Abstract
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Cell Death Dis. 2023 Feb 8;14(2):92. doi: 10.1038/s41419-023-05616-3.
Aryl hydrocarbon receptor dependent anti-inflammation and neuroprotective effects of tryptophan metabolites on retinal ischemia/reperfusion injury.
Yang Y(#)(1)(2), Wang N(#)(1)(2), Xu L(1)(2), Liu Y(1)(2), Huang L(1)(2), Gu M(1)(2), Wu Y(1)(2), Guo W(3)(4), Sun H(5)(6).
Author information: (1)Department of Ophthalmology, Shanghai 9th People’s Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China. (2)Shanghai Key Laboratory of Orbital Diseases and Ocular Oncology, Shanghai, China. (3)Department of Ophthalmology, Shanghai 9th People’s Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China. wyguo9h@163.com. (4)Shanghai Key Laboratory of Orbital Diseases and Ocular Oncology, Shanghai, China. wyguo9h@163.com. (5)Department of Ophthalmology, Shanghai 9th People’s Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China. sunhao6666@126.com. (6)Shanghai Key Laboratory of Orbital Diseases and Ocular Oncology, Shanghai, China. sunhao6666@126.com. (#)Contributed equally
Glaucoma is the major cause of irreversible blindness in the world characterized by progressive retinal neurodegeneration, in which local inflammation in retina is involved in persistent loss of retinal ganglion cells (RGCs). In order to explore whether aryl hydrocarbon receptor (AhR) and its agonists tryptophan metabolites are involved in the development of glaucoma, we collected serum and retinas from non-glaucoma controls and patients with glaucoma. Results showed altered serum tryptophan metabolism and reduced retinal AhR expression in glaucoma patients. We also showed intraperitoneally injection of tryptophan metabolite 2-(1’H-indole-3’-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) down-regulated retinal local inflammation and protected RGC apoptosis from retinal ischemia/reperfusion (IR) injury via AhR