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囊袋内长期肌成纤维细胞的持续存在导致晚期自发性囊袋内人工晶状体脱位。

Long-term myofibroblast persistence in the capsular bag contributes to the late spontaneous in-the-bag intraocular lens dislocation.

机构信息

Center for Eye Research, Department of Ophthalmology, University of Oslo and Oslo University Hospital, Kirkeveien 166, 0450, Oslo, Norway.

Institute of Clinical Medicine, University of Oslo, Oslo, Norway.

出版信息

Sci Rep. 2020 Nov 25;10(1):20532. doi: 10.1038/s41598-020-77207-7.

Abstract

Late spontaneous in-the-bag intraocular lens (IOL) dislocation is a complication presenting 6 months or later after cataract surgery. We aimed to characterize the cells in the lens capsules (LCs) of 18 patients with spontaneous late in-the-bag IOL dislocation. Patients' average age was 82.6 ± 1.5 years (range 72-98), and most of them had pseudoexfoliation syndrome (PEX). Cells from the LCs were positive for myofibroblast (αSMA), proliferation (Ki-67, PCNA), early lens development/lens progenitor (SOX2, PAX6), chemokine receptor (CXCR4), and transmembrane (N-cadherin) markers, while negative for epithelial (E-cadherin) marker. Moreover, the cells produced abundant fibronectin, type I and type V collagen in the nearby extracellular matrix (ECM). During ex vivo cultivation of dislocated IOL-LCs in toto, the cells proliferated and likely migrated onto the IOL's anterior side. EdU proliferation assay confirmed the proliferation potential of the myofibroblasts (MFBs) in dislocated IOL-LCs. Primary cultured lens epithelial cells/MFBs isolated from the LC of dislocated IOLs could induce collagen matrix contraction and continuously proliferated, migrated, and induced ECM remodeling. Taken together, this indicates that long-lived MFBs of dislocated IOLs might contribute to the pathogenic mechanisms in late in-the-bag IOL dislocation.

摘要

自发性晶状体囊袋内人工晶状体(IOL)后脱位是白内障手术后 6 个月或更长时间出现的一种并发症。我们旨在研究 18 例自发性晶状体囊袋内人工晶状体后脱位患者晶状体囊(LC)中的细胞特征。患者平均年龄为 82.6±1.5 岁(72-98 岁),其中大多数患有假性剥脱综合征(PEX)。LC 中的细胞表达肌成纤维细胞(αSMA)、增殖(Ki-67、PCNA)、早期晶状体发育/晶状体祖细胞(SOX2、PAX6)、趋化因子受体(CXCR4)和跨膜(N-钙黏蛋白)标志物,而不表达上皮(E-cadherin)标志物。此外,这些细胞在附近的细胞外基质(ECM)中产生丰富的纤连蛋白、I 型和 V 型胶原。在体外培养完全脱位的 IOL-LC 时,细胞增殖并可能迁移到 IOL 的前侧。EdU 增殖实验证实了脱位的 IOL-LC 中的肌成纤维细胞(MFB)具有增殖潜能。从脱位 IOL 的 LC 中分离出的原代培养的晶状体上皮细胞/MFB 可以诱导胶原基质收缩并持续增殖、迁移和诱导 ECM 重塑。综上所述,这表明脱位的 IOL 中的长寿 MFB 可能有助于迟发性晶状体囊袋内 IOL 脱位的发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9a/7689492/2ef8e82130c9/41598_2020_77207_Fig1_HTML.jpg

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