| Literature DB >> 33165736 |
Danyang Meng1,2, Xiaohua Ma2, Hui Li3, Xuechun Wu1, Yongjun Cao1, Zhigang Miao4,5, Xia Zhang6.
Abstract
C-type lectin-like receptor 2 (CLEC-2) is a platelet surface-activating receptor with the prominent involvement in platelet activation, which was found to be associated with the progression and prognosis of acute ischemic stroke patients. Although podoplanin is the only known endogenous ligand for CLEC-2, the role of podoplanin/CLEC-2 in cerebral ischemia injury was unclear. In this study, we examined their role by using a mouse middle cerebral artery occlusion (MCAO) model. The expression of CLEC-2 and podoplanin increased after ischemia/reperfusion (I/R) injury, peaked at 24 h, and then decreased gradually. Podoplanin and CLEC-2 co-localized mainly in the ischemia/reperfusion cortex and expressed on neurons and microglia. Anti-podoplanin antibody pretreatment reduced cerebral infarct volume from 52.67 ± 4.67 to 34.08 ± 6.04% (P < 0.05) and attenuated the neurological deficits during acute stage and recovery stage. Moreover, a significant decrease of IL-18 and IL-1β was observed in the mice pretreated with the anti-podoplanin antibody. Our results demonstrate that the podoplanin-CLEC-2 axis might play an important role in cerebral ischemia/reperfusion injury in mice by promoting inflammatory reactions.Entities:
Keywords: Anti-podoplanin; Cerebral ischemic injury; Inflammation; Ischemic stroke; Podoplanin-CLEC-2 axis
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Year: 2020 PMID： 33165736 DOI： 10.1007/s12640-020-00295-w
Source DB: PubMed Journal: Neurotox Res ISSN： 1029-8428 Impact factor: 3.911