Cigarette smoke-exposed microparticles released from T lymphocytes contribute to autophagy and apoptosis dysfunction in pulmonary microvascular endothelial cells

Abstract

Cigarette smoke can cause dysfunction of the vascular endothelium; however, the underlying mechanisms have not been fully elucidated. We hypothesized that T lymphocyte-derived microparticles (TLMPs) are involved in cigarette-related diseases, especially those involving the vascular endothelium. The effect of cigarette smoke on the release of microparticles from human lymphocytes was investigated. The contributions of TLMPs induced by cigarette smoke to endothelial proliferation/apoptosis, autophagy and cytokine levels were also measured. Notably, the potential mechanism of autophagy and apoptosis dysfunction in endothelial cells was further examined. Cigarette smoke promoted the release of microparticles from T lymphocytes. TLMPs attenuated endothelial proliferation but promoted endothelial apoptosis/autophagy and the expression of proinflammatory cytokines, especially when T lymphocytes were preexposed to cigarette smoke. The potential mechanism may involve disorders of oxidative stress and STAT3 phosphorylation. In conclusion, cigarette smoke-exposed microparticles released from T lymphocytes contribute to autophagy and apoptosis dysfunction in pulmonary microvascular endothelial cells.