The role of nitric oxide pathway in arginine transport and growth of IPEC-1 cells
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Hao Xiao1,2, Liming Zeng1,3, Fangyuan Shao4, Bo Huang1,2, Miaomiao Wu5, Bie Tan1, Yulong Yin1,6,7
1National Engineering Laboratory for Pollution Control and Waste Utilization in Livestock and Poultry Production, Key Laboratory of Agro-ecological Processes in Subtropical Region, Institute of Subtropical Agriculture, Chinese Academy of Sciences, Changsha, China
2University of the Chinese Academy of Sciences, Beijing, China
3Science College of Jiangxi Agricultural University, Nanchang, China
4Faculty of Health Sciences, University of Macau, Macau SAR, China
5Diagnostic Medicine/Pathobiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS, USA
6Laboratory of Animal Nutrition and Human Health, School of Biology, Hunan Normal University, Changsha, China
7College of Animal Science, South China Agricultural University, Guangzhou, China
Bie Tan, email: firstname.lastname@example.org
Yulong Yin, email: email@example.com
Keywords: arginine, nitric oxide synthase, mTOR, intestinal porcine epithelial cells (IPEC)
Received: December 12, 2016 Accepted: March 08, 2017 Published: March 16, 2017
L-Arginine itself and its metabolite-nitric oxide play great roles in intestinal physiology. However, the molecular mechanism underlying nitric oxide pathway regulating L-Arginine transport and cell growth is not yet fully understood. We report that inhibition of nitric oxide synthase (NOS) significantly induced cell apoptosis (p < 0.05), and promoted the rate of Arginine uptake and the expressions of protein for CAT-2 and y+LAT-1 (p < 0.05), while reduced protein expression of CAT-1. And NOS inhibition markedly decreased the activation of mammalian target of rapamycin (mTOR) and PI3K-Akt pathways by Arginine in the IPEC-1 cells (p < 0.05). Taken together, these data suggest that inhibition of NO pathway by L-NAME induces a negative feedback increasing of Arginine uptake and CAT-2 and y+LAT-1 protein expression, but promotes cell apoptosis which involved inhibiting the activation of mTOR and PI3K-Akt pathways.
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