PDF(Pubmed)
Abstract：
UNASSIGNED: Aging is a risk factor for dry eye. We sought to identify changes in the aged mouse corneal epithelial transcriptome and determine how age affects corneal sensitivity, re-epithelialization, and barrier reformation after corneal debridement.
UNASSIGNED: Corneal epithelium of female C57BL/6J (B6) mice of different ages (2, 12, 18, and 24 months) was collected, RNA extracted, and bulk RNA sequencing performed. Cornea sensitivity was measured with an esthesiometer in 2- to 3-month-old, 12- to 13-month-old, 18- to 19-month-old, and 22- to 25-month-old female and male mice. The 2-month-old and 18-month-old female and male mice underwent unilateral corneal debridement using a blunt blade. Wound size and fluorescein staining were visualized and photographed at different time points, and a re-epithelialization rate curve was calculated.
UNASSIGNED: There were 157 differentially expressed genes in aged mice compared with young mice. Several pathways downregulated with age control cell migration, proteoglycan synthesis, and collagen trimerization, assembly, biosynthesis, and degradation. Male mice had decreased corneal sensitivity compared with female mice at 12 and 24 months of age. Aged mice, irrespective of sex, had delayed corneal re-epithelialization in the first 48 hours and worse corneal fluorescein staining intensity at day 14 than young mice.
UNASSIGNED: Aged corneal epithelium has an altered transcriptome. Aged mice regardless of sex heal more slowly and displayed more signs of corneal epithelial defects after wounding than young mice. These results indicate that aging significantly alters the corneal epithelium and its ability to coordinate healing.
UNASSIGNED: Corneal epithelium of female C57BL/6J (B6) mice of different ages (2, 12, 18, and 24 months) was collected, RNA extracted, and bulk RNA sequencing performed. Cornea sensitivity was measured with an esthesiometer in 2- to 3-month-old, 12- to 13-month-old, 18- to 19-month-old, and 22- to 25-month-old female and male mice. The 2-month-old and 18-month-old female and male mice underwent unilateral corneal debridement using a blunt blade. Wound size and fluorescein staining were visualized and photographed at different time points, and a re-epithelialization rate curve was calculated.
UNASSIGNED: There were 157 differentially expressed genes in aged mice compared with young mice. Several pathways downregulated with age control cell migration, proteoglycan synthesis, and collagen trimerization, assembly, biosynthesis, and degradation. Male mice had decreased corneal sensitivity compared with female mice at 12 and 24 months of age. Aged mice, irrespective of sex, had delayed corneal re-epithelialization in the first 48 hours and worse corneal fluorescein staining intensity at day 14 than young mice.
UNASSIGNED: Aged corneal epithelium has an altered transcriptome. Aged mice regardless of sex heal more slowly and displayed more signs of corneal epithelial defects after wounding than young mice. These results indicate that aging significantly alters the corneal epithelium and its ability to coordinate healing.
摘要：
■衰老是干眼的危险因素。我们试图确定老年小鼠角膜上皮转录组的变化，并确定年龄如何影响角膜敏感性。再上皮化,角膜清创术后的屏障重建。
■收集不同年龄（2、12、18和24个月）的雌性C57BL/6J（B6）小鼠的角膜上皮，RNA提取,和进行批量RNA测序。在2至3个月大的时候用美感仪测量角膜敏感度，12到13个月大,18-19个月大,和22至25个月大的雌性和雄性小鼠。2个月大和18个月大的雌性和雄性小鼠使用钝刀片进行单侧角膜清创术。在不同的时间点观察伤口大小和荧光素染色并拍照。并计算上皮再形成率曲线。
■老年小鼠与年轻小鼠相比有157个差异表达基因。几种途径随着年龄控制细胞迁移而下调，蛋白聚糖合成，胶原蛋白三聚化，装配,生物合成，和退化。与雌性小鼠相比，雄性小鼠在12和24月龄时的角膜敏感性降低。老年老鼠,不论性别,与年轻小鼠相比，在前48小时延迟了角膜再上皮形成，在第14天角膜荧光素染色强度较差。
■衰老的角膜上皮具有改变的转录组。与年轻小鼠相比，不分性别的老年小鼠愈合更慢，并且在受伤后显示出更多的角膜上皮缺陷迹象。这些结果表明，衰老显着改变了角膜上皮及其协调愈合的能力。
■收集不同年龄（2、12、18和24个月）的雌性C57BL/6J（B6）小鼠的角膜上皮，RNA提取,和进行批量RNA测序。在2至3个月大的时候用美感仪测量角膜敏感度，12到13个月大,18-19个月大,和22至25个月大的雌性和雄性小鼠。2个月大和18个月大的雌性和雄性小鼠使用钝刀片进行单侧角膜清创术。在不同的时间点观察伤口大小和荧光素染色并拍照。并计算上皮再形成率曲线。
■老年小鼠与年轻小鼠相比有157个差异表达基因。几种途径随着年龄控制细胞迁移而下调，蛋白聚糖合成，胶原蛋白三聚化，装配,生物合成，和退化。与雌性小鼠相比，雄性小鼠在12和24月龄时的角膜敏感性降低。老年老鼠,不论性别,与年轻小鼠相比，在前48小时延迟了角膜再上皮形成，在第14天角膜荧光素染色强度较差。
■衰老的角膜上皮具有改变的转录组。与年轻小鼠相比，不分性别的老年小鼠愈合更慢，并且在受伤后显示出更多的角膜上皮缺陷迹象。这些结果表明，衰老显着改变了角膜上皮及其协调愈合的能力。
