandem stimulates endothelial cell migration. Further studies have revealed that this entails Src-mediated, phosphatidylinositol 3-kinase-mediated, and mitogen-activated protein kinase-mediated signaling that leads to the activation of Rac guanosine triphosphate hydrolase and the resultant rearrangement of the actin cytoskeleton. Furthermore, assessment of reendothelialization after perivascular electric injury in mice indicates that HDL-SR-BI-mediated stimulation of endothelial migration is operative in vivo. Recent additional work in mice also indicates that HDL activates the recruitment of endothelial progenitor cells into the intimal layer in the setting of endothelial injury. As such, signaling initiated by HDL-SR-BI promotes endothelial repair, and this novel mechanism of action may be critically involved in the impact of the lipoprotein on vascular health and disease.

Original languageEnglish (US)
Pages (from-to)156-161
Number of pages6
JournalTrends in Cardiovascular Medicine
Volume17
Issue number5
DOIs
StatePublished - Jul 2007

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Scavenger Receptors
Electric Injuries
Phosphatidylinositol 3-Kinase
Tunica Intima
HDL Lipoproteins
Guanosine Triphosphate
Mitogen-Activated Protein Kinases
Actin Cytoskeleton
Vascular Diseases
HDL Cholesterol
Lipoproteins
Cell Movement
Endothelial Cells
Cell Culture Techniques
high density lipoprotein receptors
Health
Wounds and Injuries

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

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title = "Role of High-Density Lipoprotein and Scavenger Receptor B Type I in the Promotion of Endothelial Repair",
abstract = "There is considerable experimental evidence that high-density lipoprotein (HDL) cholesterol and the principal high-affinity HDL receptor scavenger receptor B type I (SR-BI) afford cardiovascular protection. However, the fundamental mechanisms underlying the protection remain complex and not well understood. Recent work in cell culture indicates that the HDL-SR-BI tandem stimulates endothelial cell migration. Further studies have revealed that this entails Src-mediated, phosphatidylinositol 3-kinase-mediated, and mitogen-activated protein kinase-mediated signaling that leads to the activation of Rac guanosine triphosphate hydrolase and the resultant rearrangement of the actin cytoskeleton. Furthermore, assessment of reendothelialization after perivascular electric injury in mice indicates that HDL-SR-BI-mediated stimulation of endothelial migration is operative in vivo. Recent additional work in mice also indicates that HDL activates the recruitment of endothelial progenitor cells into the intimal layer in the setting of endothelial injury. As such, signaling initiated by HDL-SR-BI promotes endothelial repair, and this novel mechanism of action may be critically involved in the impact of the lipoprotein on vascular health and disease.",
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N2 - There is considerable experimental evidence that high-density lipoprotein (HDL) cholesterol and the principal high-affinity HDL receptor scavenger receptor B type I (SR-BI) afford cardiovascular protection. However, the fundamental mechanisms underlying the protection remain complex and not well understood. Recent work in cell culture indicates that the HDL-SR-BI tandem stimulates endothelial cell migration. Further studies have revealed that this entails Src-mediated, phosphatidylinositol 3-kinase-mediated, and mitogen-activated protein kinase-mediated signaling that leads to the activation of Rac guanosine triphosphate hydrolase and the resultant rearrangement of the actin cytoskeleton. Furthermore, assessment of reendothelialization after perivascular electric injury in mice indicates that HDL-SR-BI-mediated stimulation of endothelial migration is operative in vivo. Recent additional work in mice also indicates that HDL activates the recruitment of endothelial progenitor cells into the intimal layer in the setting of endothelial injury. As such, signaling initiated by HDL-SR-BI promotes endothelial repair, and this novel mechanism of action may be critically involved in the impact of the lipoprotein on vascular health and disease.

AB - There is considerable experimental evidence that high-density lipoprotein (HDL) cholesterol and the principal high-affinity HDL receptor scavenger receptor B type I (SR-BI) afford cardiovascular protection. However, the fundamental mechanisms underlying the protection remain complex and not well understood. Recent work in cell culture indicates that the HDL-SR-BI tandem stimulates endothelial cell migration. Further studies have revealed that this entails Src-mediated, phosphatidylinositol 3-kinase-mediated, and mitogen-activated protein kinase-mediated signaling that leads to the activation of Rac guanosine triphosphate hydrolase and the resultant rearrangement of the actin cytoskeleton. Furthermore, assessment of reendothelialization after perivascular electric injury in mice indicates that HDL-SR-BI-mediated stimulation of endothelial migration is operative in vivo. Recent additional work in mice also indicates that HDL activates the recruitment of endothelial progenitor cells into the intimal layer in the setting of endothelial injury. As such, signaling initiated by HDL-SR-BI promotes endothelial repair, and this novel mechanism of action may be critically involved in the impact of the lipoprotein on vascular health and disease.

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