Integrative analysis of ex vivo studies and microarray reveals the novel inhibitor effects of trehalose on the pathogenesis of pterygium

Author:

Durkal Yasin1ORCID,İnci Kubilay2ORCID,Tokgun Onur3ORCID,Yilmaz Ugur1ORCID,Yılmaz Banu Candan2

Affiliation:

1. Department of Ophthalmology, Faculty of Medicine Pamukkale University Denizli Turkey

2. Department of Cancer Molecular Biology Institution of Health Sciences, Pamukkale University Denizli Turkey

3. Department of Medical Genetics, Faculty of Medicine Pamukkale University Denizli Turkey

Abstract

AbstractPterygium is a frequent eye surface condition that is characterized by a high rate of proliferation, fibrovascular development, cellular migration, corneal infiltration, and angiogenesis. We investigated that ex vivo primary pterygium and conjunctival cell cultures were generated to analyze the effect of trehalose on cellular proliferation. After trehalose treatment, we performed microarray analysis to evaluate changes in the mRNA profile. We analyzed gene ontology (GO) and KEGG pathways to identify hub genes that changed expression levels after treatment and were associated with pterygium development. We selected three genes to verify their expression levels using qRT–PCR. The study also evaluated the impact of trehalose treatment on cell migration through a wound‐healing assay. Our results suggested that pterygium cell proliferation was inhibited in a dose‐dependent manner by trehalose. 2354 DEG were identified in pterygium and conjunctiva cells treated with trehalose compared to untreated groups. Functional enrichment analysis showed that differentially expressed mRNAs are involved in proliferation, vasculature development, and cell migration. We identified ten hub genes including upregulated (RANBP3L, SLC5A3, RERG, ANKRD1, DHCR7, RAB27B, GPRC5B, MSMO1, ASPN, DRAM1) and downregulated (TNC, PTGS2, GREM2, NPTX1, NR4A1, HMOX1, CXCL12, IL6, MYH2, TXNIP). Microarray analysis and functional investigations suggest that trehalose affects the pathogenesis of pterygium by modifying the expression of genes involved in crucial pathways related to cell function.

Publisher

Wiley

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