Homer1a reduces inflammatory response after retinal ischemia/reperfusion injury

Author:

Dou Yanan1,Fei Xiaowei1,He Xin1,Huan Yu1,Wei Jialiang1,Wu Xiuquan1,Lyu Weihao1,Fei Zhou1ORCID,Li Xia1ORCID,Fei Fei2ORCID

Affiliation:

1. Department of Neurosurgery, Xijing Hospital, Air Force Military Medical University, Xi'an, Shaanxi Province, China

2. Department of Ophthalmology, Xijing Hospital, Air Force Military Medical University, Xi'an, Shaanxi Province, China

Abstract

Abstract JOURNAL/nrgr/04.03/01300535-202407000-00042/figure1/v/2023-11-20T171125Z/r/image-tiff Elevated intraocular pressure (IOP) is one of the causes of retinal ischemia/reperfusion injury, which results in NLRP3 inflammasome activation and leads to visual damage. Homer1a is reported to play a protective role in neuroinflammation in the cerebrum. However, the effects of Homer1a on NLRP3 inflammasomes in retinal ischemia/reperfusion injury caused by elevated IOP remain unknown. In our study, animal models were constructed using C57BL/6J and Homer1flox/ /Homer1a+/ /Nestin-Cre+/ mice with elevated IOP-induced retinal ischemia/reperfusion injury. For in vitro experiments, the oxygen-glucose deprivation/reperfusion injury model was constructed with Müller cells. We found that Homer1a overexpression ameliorated the decreases in retinal thickness and Müller cell viability after ischemia/reperfusion injury. Furthermore, Homer1a knockdown promoted NF-κB P65Ser536 activation via caspase-8, NF-κB P65 nuclear translocation, NLRP3 inflammasome formation, and the production and processing of interleukin-1β and interleukin-18. The opposite results were observed with Homer1a overexpression. Finally, the combined administration of Homer1a protein and JSH-23 significantly inhibited the reduction in retinal thickness in Homer1flox/ /Homer1a+/ /Nestin-Cre+/ mice and apoptosis in Müller cells after ischemia/reperfusion injury. Taken together, these studies demonstrate that Homer1a exerts protective effects on retinal tissue and Müller cells via the caspase-8/NF-κB P65/NLRP3 pathway after I/R injury.

Publisher

Medknow

Subject

Developmental Neuroscience

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