天堂网亚洲,天天操天天搞,91视频高清,菠萝蜜视频在线观看入口,美女视频性感美女视频,95丝袜美女视频国产,超高清美女视频图片

ChemicalBook >> journal list >> Experimental eye research >>article
Experimental eye research

Experimental eye research

IF: 3
Download PDF

MiR-23a-3p targets PTEN as a novel anti-ferroptosis regulator in Fuchs endothelial corneal dystrophy

Published:22 November 2024 DOI: 10.1016/j.exer.2024.110180 PMID: 39581360
Miaomiao Chi, Yaning Zhao, Jing Hong

Abstract

Fuchs endothelial corneal dystrophy (FECD) is the leading cause of keratoplasty without drug treatment. Research indicated that oxidative stress and lipid peroxidation play significant roles in FECD. However, the underlying pathogenesis and potential treatment remain poorly understood. We analyzed the mRNA expression of FECD using the GEO database (GSE171830). Utilizing the STRING database and Cytoscape's MCODE plugin, we identified hub genes that intersect with ferroptosis-related genes listed in FerrDb. FECD cell and animal models were developed, induced by Ultraviolet A exposure. We assessed ferroptosis by measuring GPX4 expression and ROS fluorescence intensity. MiR-23a-3p was compared between FECD model and normal control, and the target gene PTEN was confirmed through Western blot and dual-luciferase reporter assays. Treatment with PTEN, PI3K, Akt, and mTOR inhibitors provided insights into the role of the PTEN/PI3K/Akt/mTOR pathway in FECD model. Corneal endothelium and cellular structure were evaluated before and after delivery of miR-23a-3p. Bioinformatics analysis of the GSE171830 revealed the top five hub genes: TP53, PTEN, EGFR, EPAS1, and IL-1β. Ferroptosis is the predominant mechanism in FECD pathogenesis, distinct from apoptosis and necrosis. We uncovered a protective role for miR-23a-3p in corneal endothelial cells (CEnCs), mitigating ferroptosis by downregulating PTEN. Corroborating this, bpV (a PTEN inhibitor) was found to attenuate ferroptosis in CEnCs. Mechanistically, PTEN inhibition coupled with sustained PI3K/Akt/mTOR pathway activation emerged as a protective strategy against ferroptosis in CEnCs. Ferroptosis contributes to FECD pathogenesis, and targeted delivery of miR-23a-3p as a ferroptosis inhibitor may offer therapeutic potential by regulating PTEN/PI3K/Akt/mTOR signaling.

Substances (5)

Materials
Procduct Name CAS Molecular Formula Supplier Price
4',6-Diamidino-2-phenylindole dihydrochloride 28718-90-3 C16H16ClN5 296 suppliers $14.10-$4800.00
Sincalide 25126-32-3 C49H62N10O16S3 263 suppliers $75.00-$8505.00
Necrostatin-1 4311-88-0 C13H13N3OS 174 suppliers $26.00-$2000.00
Torin 1 1222998-36-8 C35H28F3N5O2 157 suppliers $28.00-$4500.00
2-[1-[4-[2-(4-Chlorophenoxy)acetyl]-1-piperazinyl]ethyl]-3-(2-ethoxyphenyl)-4(3H)-Quinazolinone 571203-78-6 C30H31ClN4O4 153 suppliers $44.00-$2691.10

Similar articles

IF:5.9

Creatine monohydrate as a therapeutic aid in muscular dystrophy.

Nutrition reviews Jared Pearlman,?R. Fielding,etc Published: 1 February 2006
IF:3.4

Exosomal miR‐155‐5p Facilitates Lipopolysaccharide Transport and Foam Cell Formation: A Novel Link Between Periodontitis and Atherosclerosis

Journal of periodontal research Wen‐Wen Yang, Qing‐Xiang Li,etc Published: 27 November 2024