Upregulation of TRPM7 augments cell proliferation and interleukin-8 release in airway smooth muscle cells of rats exposed to cigarette smoke.

Proliferation and synthetic function (i.e. the capacity to release numerous chemokines and cytokines) of airway smooth muscle cells (ASMCs) are important in airway remodeling induced by cigarette smoke exposure. However, the molecular mechanism has not been clarified. Transient receptor potential cation channel subfamily M member 7 (TRPM7) is expressed ubiquitously and is crucial for the cellular physiological function of many cell types. The present study aimed to detect the expression of TRPM7 in ASMCs from smoke­exposed rats and determine the importance of TRPM7 in proliferation and interleukin­8 (IL­8) release. ASMCs were isolated and cultured from smoke­exposed rats. Expression levels of TRPM7 were determined by reverse transcription­polymerase chain reaction, western blot analysis and immunofluorescence. TRPM7 was silenced with TRPM7­short hairpin RNA lentivirus vector. DNA synthesis, cell number and IL­8 release of ASMCs induced by cigarette smoke extract (CSE) and tumor necrosis factor­α (TNF­α) were assessed using [3H]-thymidine incorporation assay, hemocytometer and enzyme­linked immunosorbent assay, respectively. It was determined that mRNA and protein expression levels of TRPM7 were increased in ASMCs from smoke­exposed rats. Stimulation with CSE or TNF­α elevated DNA synthesis, cell number and IL­8 release were more marked in ASMCs from smoke­exposed rats. Silencing of TRPM7 reduced DNA synthesis, cell number and IL­8 release induced by CSE or TNF­α in ASMCs from smoke-exposed rats. In conclusion, expression of TRPM7 increased significantly in ASMCs from smoke­exposed rats and the upregulation of TRPM7 led to augmented cell proliferation and IL-8 release in ASMCs from rats exposed to cigarette smoke.