Ascorbic acid ameliorates corneal endothelial dysfunction and enhances cell proliferation via the noncanonical GLUT1-ERK axis - 13/11/21
, Yaa-Jyuhn James Meir b, c , Jui-Yang Lai d, e, f , Chieh-Cheng Huang b, g , Tsai-Te Lu b, g , David Hui-Kang Ma a, b, h , Chao-Min Cheng b, g , Wei-Chi Wu a, i , Hung-Chi Chen a, b, i, ⁎ Bienvenue sur EM-consulte, la référence des professionnels de santé.
L’accès au texte intégral de cet article nécessite un abonnement.
| pages | 10 |
| Iconographies | 7 |
| Vidéos | 0 |
| Autres | 0 |
Abstract |
Background |
The pumping function of corneal endothelial cells (CECs) plays a pivotal role in the maintenance of corneal water homeostasis. Corneal endothelial dysfunction (CED) leads to corneal edema and opacity, but with the exception of keratoplasty, no optimal therapeutic strategies have been established for CED. In this study, we aimed to investigate the ameliorative effect of ascorbic acid (AA) on CED and the underlying mechanism of action in the corneal endothelium.
Methods |
Rabbit corneal endothelial damage was induced by anterior chamber injection of benzalkonium chloride (BAK). AA was topically administered to the corneal surface, and the transparency and thickness of the cornea were assessed by external eye photography, slit-lamp photography, and ultrasonic pachymetry. To further analyze the mechanism, rabbit CECs and immortalized human CECs (B4G12 cells) were cultured. A ferric reducing/antioxidant and AA (FRASC) assay was performed to measure the AA concentration. Cell proliferation was evaluated by cell counting and bromodeoxyuridine (BrdU) labeling assays, and protein expression was examined by liquid chromatography–mass spectrometry (LC/MS) and immunoblotting. The involvement of glucose transporter 1 (GLUT1) and phospho-ERK was evaluated via GLUT1-siRNA and phospho-ERK inhibitor (PD98059) treatment.
Interpretation |
We observed that topical AA ameliorates BAK-induced rabbit corneal endothelial damage. Furthermore, we demonstrated that AA is transported into B4G12 cells via GLUT1, and afterward, AA increases ERK phosphorylation and promotes cell proliferation. Our findings indicate that CEC proliferation stimulated via the noncanonical AA-GLUT1-ERK axis contributes to AA-enhanced healing of CED.
Le texte complet de cet article est disponible en PDF.Abbreviation : HCEC, CEC, ECD, AA, DHA, GPA, BAK, GLUT1 SLC2A1, DMEM, AO, basic-FGF, BrdU, LC/MS, IND, RPE, PI3K, Akt, mTOR, RAS, Raf, MEK, ERK, RSK
Keywords : Corneal endothelial dysfunction (CED), Ascorbic acid, Proliferation, Glucose transporter 1 (GLUT1), Noncanonical ERK pathway
Plan
Vol 144
Article 112306- décembre 2021 Retour au numéro
Article précédent
- JKST6, a novel multikinase modulator of the BCR-ABL1/STAT5 signaling pathway that potentiates direct BCR-ABL1 inhibition and overcomes imatinib resistance in chronic myelogenous leukemia
- Haidée Aranda-Tavío, Carlota Recio, Pedro Martín-Acosta, Miguel Guerra-Rodríguez, Yeray Brito-Casillas, Rosa Blanco, Vanessa Junco, Javier León, Juan Carlos Montero, Lucía Gandullo-Sánchez, Grant McNaughton-Smith, Juan Manuel Zapata, Atanasio Pandiella, Angel Amesty, Ana Estévez-Braun, Leandro Fernández-Pérez, Borja Guerra
- Alpinia officinarum water extract inhibits the atopic dermatitis-like responses in NC/Nga mice by regulation of inflammatory chemokine production
- Hyun-Kyung Song, Sun Haeng Park, Hye Jin Kim, Seol Jang, Taesoo Kim
Bienvenue sur EM-consulte, la référence des professionnels de santé.
L’accès au texte intégral de cet article nécessite un abonnement.
Bienvenue sur EM-consulte, la référence des professionnels de santé.
L’achat d’article à l’unité est indisponible à l’heure actuelle.
Déjà abonné à cette revue ?