Literature DB >> 31415077

Corneal Denervation Causes Epithelial Apoptosis Through Inhibiting NAD+ Biosynthesis.

Ya Li1,2, Xiubin Ma1, Jing Li3, Lingling Yang2, Xiaowen Zhao2, Xia Qi2, Xiaoping Zhang1, Qingjun Zhou2, Weiyun Shi2.   

Abstract

Purpose: To determine if trigeminal innervations of the corneal epithelium maintains its integrity and homeostasis through controlling the nicotinamide adenine dinucleotide (NAD) content of this tissue.
Methods: Corneal denervation of C57BL/6 mice was induced by squeezing the nerve bundles that derive from the trigeminal ganglion and was confirmed by whole-mount corneal nerve staining and the sensation test. The apoptosis of the corneal epithelium was examined by TUNEL assay and annexin V/propidium iodide staining. NAD biosynthesis-related enzymes were analyzed by quantitative PCR, immunofluorescence staining, and Western blotting. FK866, an inhibitor of nicotinamide phosphoribosyltransferase (NAMPT), exogenous nicotinamide mononucleotide (NMN), and NAD+ were used to evaluate the effect of NAD+ on the apoptosis of cultured corneal epithelial cells and epithelial detachment in denervated mice. Protein expression that related to apoptosis and phosphorylation were analyzed by Western blotting.
Results: The denervated mice showed spontaneous corneal epithelial detachment and cell apoptosis accompanied with impaired epithelial NAD+ contents due to low levels of NAMPT. Similarly, inhibition of NAMPT recapitulated epithelial detachment as in denervated mice and induced apoptosis in cultured corneal epithelial cells. The replenishment of NMN or NAD+ partially slowed down corneal nerve fiber degeneration, reduced the epithelial defect in denervated mice, and improved apoptosis induction in FK866-treated cells by restoring the activation levels of SIRT1, AKT, and CREB. Conclusions: Corneal denervation lowered epithelial NAD+ contents through reducing the expression of NAMPT and caused cell apoptosis and epithelial defects, suggesting that corneal innervations contribute to epithelial homeostasis by regulating NAD+ biosynthesis.

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Year:  2019        PMID: 31415077     DOI: 10.1167/iovs.19-26909

Source DB:  PubMed          Journal:  Invest Ophthalmol Vis Sci        ISSN: 0146-0404            Impact factor:   4.799


  4 in total

Review 1.  The impact of sensory neuropathy and inflammation on epithelial wound healing in diabetic corneas.

Authors:  Fu-Shin X Yu; Patrick S Y Lee; Lingling Yang; Nan Gao; Yangyang Zhang; Alexander V Ljubimov; Ellen Yang; Qingjun Zhou; Lixin Xie
Journal:  Prog Retin Eye Res       Date:  2022-01-04       Impact factor: 19.704

Review 2.  Implications of NAD+ Metabolism in the Aging Retina and Retinal Degeneration.

Authors:  Ravirajsinh N Jadeja; Menaka C Thounaojam; Manuela Bartoli; Pamela M Martin
Journal:  Oxid Med Cell Longev       Date:  2020-05-09       Impact factor: 6.543

3.  Nicotinamide Mononucleotide Alleviates Hyperosmolarity-Induced IL-17a Secretion and Macrophage Activation in Corneal Epithelial Cells/Macrophage Co-Culture System.

Authors:  Yi-Fang Meng; Qi Pu; San-You Dai; Qian Ma; Xinyu Li; Wei Zhu
Journal:  J Inflamm Res       Date:  2021-02-22

Review 4.  Nicotinamide Mononucleotide: A Promising Molecule for Therapy of Diverse Diseases by Targeting NAD+ Metabolism.

Authors:  Weiqi Hong; Fei Mo; Ziqi Zhang; Mengyuan Huang; Xiawei Wei
Journal:  Front Cell Dev Biol       Date:  2020-04-28
  4 in total

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