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. 2019 Dec 17;5:30. doi: 10.1186/s41016-019-0178-3

Table 1.

A summary of the cell types that express SR-B1, and their functions pertaining to the pathology of stroke and other neurological disorders

Cell type Function Reference
Epithelial cells

- Upregulates wound tissue repair by affecting the proliferative and migratory properties of keratinocytes

- Regulates ceramide levels and maintain barrier function of keratinocytes

- Vitamin E uptake might be regulated by SR-B1 in pneumocytes

- Functions as plasma membrane cholesterol sensor

Muresan et al. [34], Muresan et al. [35], Kolleck et al. [36], Morel et al. [20]
Smooth muscle cells

- rHDL inhibits smooth muscle cell chemokine expression, p65, and proliferation through SR-B1

- HDL-associated lysosphinoglipids function to reduce ROS generation, which requires SR-B1 coordinate signaling

Van der Vorst et al. [37], Tolle et al. [38]
Monocytes - Subclinical endotoxemia promotes atherosclerosis by converting monocytes into a persistent inflammatory state with reduced SR-B1 Geng et al. [39]
Macrophages - SR-B1 invalidation reduces free-cholesterol-induced apoptosis and promotes atherosclerosis Galle-Treger et al. [40]
Endothelial cells

- Functions as plasma membrane cholesterol sensor

- Binding of SR-B1 with HDL activates endothelial NO synthase and stimulates endothelial cell migration

- Apolipoprotein A-1 promotes endothelial repair through SR-B1

- SR-B1 acts as a mechanosensor in response to shear stress

- SR-B1 is involved in transendothelial cholesterol transport

Saddar et al. [41], Yuhanna et al. 2001, Seetharam et al. [42], He et al. [43], Zhang et al. [44], Miao et al. [21]
Steroidogenic cells

- Estrogen increases brain SR-B1 levels

- SR-B1 facilitates vasorelaxation pathway via interactions with DHEA-enriched HDL

Srivastava et al. [45], Paatela et al. [46]
Astrocytes -Impairment of amyloid β uptake in Alzheimer’s correlated with a lower expression of SR-B1 Iram et al. [47]
Hepatocytes - Mediates uptake of HDL-derived cholesterol ester Acton et al. [17]