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Therapeutic Effect of Histone Acetyltransferase Inhibitors on Galactose-Induced Cataract in Rats

ABSTRACT: Therapeutic Effect of Histone Acetyltransferase Inhibitors on Galactose-Induced Cataract in Rats

PROVIDER: PRJNA773070 | ENA |

REPOSITORIES: ENA

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Therapeutic Effect of Histone Acetyltransferase Inhibitors on Galactose-Induced Cataract in Rats

Project description:We investigated the therapeutic effects of histone acetyltransferase (HAT) inhibitors on cataracts using an ex vivo model of galactose-induced cataracts in the rat lens.Among the tested HAT inhibitors, TH1834 was the only inhibitor that could completely reverse white opacities once formed in the lens. Combination treatment with C646/CPTH2 and CBP30/CPTH2 also had therapeutic effects. To identify the genes regulated by HAT inhibitors, we conducted microarray analysis of treated and untreated cataract samples.

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Project description:The addition of Pyruvate to the lens induced by galactose eliminated the white clouding formed and showed a therapeutic effect. Genes regulated by pyruvate addition were identified by microarray analysis. A total of seven samples were used in this analysis: two samples without galactose (control), three samples with galactose (galactose) and two samples with Pyruvate (Pyruvate).

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Project description:Diabetic cataracts can occur at an early age, causing visual impairment or blindness. The detailed molecular mechanisms of diabetic cataract formation remain incompletely understood, and there is no well-documented prophylactic agent. Galactose-fed rats and ex vivo treatment of lenses with galactose are used as models of diabetic cataract. To assess the role of histone acetyltransferases, we conducted cataract prevention screening with known histone acetyltransferase (HAT) inhibitors. Ex vivo treatment with a HAT inhibitor strongly inhibited the formation of lens turbidity in high-galactose conditions, while addition of a histone deacetylase (HDAC) inhibitor aggravated turbidity. We conducted a microarray to identify genes differentially regulated by HATs and HDACs, leading to discovery of a novel cataract causative factor, Plk3. Plk3 mRNA levels correlated with the degree of turbidity, and Plk3 inhibition alleviated galactose-induced cataract formation. These findings indicate that epigenetically controlled Plk3 influences cataract formation. Our results demonstrate a novel approach for prevention of diabetic cataract using HAT and Plk3 inhibitors.

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Expression data from lens epithelial cells (LECs) from Shumiya cataract rats (SCR) with or without cataract (Cat+ or Cat-)

Project description:The Shumiya cataract rat (SCR) is a model for hereditary cataract. Two-third of these rats develop lens opacity within 10-11-weeks. Onset of cataract is attributed to the synergetic effect of lanosterol synthase (Lss) and farnesyl-diphosphate farnesyltransferase 1 (Fdft1) mutant alleles that lead to cholesterol deficiency in the lenses, which in turn adversely affects lens biology including the growth and differentiation of lens epithelial cells (LECs). Nevertheless, the molecular events and changes in gene expression associated with the onset of lens opacity in SCR is poorly understood. Our study aimed to identify the gene expression patterns during cataract formation in SCRs, which may be responsible for cataractogenesis in SCR.

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Project description:Cataract, a disease that causes opacity of the lens, is the leading cause of blindness worldwide. Cataracts secondary to diabetes are common, even in young patients, so they are of significant clinical importance. Here, we used an ex vivo model of galactose-induced cataracts in the rat lens to investigate the therapeutic effects of histone acetyltransferase (HAT) inhibitors. Among the tested HAT inhibitors, TH1834 was the only one that could reverse most of the opacity once it had formed in the lens. Combination treatment with C646/CPTH2 and CBP30/CPTH2 also had therapeutic effects. In lens cross-sections, vacuoles were present in the tissue of the cortical equatorial region of untreated cataract samples. In treated cataract samples, lens tissue regenerated to fill the vacuoles. To identify the genes regulated by HAT inhibitors, qRT-PCR was performed on treated and untreated cataract samples to determine candidate genes. Expression of Acta1 and Stmn4, both of which are involved in the cytoskeleton, were altered significantly in C646+CPTH2 samples. Expression of Emd, a nuclear membrane protein, and Prtfdc1, which is involved in cancer cell proliferation, were altered significantly in CBP30+CPTH2 samples. Acta1, Acta2, Arrdc3, Hebp2, Hist2h2ab, Pmf1, Ppdpf, Rbm3, RGD1561694, Slc16a6, Slfn13, Tagln, Tgfb1i1, and Tuba1c in TH1834 samples were significantly altered. These genes were primarily related to regulation of cell proliferation, the cytoskeleton, and cell differentiation. Expression levels increased with the onset of cataracts and was suppressed in samples treated with HAT inhibitors.

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Microarray data of lenses with 2ME2

Project description:The addition of 2ME2 (HIF-1 inhibitor) to rat model of galactose-induced cataract decreased opacity and therapeutic effect. Genes regulated by 2ME2 addition were identified by microarray analysis. A total of 7 samples were analyzed: samples with no cataract (Control_Day4, Control_Day6), samples with cataract (Galactose-1, Galactose-2, Galactose-3), samples with decreased lens opacity (2ME2, 2ME2-2)

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