Dataset Information

RNA-seq analysis reveals differentially expressed inflammatory chemokines in a rat retinal degeneration model induced by sodium iodate.

ABSTRACT:

Objective

Retinal degeneration (RD) is a group of serious blinding eye diseases characterized by photoreceptor cell apoptosis and progressive degeneration of retinal neurons. However, the underlying mechanism of its pathogenesis remains unclear.

Methods

In this study, retinal tissues from sodium iodate (NaIO₃)-induced RD and control rats were collected for transcriptome analysis using RNA-sequencing (RNA-seq). Analysis of white blood cell-related parameters was conducted in patients with retinitis pigmentosa (RP) and age-related cataract (ARC) patients.

Results

In total, 334 mRNAs, 77 long non-coding RNAs (lncRNAs), and 20 other RNA types were identified as differentially expressed in the retinas of NaIO₃-induced RD rats. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses showed that differentially expressed mRNAs were mainly enriched in signaling pathways related to immune inflammation. Moreover, we found that the neutrophil-to-lymphocyte ratio was significantly higher in RP patients than in ARC patients.

Conclusion

Overall, this study suggests that multiple chemokines participating in systemic inflammation may contribute to RD pathogenesis.

SUBMITTER: Chen S

PROVIDER: S-EPMC9434683 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature

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Publications

RNA-seq analysis reveals differentially expressed inflammatory chemokines in a rat retinal degeneration model induced by sodium iodate.

Chen Sheng S Liu Guo G Liu Xin X Wang Yun Y He Fen F Nie Danyao D Liu Xinhua X Liu Xuyang X

The Journal of international medical research 20220801 8

<h4>Objective</h4>Retinal degeneration (RD) is a group of serious blinding eye diseases characterized by photoreceptor cell apoptosis and progressive degeneration of retinal neurons. However, the underlying mechanism of its pathogenesis remains unclear.<h4>Methods</h4>In this study, retinal tissues from sodium iodate (NaIO<sub>3</sub>)-induced RD and control rats were collected for transcriptome analysis using RNA-sequencing (RNA-seq). Analysis of white blood cell-related parameters was conducte ...[more]

PMID: 36036255

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Project description:PurposeTo investigate the effect of Ca2+/calmodulin-dependent protein kinase II (CAMKII) δ subtypes (CAMK2D) on sodium iodate (NaIO3)-induced retinal degeneration in mice.MethodsBioinformatics analysis and Western blot experiments were used to screen the significantly differentially expressed genes in age-related macular degeneration (AMD) disease. CAMK2D knockdown and overexpression models were constructed by lentivirus (LV) infection of adult retinal pigment epithelial cell line-19 (ARPE-19) cells in vitro. Flow cytometry was used to detect ARPE-19 cell apoptosis induced by NaIO3. In vivo, CAMK2D knockdown and overexpression mouse models were generated by infecting mouse retinal pigment epithelium (RPE) with adeno-associated virus (AAV). Retinography, optical coherence tomography (OCT), and histological analysis (hematoxylin and eosin staining) were used to detect NaIO3-induced retinal structural changes in mice. Electroretinography (ERG) was used to detect NaIO3-induced retinal function changes in mice. TdT-mediated dUTP nick-end labeling (TUNEL) staining was used to detect the apoptosis of retinal cells induced by NaIO3. RNA sequencing (RNA-Seq) and bioinformatics analysis were used to screen for target genes affected by CAMK2D in CAMK2D-overexpressing ARPE-19 cells. And flow cytometry, OCT, and ERG were used to evaluate the regulatory effect of CAMK2D on target genes.ResultsBioinformatics analysis found the expression of genes related to Ca2+ signal was significantly reduced in AMD patients. Western blot showed that in a mouse model of dry AMD induced by NaIO3, CAMK2D expression in RPE-Choroid tissue significantly lower than normal mice. In vitro, our results showed that overexpression of CAMK2D in ARPE-19 cells decreased apoptosis induced by NaIO3 and knockdown increased apoptosis. In vivo, CAMK2D overexpression in RPE cells can attenuate the retina degeneration induced by NaIO3 and CAMK2D knockdown aggravated degeneration. The bioinformatics analysis indicated that CAMK2D might affect AMD pathology through complement factor I (CFI). In vitro, knockdown of CFI in ARPE-19 cells increased apoptosis induced by NaIO3. In knockdown CFI ARPE-19 cells, overexpression of CAMK2D reduced the above apoptosis. In mice retina, CFI knockdown can aggravate the retina degeneration induced by NaIO3. In knockdown CFI mice, overexpression of CAMK2D in RPE can attenuate the above retina degeneration. Western blot confirmed that CAMK2D regulated the expression of CFI in mice.ConclusionsCAMK2D can attenuate the retinal degeneration induced by NaIO3, which was achieved by regulating the CFI.

Project description:BackgroundAge-related macular degeneration (AMD) is one of the major causes of blindness in the elderly over the age of 60. AMD is divided into dry AMD and wet AMD. Although there are certain treatment methods for wet age-related macular degeneration (AMD), there are no effective treatments for dry AMD yet, and finding new drugs or treatment methods for dry AMD has become a priority. For this purpose, this study explored Glabridin (Glab), an isoflavane found in the root extract of licorice, which has never been investigated in relation to eye diseases.PurposeTo investigate the effect of Glab on the sodium iodate (NaIO3) induced retinal degeneration in vitro and in vivo.MethodsIn vitro, cell viability and cytotoxicity were tested with methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay among the groups of ARPE-19 cells. The cell apoptosis was tested with Hoechst 33342 staining and flow cytometry. The level of Reactive oxygen species (ROS) was measured to check the effect on oxidative stress. The protein expressions of phosphorylation of ERK1/2 and p38 were detected by Western blotting. In vivo, C57BL/6J mice were pretreated with Glab intraperitoneally for one week and continued for 4 weeks. NaIO3 was given to mice through tail vein intravenous injection after 1 week of Glab administration. The retinas of mice were monitored by Optical coherence tomography (OCT) and electroretinography (ERG) at 1w, 2w, 3w, and 4w, respectively, followed by H&E staining.ResultsIn vitro, the Glab protected the retinal pigment epithelial (RPE) cells against oxidative stress and apoptosis by inhibiting phosphorylation of ERK1/2 and the p38 MAPK pathway. In vivo, Glab significantly prevented retinal damage by stopping the progression of retinal degeneration and reducing the formation of deposits on the RPE layer induced by NaIO3. According to the findings of electroretinogram (ERG), Glab helped to maintain the normal function of the retina.ConclusionGlabridin has a protective effect against retinal degeneration. It is suggested that Glab be further investigated for the treatment of retinal degeneration diseases.

Dataset Information

RNA-seq analysis reveals differentially expressed inflammatory chemokines in a rat retinal degeneration model induced by sodium iodate.

Objective

Methods

Results

Conclusion

Publications

RNA-seq analysis reveals differentially expressed inflammatory chemokines in a rat retinal degeneration model induced by sodium iodate.

Similar Datasets

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