Propofol Affects Non-Small-Cell Lung Cancer Cell Biology By Regulating the miR-21/PTEN/AKT Pathway In Vitro and In Vivo.

Background: Propofol is a common sedative-hypnotic drug traditionally used for inducing and maintaining general anesthesia. Recent studies have drawn attention to the nonanesthetic effects of propofol, but the potential mechanism by which propofol suppresses non-small-cell lung cancer (NSCLC) progression has not been fully elucidated.

Methods: For the in vitro experiments, we used propofol (0, 2, 5, and 10 µg/mL) to treat A549 cells for 1, 4, and 12 hours and Cell Counting Kit-8 (CCK-8) to detect proliferation.

Cigarette smoke extract inhibits the proliferation of alveolar epithelial cells and augments the expression of P21WAF1.

Cigarette smoking is intimately related with the development of chronic obstructive pulmonary diseases, and alveolar epithelium is a major target for the exposure of cigarette smoke extract. In order to investigate the effect of cigarette smoke extract on the proliferation of alveolar epithelial cell type II and its relationship with P21WAF1, the alveolar epithelial type II cell line (A549) cells were chosen as surrogate cells to represent alveolar epithelial type II cells. MTT assay was used to detect cell viability after interfered with different concentrations of cigarette smoke extract.

Angiotensin II directly triggers endothelial exocytosis via protein kinase C-dependent protein kinase D2 activation.

Angiotensin II (AII) has been reported to induce leukocyte adhesion to endothelium through up-regulation of P-selectin surface expression. However, the underlying molecular and cellular mechanisms remain unknown. P-selectin is stored in Weibel-Palade bodies (WPBs), large secretory granules, in endothelial cells.

Transdifferentiation of pulmonary arteriolar endothelial cells into smooth muscle-like cells regulated by myocardin involved in hypoxia-induced pulmonary vascular remodelling.

Myocardin gene has been identified as a master regulator of smooth muscle cell differentiation. Smooth muscle cells play a critical role in the pathogenesis of hypoxia-induced pulmonary hypertension (PH) and pulmonary vascular remodelling (PVR). The purpose of this study was to investigate the change of myocardin gene expression in the pulmonary vessels of hypoxia-induced PH affected by Sildenafil treatment and the involvement of endothelial cells transdifferentiation into smooth muscle cells in the process of hypoxia-induced PH and PVR.

[The role of myocardin in hypoxia-induced transdifferentiation of pulmonary artery endothelial cells into smooth muscle-like cells].

Objective: To investigate the transdifferentiation of pulmonary artery endothelial cells (PAECs) into smooth muscle-like cells under hypoxia and the role of myocardin therein.

Methods: Recombinant plasmid psimyocardin (pSi), capable of silencing the expression of myocardin gene, was constructed by RNAi to be used to transfect the PAECs. Endothelial cells of adult pig pulmonary small arteries were purified by immunomagnetic purification technique, and divided into 4 groups: normoxia group (to be cultured in normoxic cell culture box containing 21% O(2), 5% CO2, and 74% N(2)), normoxia + pSi group, hypoxia group (to be cultured in cell box containing 1% O(2), 5% CO2, and 74% N(2)), and hypoxia + pSi group to be cultured for 1, 4, and 7 days respectively.

[Effects of cigarette smoke extract on the proliferation and the expression of TGF-beta1 and EGF in human embryonic lung fibroblasts].

Objective: To observe the effects of cigarette smoke extract (CSE) on the proliferation and the expression of TGF-beta(1) and EGF in human embryonic lung fibroblasts (HELF).

Methods: The cultures of HELF were incubated with CSE (1:50, 1:25 and 1:10) for examining the effects of CSE on the proliferation and the proliferating cell nuclear antigen (PCNA) levels in HELF. The total RNA was extracted from the cells incubated with CSE at different doses.

[Changes of the actin and transforming growth factor-beta1 expression in the small airways of the rat with chronic obstructive lung disease].

Objective: To study the roles of actin and transforming growth factor (TGF)-beta(1) in the injury repair and the development of emphysema.

Methods: Wistar rats were randomly divided into two groups: the smoking and infection group (group SI) and the control group (group C). The rats of group SI received smoking irritation accompanying with repeated intranasal infection.