Transforming growth factor‐β blocks glucose‐induced inflammation and apoptosis in corneal epithelial cells

Abstract

Diabetic retinopathy is the most important ocular complication associated with diabetes. Corneal defects due to diabetes mellitus ( DM ) may cause severe vision impairments. This study aimed to identify the effect of transforming growth factor‐β ( TGF ‐β) on biological events, such as apoptosis and inflammation, in the diabetic cornea. High‐glucose treatment induced reactive oxygen species ( ROS ) production and several biological events, including apoptosis and inflammatory cytokine secretion, in human corneal epithelial cells. However, administration of TGF ‐β significantly decreased ROS production, Annexin V‐positive cells, and levels of inflammatory cytokines. Sprague Dawley rats were injected with streptozotocin (STZ) as a model of DM . Inflammatory cytokine secretion, apoptosis, and inflammation were all increased by STZ treatment. However, apoptosis and inflammation were markedly reduced following TGF ‐β treatment. In conclusion, TGF ‐β can ameliorate the enhancement of apoptosis and inflammation in diabetic cornea in in vivo and in vitro .

The role of the PI3K/AKT signalling pathway in the corneal epithelium: recent updates

“…Diabetes-associated hyperglycaemia stimulates apoptosis and inflammation but inhibits migration and tight junctions in CECs, thus causing DK [ 20 ].…”

“…The PI3K/AKT signalling pathway plays an important role in the biological responses of CECs [ 16 – 19 ]. Importantly, dysregulation of CE homeostasis caused by impaired CEC responses is associated with many corneal diseases, such as DK, DED, and keratitis [ 18 , 20 , 21 ]. Therefore, an in-depth understanding of the pathophysiology of CE with a focus on the PI3K/AKT signalling pathway is important for maintaining the integrity of patients’ corneas and seeking reliable treatments and new drugs [ 22 , 23 ].…”

Uric Acid Promotes Diabetic Retinopathy Progression through Transforming Growth Factor β2(TGF-β2) Signaling and Beneficial Effects of Fenofibrate

“…1B). There was evidence that TGF-β can ameliorate the apoptosis in corneal epithelial cells cultured in high glucose (14). Next, to investigate the link between TGF-β2, a polypeptide member of TGF-β superfamily, and HRECs apoptosis in high glucose mixed high uric acid, we incubated HRECs with high glucose, high uric acid and high glucose mixed high uric acid seperately and analyzed each expression of TGF-β2 and smad2/3, mediators of intracellular signaling, at protein and mRNA levels.…”

β‐Hydroxybutyrate exacerbates lipopolysaccharide/d‐galactosamine‐induced inflammatory response and hepatocyte apoptosis in mice

“…Recently, the upregulation of NADPH oxidase 4 has been suggested to be responsible to the oxidative stress in BHB‐treated endothelial cells and hepatocytes . In addition to direct tissue injury, ROS also functions as a crucial regulator in inflammation and apoptosis . Therefore, the induction of ROS might mediate the proinflammatory and proapoptotic activities of BHB.…”