Aim: To investigate the effect of interleukin-8 (IL-8) on neural retinal ganglion cells (RGCs) and whether it can be alleviated by G31P.
Methods: RGC-5 cells were exposed to IL-8 with or without its specific receptor antagonist G31P for 24h, and the cell viability was assessed by Cell Counting Kit 8 (CCK-8). Apoptosis was measured by examining nuclear morphology and quantifying with flow cytometry. Reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR) and Western blot were used to investigate the expression of apoptosis-related genes.
Results: CCK-8 assay showed that IL-8 significantly inhibits the viability of RGC-5 cells in a dose-dependent manner. Cell apoptosis assays exhibited higher apoptotic rate in IL-8 treatment group compared to control group. We further found that IL-8 could promote Bax and caspase-3 expressions, but decrease the level of Bcl-2 in the aspect of mRNA and protein. However, pre-treatment with G31P partly attenuated these effects in RGC-5 cells (<0.05).
Conclusion: These results indicate that anti-proliferation effects of IL-8 through induction of cell apoptosis regulated by Bcl-2, Bax and caspase-3 expressions, can be ameliorated by G31P.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6090122 | PMC |
http://dx.doi.org/10.18240/ijo.2018.08.05 | DOI Listing |
Exp Eye Res
January 2025
Institutes of Biology and Medical Sciences, Soochow University, Suzhou, 215000, China; Key Laboratory of Geriatric Diseases and Immunology, Ministry of Education, Institutes of Biology and Medical Sciences, Suzhou Medical College of Soochow University, Suzhou, 215123, China. Electronic address:
Due to its unique physiological structure and functions, the eye has received considerable attention in the field of adeno-associated virus (AAV) gene therapy. Inherited retinal degenerative diseases, which arise from pathogenic mutations in mRNA transcripts expressed in the eye's photoreceptor cells or retinal pigment epithelium (RPE), are the most common cause of vision loss. However, current retinal gene therapy mostly involves subretinal injection of therapeutic genes, which treats a limited area, entails retinal detachment, and requires sophisticated techniques.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Interdisciplinary Centre for Preclinical and Clinical Research, College of Natural Sciences, University of Rzeszow, Werynia 2a, 36-100 Kolbuszowa, Poland.
Degenerative retinal diseases can lead to blindness if left untreated. At present, there are no curative therapies for retinal diseases. Therefore, effective treatment strategies for slowing the progression of retinal diseases and thus improving patients' life standards are urgently needed.
View Article and Find Full Text PDFInsect Sci
September 2024
Integrative Science Center of Germplasm Creation in Western China (CHONGQING) Science City & Southwest University, Biological Science Research Center, Southwest University, Chongqing, China.
J Med Food
November 2024
Electroanalytical Chemistry, Changchun Institute of Applied Chemistry, National Center of Mass Spectrometry in Changchun and Jilin Provincial Key Laboratory of Chinese Medicine Chemistry and Mass Spectrometry, Chinese Academy of Sciences, Changchun, China.
Commun Biol
July 2024
Tianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, No. 251, Fukang Road, Nankai District, Tianjin, 300384, China.
Glaucoma is the leading cause of irreversible blindness and is characterized by progressive retinal ganglion cell (RGC) loss and retinal nerve fiber layer thinning. Currently, no existing treatment is effective for the preservation of RGCs. MicroRNA-22-3p (miR22) and small extracellular vesicles derived from mesenchymal stem cells (MSC-sEVs) have neuroprotective effects.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!