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Mir-204-5p alleviates mitochondrial dysfunction by targeting IGFBP5 in diabetic cataract.
Xie, Jin; Chen, Peng; Mao, Shilan; Zang, Xinyi; Cao, Rui; Liu, Wenhui; Wang, Xiaolei; Dai, Yunhai.
Afiliación
  • Xie J; State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Eye Institute of Shandong First Medical University, Qingdao, China.
  • Chen P; Qingdao Eye Hospital of Shandong First Medical University, Qingdao, China.
  • Mao S; Department of Human Anatomy, Histology and Embryology, School of Basic Medicine, Qingdao University, Qingdao, China.
  • Zang X; Institute of Stem Cell Regeneration Medicine, School of Basic Medicine, Qingdao University, Qingdao, China.
  • Cao R; Shandong First Medical University, Jinan, China.
  • Liu W; School of Ophthalmology, Shandong First Medical University, Qingdao, China.
  • Wang X; Weifang Medical University, Weifang, China.
  • Dai Y; State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Eye Institute of Shandong First Medical University, Qingdao, China.
Mol Biol Rep ; 51(1): 755, 2024 Jun 14.
Article en En | MEDLINE | ID: mdl-38874707
ABSTRACT

BACKGROUND:

Cataract contributes to visual impairment worldwide, and diabetes mellitus accelerates the formation and progression of cataract. Here we found that the expression level of miR-204-5p was diminished in the lens epithelium with anterior lens capsule of cataract patients compared to normal donors, and decreased more obviously in those of diabetic cataract (DC) patients. However, the contribution and mechanism of miR-204-5p during DC development remain elusive. METHODS AND

RESULT:

The mitochondrial membrane potential (MMP) was reduced in the lens epithelium with anterior lens capsule of DC patients and the H2O2-induced human lens epithelial cell (HLEC) cataract model, suggesting impaired mitochondrial functional capacity. Consistently, miR-204-5p knockdown by the specific inhibitor also attenuated the MMP in HLECs. Using bioinformatics and a luciferase assay, further by immunofluorescence staining and Western blot, we identified IGFBP5, an insulin-like growth factor binding protein, as a direct target of miR-204-5p in HLECs. IGFBP5 expression was upregulated in the lens epithelium with anterior lens capsule of DC patients and in the HLEC cataract model, and IGFBP5 knockdown could reverse the mitochondrial dysfunction in the HLEC cataract model.

CONCLUSIONS:

Our results demonstrate that miR-204-5p maintains mitochondrial functional integrity through repressing IGFBP5, and reveal IGFBP5 may be a new therapeutic target and prognostic factor for DC.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Catarata / Proteína 5 de Unión a Factor de Crecimiento Similar a la Insulina / MicroARNs / Complicaciones de la Diabetes / Células Epiteliales / Mitocondrias Límite: Female / Humans / Male / Middle aged Idioma: En Revista: Mol Biol Rep Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Países Bajos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Catarata / Proteína 5 de Unión a Factor de Crecimiento Similar a la Insulina / MicroARNs / Complicaciones de la Diabetes / Células Epiteliales / Mitocondrias Límite: Female / Humans / Male / Middle aged Idioma: En Revista: Mol Biol Rep Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Países Bajos