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微小RNA-26缺乏会导致晶状体转录组改变，并引发成人期白内障。

miR-26 deficiency causes alterations in lens transcriptome and results in adult-onset cataract.

作者信息

Upreti Anil, Hoang Thanh V, Li Minghua, Tangeman Jared A, Dierker David S, Wagner Brad D, Tsonis Panagiotis A, Liang Chun, Lachke Salil A, Robinson Michael L

机构信息

Cell, Molecular and Structural Biology Program, Miami University, Oxford, OH 45056, USA.

Department of Biology and Center for Visual Sciences, Miami University, Oxford, OH 45056, USA.

出版信息

bioRxiv. 2024 Jan 30:2024.01.29.577818. doi: 10.1101/2024.01.29.577818.

DOI:10.1101/2024.01.29.577818
PMID:38352453
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10862774/
Abstract

PURPOSE

Despite strong evidence demonstrating that normal lens development requires regulation governed by miRNAs, the functional role of specific miRNAs in mammalian lens development remains largely unexplored.

METHODS

A comprehensive analysis of miRNA transcripts in the newborn mouse lens, exploring both differential expression between lens epithelial cells and lens fiber cells and overall miRNA abundance was conducted by miRNA-seq. Mouse lenses lacking each of three abundantly expressed lens miRNAs: miR-184, miR-26 and miR-1 were analyzed to explore the role of these miRNAs in lens development.

RESULTS

Mice lacking all three copies of () developed postnatal cataracts as early as 4-6 weeks of age. RNA-seq analysis of neonatal lenses from mice exhibited abnormal reduced expression of a cohort of genes found to be lens-enriched and linked to cataract (, , , and numerous crystallin genes), and abnormal elevated expression of genes related to neural development ( ), inflammation (, the complement pathway, and epithelial to mesenchymal transition ().

CONCLUSION

miR-1, miR-184 and miR-26 are each dispensable for normal embryonic lens development. However, loss of miR-26 causes lens transcriptome changes and drives cataract formation.

摘要

目的

尽管有强有力的证据表明正常晶状体发育需要受微小RNA（miRNA）调控，但特定miRNA在哺乳动物晶状体发育中的功能作用在很大程度上仍未被探索。

方法

通过miRNA测序对新生小鼠晶状体中的miRNA转录本进行全面分析，探究晶状体上皮细胞和晶状体纤维细胞之间的差异表达以及整体miRNA丰度。对缺乏三种高表达晶状体miRNA（miR - 184、miR - 26和miR - 1）中每一种的小鼠晶状体进行分析，以探索这些miRNA在晶状体发育中的作用。

结果

缺乏所有三个拷贝（）的小鼠早在4 - 6周龄时就出现了产后白内障。对来自小鼠的新生晶状体进行RNA测序分析显示，一组在晶状体中富集且与白内障相关的基因（，，，和众多晶状体蛋白基因）表达异常降低，而与神经发育（）、炎症（，补体途径）以及上皮 - 间充质转化（）相关的基因表达异常升高。

结论

miR - 1、miR - 184和miR - 26对正常胚胎晶状体发育均非必需。然而，miR - 26的缺失会导致晶状体转录组变化并引发白内障形成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a9/10862774/325ccb089aff/nihpp-2024.01.29.577818v1-f0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a9/10862774/7e166a547886/nihpp-2024.01.29.577818v1-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a9/10862774/7bbe593b565a/nihpp-2024.01.29.577818v1-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a9/10862774/f6854b5754ef/nihpp-2024.01.29.577818v1-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a9/10862774/42034ee7c0e3/nihpp-2024.01.29.577818v1-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a9/10862774/fb515d3f7a0c/nihpp-2024.01.29.577818v1-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a9/10862774/574deb95365c/nihpp-2024.01.29.577818v1-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a9/10862774/c8f6b355d761/nihpp-2024.01.29.577818v1-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a9/10862774/325ccb089aff/nihpp-2024.01.29.577818v1-f0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a9/10862774/7e166a547886/nihpp-2024.01.29.577818v1-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a9/10862774/7bbe593b565a/nihpp-2024.01.29.577818v1-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a9/10862774/f6854b5754ef/nihpp-2024.01.29.577818v1-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a9/10862774/42034ee7c0e3/nihpp-2024.01.29.577818v1-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a9/10862774/fb515d3f7a0c/nihpp-2024.01.29.577818v1-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a9/10862774/574deb95365c/nihpp-2024.01.29.577818v1-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a9/10862774/c8f6b355d761/nihpp-2024.01.29.577818v1-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a9/10862774/325ccb089aff/nihpp-2024.01.29.577818v1-f0008.jpg

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