Dual Effects of Cigarette Smoke Extract on Proliferation of Endothelial Progenitor Cells and the Protective Effect of 5-aza-2′-deoxycytidine on EPCs against the Damage Caused by CSE

Abstract

Cigarette smoke is a major public health problem associated with multitude of diseases, including pulmonary and vascular diseases. Endothelial progenitor cells (EPCs) contribute to neovascularization and play an important role in the development of these diseases. The effect of CSE on EPCs is seldom studied. The aim of the current study is to observe the effect of CSE on biological behavior of EPCs and, further, to search for potential candidate agent in protection of proliferation of EPCs against the damage caused by CSE exposure in vitro. Methods. The proliferations of EPCs isolated from bone marrow of C57BL/6J mice were assessed by MTT after incubating the EPCs with a series of concentrations of CSE (1.0%, 2.5%, 5.0%, and 10.0%) for different times (3, 6, and 24 hours) as well as with 1.0% CSE in presence of 5-AZA-CdR for 24 hours. Results. The proliferations of EPCs were significantly enhanced after 3 hours of exposure to concentrations of 1.0% and 2.5% CSE but depressed when exposed to concentrations of 5.0% and 10.0% CSE. Furthermore, the 5-AZA-CdR in concentrations of 2.0 μmol/L and 5.0 μmol/L partly protected against the depression of proliferation of EPCs caused by CSE exposure. Conclusions. The CSE showed dual effects on proliferation of EPCs isolated from mice. The 5-AZA-CdR partly protected the proliferation of EPCs against the damage caused by CSE exposure in vitro, suggesting that DNA methylation may be involved in the dysfunction of EPCs induced by CSE.

Comparison between cigarette smoke-induced emphysema and cigarette smoke extract-induced emphysema

“…As the surrogate of CS, CSE could be considered to play the same role as CS in emphysema and COPD. CSE could decrease the function of endothelial progenitor cells (EPCs) [ 43 ], induce the apoptosis of pulmonary endothelial cells [ 44 ]. Intraperitoneal injection of CSE is a relatively new method of short-term modeling of emphysema, which was firstly reported by Taraseviciene-Stewart et al in 2007 [ 45 ].…”

Cigarette smoke extracts induced the colon cancer migration via regulating epithelial mesenchymal transition and metastatic genes in human colon cancer cells

“…In another study with HT‐29 cells, nicotine induced the production of mitochondrial reactive oxygen species (mROS) associated with a disruption of the mitochondrial membrane potential and endoplasmic reticulum (ER) stress, and thus nicotine caused apoptosis mediated by caspase‐3 activation in this study (Pelissier‐Rota et al, ). As shown in the previous studies, cigarette smoking has often contrary dual effects on cellular proliferation or damage (He et al, ). Therefore, in the relation with the effect of CSEs on cell proliferation, we conducted Western blot analysis to determine the expression levels of the cell cycle‐related proteins, p21, cyclin D1, p27, and cyclin E1, in SW‐620 cells.…”

5-Aza-2'-deoxycytidine protects against emphysema in mice via suppressing p16^Ink4a expression in lung tissue

“… 8 – 10 EPC function is decreased after chronic stimulation by CSE. 42 Peripheral infusion of rat bone marrow-derived EPCs is helpful in vascular repair and damage-healing processes by homing in on impaired locations. 43 Autologous transplantation of circulating EPCs effectively attenuates acute lung injury by direct endothelial repair and indirect immunomodulation.…”