Thymosin-β4 Inhibits Corneal Epithelial Cell Apoptosis after Ethanol Exposure In Vitro

Abstract

Tbeta(4) plays an antiapoptotic role under conditions of epithelial cell challenge with an external stress such as exposure to ethanol. Tbeta(4) may function as an antiapoptotic agent by inhibiting the release of cytochrome c from mitochondria and by suppressing the activation of caspases.

Coenzyme Q10 Rescues Ethanol-induced Corneal Fibroblast Apoptosis through the Inhibition of Caspase-2 Activation

“…Chronic EtOH con- sumption would induce caspase-2-mediated apoptosis in aged animals (64). Mitochondrial dysfunction in apoptotic signaling after exposure to EtOH has been specifically addressed in the context of apoptosis in the corneal fibroblasts as well as in the corneal epithelium (2,29). In agreement with previous observations, our results also demonstrate that corneal fibroblasts engage the intrinsic pathway of apoptosis.…”

“…It has been known that ethanol (EtOH) may induce apoptosis, programming cell death in a variety of tissues, including the corneal epithelial cells (1,2), corneal fibroblasts (3), liver (4), and brain (5). In ophthalmology, it is one of the methods used in the removal of the epithelium during the procedures of refractive surgery, such as photorefractive surgery (PRK) and laser subepithelial keratomileusis (LASEK) (6,7).…”

γδ T Cells Are Necessary for Platelet and Neutrophil Accumulation in Limbal Vessels and Efficient Epithelial Repair after Corneal Abrasion

“…46 There is evidence for anti-inflammatory activity through the production and release of thymosin-␤4, 40 of possible interest in the cornea given published data for an anti-inflammatory and beneficial wound-healing effect of thymosin-␤4 in the cornea. 48,49 The finding that ICAM-1 Ϫ/Ϫ mice exhibited reduced accumulation of ␥␦ T cells and delayed, abbreviated epithelial basal cell division remains to be explained, especially because the CD11a Ϫ/Ϫ mice were not significantly different from wild type. ICAM-1 is known to be a dominant ligand for CD11a/CD18 (LFA-1), but in this specific inflammatory condition, it seems to be functioning in some other capacity.…”

Expression of thymosin β4 in odontoblasts during mouse tooth development

“…Treatment with Tβ4 accelerates wound-healing in mouse skin and inhibits apoptosis by inducing an increase in Bcl-2 expression and reducing caspase activity (8,9). Tβ4 promotes the migration and differentiation of hair follicle stem cells, stimulates endothelial cell differentiation during vessel formation.…”