Université de Fribourg

Arginase-II activates mTORC1 through myosin-1b in vascular cell senescence and apoptosis

Yu, Yi ; Xiong, Yuyan ; Montani, Jean-Pierre ; Yang, Zhihong ; Ming, Xiu-Fen

In: Cell Death & Disease, 2018, vol. 9, no. 3, p. 313

Type-II L-arginine:ureahydrolase, arginase-II (Arg-II), is shown to activate mechanistic target of rapamycin complex 1 (mTORC1) pathway and contributes to cell senescence and apoptosis. In an attempt to elucidate the underlying mechanism, we identified myosin-1b (Myo1b) as a mediator. Overexpression of Arg-II induces re-distribution of lysosome and mTOR but not of tuberous sclerosis complex...

Université de Fribourg

"En Face" detection of nitric oxide and superoxide in endothelial layer of intact arteries

Yu, Yi ; Xiong, Yuyan ; Montani, Jean-Pierre ; Yang, Zhihong ; Ming, Xiu-Fen

In: Journal of Visualized Experiments, 2016, no. 108, p. -

Endothelium-derived nitric oxide (NO) produced from endothelial NO-synthase (eNOS) is one of the most important vasoprotective molecules in cardiovascular physiology. Dysfunctional eNOS such as uncoupling of eNOS leads to decrease in NO bioavailability and increase in superoxide anion (O₂.−) production, and in turn promotes cardiovascular diseases. Therefore, appropriate...

Université de Fribourg

P38 mitogen-activated protein kinase is involved in arginase-II-mediated eNOS-Uncoupling in Obesity

Yu, Yi ; Rajapakse, Angana G. ; Montani, Jean-Pierre ; Yang, Zhihong ; Ming, Xiu-Fen

In: Cardiovascular Diabetology, 2014, vol. 13, no. 1, p. 113

Background Endothelial nitric oxide synthase (eNOS)-uncoupling links obesity-associated insulin resistance and type-II diabetes to the increased incidence of cardiovascular disease. Studies have indicated that increased arginase is involved in eNOS-uncoupling through competing with the substrate L-arginine. Given that arginase-II (Arg-II) exerts some of its biological functions through crosstalk...

Université de Fribourg

Arginase‐II induces vascular smooth muscle cell senescence and apoptosis through p66Shc and p53 independently of its l‐arginine ureahydrolase activity: implications for atherosclerotic plaque vulnerability

Xiong, Yuyan ; Yu, Yi ; Montani, Jean‐Pierre ; Yang, Zhihong ; Ming, Xiu‐Fen

In: Journal of the American Heart Association, 2013, vol. 2, no. 4, p. e000096

Background Vascular smooth muscle cell (VSMC) senescence and apoptosis are involved in atherosclerotic plaque vulnerability. Arginase‐II (Arg‐II) has been shown to promote vascular dysfunction and plaque vulnerability phenotypes in mice through uncoupling of endothelial nitric oxide synthase and activation of macrophage inflammation. The function of Arg‐II in VSMCs with respect to plaque...