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Knockdown of ChREBP ameliorates retinal microvascular endothelial cell injury and angiogenic responses in diabetic retinopathy.
Sui, Yao; Du, Chunyang; Wang, Ming; Liu, Xiaoli; Chai, Qiannan; Liang, Shuang; Ma, Jingxue; Duan, Jialiang.
Afiliación
  • Sui Y; Department of Ophthalmology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
  • Du C; Department of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province, Shijiazhuang, China; Center of Metabolic Diseases and Cancer research, Institute of Medical and Health Science, Hebei Medical University, Shijiazhuang, China.
  • Wang M; Department of Ophthalmology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
  • Liu X; Department of Ophthalmology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
  • Chai Q; Department of Ophthalmology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
  • Liang S; Department of Ophthalmology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
  • Ma J; Department of Ophthalmology, The Second Hospital of Hebei Medical University, Shijiazhuang, China. Electronic address: majingxue99@126.com.
  • Duan J; Department of Ophthalmology, The Second Hospital of Hebei Medical University, Shijiazhuang, China. Electronic address: duanjialiang@hebmu.edu.cn.
Biochem Biophys Res Commun ; 694: 149389, 2024 01 29.
Article en En | MEDLINE | ID: mdl-38128383
ABSTRACT

PURPOSE:

To examine whether and how carbohydrate response element-binding protein (ChREBP) plays a role in diabetic retinopathy.

METHODS:

Western blotting was used to detect ChREBP expression and location following high glucose stimulation of Human Retinal Microvascular Endothelial Cells (HRMECs). Flow cytometry, TUNEL staining, and western blotting were used to evaluate apoptosis following ChREBP siRNA silencing. Cell scratch, transwell migration, and tube formation assays were used to determine cell migration and angiogenesis. Diabetic models for wild-type (WT) and ChREBP knockout (ChKO) mice were developed. Retinas of WT and ChKO animals were cultivated in vitro with vascular endothelial growth factor + high glucose to assess neovascular development.

RESULTS:

ChREBP gene knockdown inhibited thioredoxin-interacting protein and NOD-like receptor family pyrin domain containing protein 3 expression in HRMECs, which was caused by high glucose stimulation, reduced apoptosis, hindered migration, and tube formation, and repressed AKT/mTOR signaling pathway activation. Compared with WT mice, ChKO mice showed suppressed high glucose-induced alterations in retinal structure, alleviated retinal vascular leakage, and reduced retinal neovascularization.

CONCLUSIONS:

ChREBP deficiency decreased high glucose-induced apoptosis, migration, and tube formation in HRMECs as well as structural and angiogenic responses in the mouse retina; thus, it is a potential therapeutic target for diabetic retinopathy.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Diabetes Mellitus / Retinopatía Diabética Límite: Animals / Humans Idioma: En Revista: Biochem Biophys Res Commun Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos
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: Diabetes Mellitus / Retinopatía Diabética Límite: Animals / Humans Idioma: En Revista: Biochem Biophys Res Commun Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos