17β-Hydroxysteroid Dehydrogenase Type 2 Expression Is Induced by Androgen Signaling in Endometrial Cancer.

Endometrial cancer is one of the most common female pelvic cancers and has been considered an androgen-related malignancy. Several studies have demonstrated the anti-cell proliferative effect of androgen on endometrial cancer cells; however, the mechanisms of the anti-cancer effect of androgen remain largely unclear. 17β-hydroxysteroid dehydrogenase type 2 (17β-HSD2), which catalyzes the conversion of E2 to E1, is known to be upregulated by androgen treatment in breast cancer cells.

The role of 5α-reductase type 1 associated with intratumoral dihydrotestosterone concentrations in human endometrial carcinoma.

Endometrial carcinoma, especially endometrioid endometrial adenocarcinoma, is an estrogen-dependent tumor that is similar to breast cancer. Androgen is closely associated with other steroid hormones, but its correlation with endometrioid endometrial adenocarcinoma remains largely unclear. We previously demonstrated the expression of the androgen receptor, 5α-reductase type 1, and 5α-reductase type 2 in endometrioid endometrial adenocarcinoma tissue, but androgen action and its correlation with prognosis are unknown.

Ezetimibe improves endothelial function and inhibits Rho-kinase activity associated with inhibition of cholesterol absorption in humans.

Background: Ezetimibe is an inhibitor of cholesterol absorption in the intestine. We examined whether ezetimibe improves endothelial function, and if so, what mechanisms are involved.

Methods And Results: Nineteen healthy subjects (male/female 14/5; mean age, 31±3 [SD] years-old) were randomized to receive ezetimibe (10mg/day) or pravastatin (10mg/day) for 4 weeks in a cross-over manner with a 4-week washout interval.

Enhanced pulsatile pressure accelerates vascular smooth muscle migration: implications for atherogenesis of hypertension.

Aims: Clinical studies have suggested that pulsatile pressure is an independent risk factor for atherosclerosis. However, it is unknown whether enhanced pulsatile pressure per se directly accelerates vascular smooth muscle cell (VSMC) migration, an important process of atherosclerosis.

Methods And Results: Using our original Pressure-loading system with a Boyden chamber, we examined the direct effects of variable pressures and pulse rates on migration of rat aortic VSMCs in vitro.

Increased static pressure promotes migration of vascular smooth muscle cells: involvement of the Rho-kinase pathway.

Vascular smooth muscle cell (VSMC) migration plays a pivotal role in the pathogenesis of arteriosclerosis, under influences of various mechanical factors. Thus, we examined whether static pressure promotes VSMC migration and if so, whether Rho-kinase is involved. Rat VSMCs were cultured on chambers coated on fibronectin, vitronectin, laminin, or type IV collagen, under pressure-free conditions and at 90 and 180 mm Hg.