PM2.5 exposure could result in delay of corneal epithelium wound healing by inhibiting cell migration, thus more attention should be paid to the potential risk of corneal infection and effort should be made to protect eyes against impairment induced by PM2.5.
Inflammation is considered to be critical in the pterygium progression and recurrence. However, the underlying molecular mechanism is not well understood. Herein, we investigated the potential role of RNA binding protein human antigen R (HuR) responsible for the impact of inflammation on pterygium development. The expression of HuR and matrix metallopeptidase‐9 (MMP‐9) in pterygium and normal conjunctiva was detected with immunohistochemistry and quantitative reverse transcription polymerase chain reaction (qRT‐PCR). The influence of interleukin‐1β (IL‐1β) on HuR expression and cellular distribution was determined with western blot and immunofluorescence. The pterygium fibroblast (PTF) migration was determined with scratch wound healing assay and Transwell migration assay. MMP‐9 production was determined with qRT‐PCR and gelatin zymography. The interaction between HuR and MMP‐9 was investigated with RNP immunoprecipitation (IP) followed by RT‐PCR and messenger RNA (mRNA) stability analysis. HuR and MMP‐9 expression are elevated in pterygium, especially progressive pterygium compared with normal conjunctiva. IL‐1β could increase the expression and nucleus–cytoplasm shuttle of HuR in cultured PTFs. HuR mediated the stimulatory effect of IL‐1β on PTF migration and MMP‐9 production. HuR bound to MMP‐9 mRNA and in turn increased it stability. Our results suggest that posttranscriptional regulation of MMP‐9 via stabilizing mRNA by HuR might contribute to the stimulatory effect of inflammatory factor IL‐1β on pterygium progression. These findings shed light on the pathogenesis of pterygium and provide a promising target for adjuvant treatment of pterygium.
Pterygium is a common ocular surface disease induced by a variety of factors. The exact pathogenesis of pterygium remains unclear. Numbers of genes and proteins are discovered in pterygium and they function differently in the occurrence and development of this disease. We searched the Web of Science and PubMed throughout history for literatures about the subject. The keywords we used contain pterygium, gene, protein, angiogenesis, fibrosis, proliferation, inflammation, pathogenesis and therapy. In this review, we summarize the aberrant expression of a range of genes and proteins in pterygium compared with normal conjunctiva or cornea, including growth factors, matrix metalloproteinases and tissue inhibitors of metalloproteinases, interleukins, tumor suppressor genes, proliferation related proteins, apoptosis related proteins, cell adhesion molecules, extracellular matrix proteins, heat shock proteins and tight junction proteins. We illustrate their possible mechanisms in the pathogenesis of pterygium as well as the related intervention based on them for pterygium therapy.
Myopia has become a major public health issue worldwide. Identification of genetic loci related to myopia in young children may advance our knowledge of the pathogenesis of myopia. Fibroblast growth factor 10 (FGF10) plays essential roles for the development of myopia through modulating extracellular matrix‐associated genes. Studies revealed that genetic variants of FGF10 were associated with extreme myopia in adults. However, their associations with susceptibility of myopia in young children, which are less affected by confounding factors and more suitable for studying genetic factors of myopia, have not been explored. In the current study, we evaluated 13 tagSNPs that captured 100% of genetic variation in the FGF10 gene region for their associations with myopia in a large Chinese case‐control study with 900 myopia children and 900 nonmyopia children. We found rs2973644 was significantly associated with increased risk of myopia (odds ratio [OR]: 1.26; 95% confidence intervals [CI]: 1.06‐1.49; P = 0.009). furthermore, rs339501 (OR: 1.73; 95% CI: 1.18‐2.53; P = 0.005), rs2973644 (OR: 1.57; 95% CI: 1.13‐2.19; P = 0.007), and rs79002828 (OR: 1.83; 95% CI: 1.20‐2.77; P = 0.005) were significantly associated with increased risk of high myopia in young children. Functional assessment of rs2973644 by luciferase assays revealed the risk G allele causes a higher expression level of FGF10 than the protective A allele. Our results do support that genetic variants of cytokine FGF10 are associated with susceptibility of myopia (as well as high myopia) in young children and further exploration are needed for myopia in children.
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