Overexpression of the steroidogenic acute regulatory protein increases the expression of ATP-binding cassette transporters in microvascular endothelial cells (bEnd.3).

Objective: To determine the effect of steroidogenic acute regulatory protein (StAR) overexpression on the levels of adenosine triphosphate (ATP)-binding cassette transporter A1 (ABCA1) and ATP-binding cassette transporter G1 (ABCG1) in an endothelial cell line (bEnd.3).

Methods: The StAR gene was induced in bEnd.

[Cardiac mast cells accumulation and degranulation contribute to collagen deposition after coronary microembolization].

Objective: To investigate potential pathophysiological role of cardiac mast cells accumulation and degranulation on the collagen deposition after coronary microembolization (CME).

Methods: CME was induced in miniswine by selective infusion of 15X10(4) microspheres (diameter, 45 mum) into the left anterior descending artery groups (CME group, n=8). Some CME-induced animals were pretreated with the MC stabilizer tranilast (50 mg/kg, twice daily), beginning 2 weeks before CME and thereafter throughout the experimental period (CME +tranilast group, n=8), while some animals received tranilast without CME (tranilast group, n=8).

Tranilast stabilizes the accumulation and degranulation of resident mast cells while reducing cardiomyocyte apoptosis in a swine model of coronary microembolisation.

1. Coronary microembolisation (CME) is associated with progressive myocardial dysfunction, and mast cells (MC) might have an important role in myocardial apoptosis after CME. We investigated whether the MC stabilizer tranilast suppresses the accumulation and degranulation of MC while reducing cardiomyocyte apoptosis after CME.

Effects of RNA interference-induced tryptase down-regulation in P815 cells on IL-6 and TNF-alpha release of endothelial cells.

Objective: To explore the effects of down-regulated tryptase expression in mast cells on the synthesis and release of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) of vascular endothelial cells.

Methods: Tryptase-siRNA (small-interfering RNA) vector was constructed to inhibit tryptase expression in P815 cells. The medium of P815 cells treated by the tryptase-siRNA (RNAi-P815 group) or pure vector (P815 group) was collected and used to culture bEnd.

The reinforcement of invasion in epithelial ovarian cancer cells by 17 beta-Estradiol is associated with up-regulation of Snail.

Objective: The transcription factor Snail, which is implicated in the triggering of epithelial-mesenchymal transitions (EMT), plays an important role in adhesion, invasion and metastasis of tumor cells. In the present study, we assessed 17beta-Estradiol (E2)'s effect on Snail, E-cadherin and MMP-2 expression of epithelial ovarian cancer cell line ES-2 and SKOV3. Then we induced Snail gene silencing by RNA interference to explore the effect of E2 on E-cadherin and MMP-2 expression when Snail gene expression was blocked.

Up regulation of interleukin-8 expressions induced by mast cell tryptase via protease activated receptor-2 in endothelial cell line.

Background: Protease activated receptor-2 is cleaved and activated by trypsin or mast cell tryptase and may play an important role in inflammation. However, it is unknown whether PAR-2 can mediate tryptase-induced inflammatory reaction. This study was conduct to investigate whether PAR-2 could be the activated by mast cell tryptase and medicated the tryptase induced interleukin-8 expression in endothelial cells.

[Primary study of vasculogenic mimicry induced by hypoxia in epithelial ovarian carcinoma].

Objective: To explore possibility of vasculogenic mimicry induced by hypoxia and the inhibitive effect by sirolimus in epithelial ovarian carcinoma in vitro.

Methods: Based on three-dimensional cell culture system developed by Matrigel, ovarian cell lines SKOV3 and ES2 were induced under conditions of hypoxia, hypoxia added with sirolimus and no-hypoxia, respectively. Potential formation of tumor channels and their characterization of network were observed by light microscopy and scanning electronic microscopy.