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CD99 mediates neutrophil transmigration through the bEnd.3 monolayer via the induction of oxygen-glucose deprivation.

Abstract：

AIM/BACKGROUND:CD99 participate in neutrophil infiltration after inflammatory events; however, despite the important role of inflammation in ischemic stroke, the role of CD99 in ischemic stroke remains unclear. METHOD:In the present study, we detected the protein expression of CD99, ICAM-1, and CD31 (PECAM-1) in oxygen-glucose deprivation (OGD)-induced bEnd.3 cells and neutrophils and explored the influence of HIF-1α and IL-1β on their expression. We also explored the role of CD99 in the OGD-induced transmigration of neutrophils. RESULTS:Our results showed that OGD induction upregulated CD99 in bEnd.3 cells and that this effect could be abolished by the preadministration of IL-1β and was not mediated by HIF-1α. However, the activation of ICAM-1 by OGD remained activated with IL-1β treatment. No significant influence of IL-1β on OGD-induced CD31. Finally, we found a significant increase in infiltrated neutrophils after OGD induction compared with the control and OGD + anti-CD99 groups. CONCLUSION:Our results indicated that CD99 mediates neutrophil infiltration and transmigration via OGD induction and thus constitutes a potential therapeutic target for anti-inflammatory treatment after ischemic stroke.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Hu T,Sun R,Huang F,Liu X,Duan Z,Ye R,Li Y,Xiao L,Guo Z,Liu Q,Zhu W

doi

10.1016/j.bbrc.2020.03.159

subject

Has Abstract

pub_date

2020-06-04 00:00:00

pages

799-804

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(20)30657-4

journal_volume

526

pub_type

杂志文章

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