Increased STIM1 expression induced by cigarette smoking extracts regulates the proliferation and production of inflammatory cytokines in human airway smooth muscle cells

Cigarette smoking extracts (CSE) induces increased proliferation and production of inflammatory cytokines in human airway smooth muscle cells (hASMCs), which might contribute to the airway remolding in COPD. However, the underlying mechanism is not fully addressed. Stromal Interaction Molecule 1 (STIM1) mediates Store-operated Calcium Entry (SOCE) to sustain the calcium levels of Sarcoplasmic Reticulum (SR) in hASMCs. To investigate whether CSE regulates the STIM1 expression in hASMCs, and its effects on the proliferative and secretory ability of hASMCs, hASMCs were incubated with siRNA targeting STIM1 with or without stimulation of CSE (varied from 0.25% to 4%); the relative expression of STIM1, PCNA, IL-6, IL-8, TNF-alpha and fibronectin were determined by qPCR, the proliferation of hASMCs were assessed by CCK8 assay. We observed increased expression of STIM1, PCNA, IL-6, IL-8 and TNF-alpha, as well as increased proliferation in the hASMCs treated with CSE, whereas the fibronectin expression in hASMCs was not affected by CSE; the decrease of STIM1 expression by siRNA reduced the IL-6, IL-8, TNF-alpha production and the proliferation of hASMCs excited by CSE (P This study was supported by NSFC funds NO. 81800015 and 81670038.