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  3. BAFF deficiency aggravated optic nerve crush-induced retinal ganglion cells damage by regulating apoptosis and neuroinflammation via NF-κB-IκBα signaling

BAFF deficiency aggravated optic nerve crush-induced retinal ganglion cells damage by regulating apoptosis and neuroinflammation via NF-κB-IκBα signaling

  • Int Immunopharmacol. 2023 Dec 1:126:111287. doi: 10.1016/j.intimp.2023.111287.
Jiali Lin 1,  Wen Deng 1,  Jing Liao 1,  Diyang Ke 1,  Ling Cui 1,  Haibin Zhong 1,  Kongqian Huang 1,  Li Jiang 1,  Qi Chen 2,  Fan Xu 3,  Fen Tang 4
Affiliations

Affiliations

  • 1 Department of Ophthalmology, the People's Hospital of Guangxi Zhuang Autonomous Region & Guangxi Key Laboratory of Eye Health & Guangxi Health Commission Key Laboratory of Ophthalmology and Related Systemic Diseases Artificial Intelligence Screening Technology & Institute of Ophthalmic Diseases, Guangxi Academy of Medical Sciences, 534000, 0771-2186574 Nanning, Guangxi, China.
  • 2 Department of Ophthalmology, the People's Hospital of Guangxi Zhuang Autonomous Region & Guangxi Key Laboratory of Eye Health & Guangxi Health Commission Key Laboratory of Ophthalmology and Related Systemic Diseases Artificial Intelligence Screening Technology & Institute of Ophthalmic Diseases, Guangxi Academy of Medical Sciences, 534000, 0771-2186574 Nanning, Guangxi, China. Electronic address: [email protected].
  • 3 Department of Ophthalmology, the People's Hospital of Guangxi Zhuang Autonomous Region & Guangxi Key Laboratory of Eye Health & Guangxi Health Commission Key Laboratory of Ophthalmology and Related Systemic Diseases Artificial Intelligence Screening Technology & Institute of Ophthalmic Diseases, Guangxi Academy of Medical Sciences, 534000, 0771-2186574 Nanning, Guangxi, China. Electronic address: [email protected].
  • 4 Department of Ophthalmology, the People's Hospital of Guangxi Zhuang Autonomous Region & Guangxi Key Laboratory of Eye Health & Guangxi Health Commission Key Laboratory of Ophthalmology and Related Systemic Diseases Artificial Intelligence Screening Technology & Institute of Ophthalmic Diseases, Guangxi Academy of Medical Sciences, 534000, 0771-2186574 Nanning, Guangxi, China. Electronic address: [email protected].
PMID: 38041956 DOI: 10.1016/j.intimp.2023.111287
Abstract

Loss of retinal ganglion cells (RGCs) is a primary cause of visual impairment in glaucoma, the pathological process is closely related to neuroinflammation and Apoptosis. B-cell activating factor (BAFF) is a fundamental survival factor mainly expressed in the B cell lineage. Evidence suggests its neuroprotective effect, but the expression and role in the retina have not yet been investigated. In this study, we adopt optic nerve crush (ONC) as an in vivo model and oxygen-glucose deprivation/reoxygenation (OGD/R) of RGCs as an in vitro model to investigate the expression and function of BAFF. We found that BAFF and its receptors were abundantly expressed in the retina and BAFF inhibition exacerbated the Caspase 3-mediated RGCs Apoptosis, glial cell activation and pro-inflammatory cytokines expression, which may be caused by the activation of the NF-κB pathway in vivo. In addition, we found that BAFF treatment could alleviate RGCs Apoptosis, pro-inflammatory cytokines expression and NF-κB pathway activation, which could be reversed the effect by blockade of the NF-κB pathway in vitro. Meanwhile, we found that microglia induced to overexpress BAFF in the inflammatory microenvironment in a time-dependent manner. Taken together, our results indicated that BAFF deficiency promoted RGCs Apoptosis and neuroinflammation through activation of NF-κB pathway in ONC retinas, suggesting that BAFF may serve as a promising therapeutic target for the treatment of glaucoma.

Keywords

Apoptosis; BAFF; NF-κB; Neuroinflammation.

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