Resistin-like molecule β (RELMβ) secreted by macrophages promotes epithelial-mesenchymal transition of alveolar epithelial cells in diabetic lungs

Abstract

Abstract Aims: To explore the characteristics of diabetic lung injury and the role of resistin-like molecule β (RELMβ). Methods: The experimental diabetic mice were established by intraperitoneal injection of streptozotocin (STZ), the lung function, tissue structure and protein expression levels of the mice were observed. The role of RELMβ on the epithelial to mesenchymal transition (EMT) in A549 cells exposed to high glucose was explored. Results: The function and structure of the diabetic lungs were significantly impaired, with extensive collagen fibers and macrophages deposited in the alveolar septum, with declined expression of epithelial marker (E-cadherin) and increased expression of mesenchymal markers (α-SMA and Vimentin) and RELMβ. The expression and secretion of RELMβ in macrophages were stimulated by high glucose, and the EMT level in A549 cells was up-regulated by recombinant human RELMβ or co-culture with macrophages. Conclusions: Diabetic mice showed declined lung function and increased fibrotic changes in lung tissues. Macrophages exposed to high glucose can promote the EMT progression in A549 cells via secreting RELMβ.