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Volume 29 Issue 4
August 2014
    Citation: Meiwan Cao, Min Yang, Zhiying Ou, Dingyou Li, Lanlan Geng, Peiyu Chen, Huan Chen, Sitang Gong. Involvement of aquaporins in a mouse model of rotavirus diarrhea .VIROLOGICA SINICA, 2014, 29(4) : 211-217.  http://dx.doi.org/10.1007/s12250-014-3469-z
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    Involvement of aquaporins in a mouse model of rotavirus diarrhea

    • 1.

      Department of Gastroenterology, Guangzhou Women and Children's Medical Center, Guangzhou 510623, China

    • 2.

      Department of Gastroenterology, Children's Mercy Hospital, University of Missouri Kansas City School of Medicine, 2401 Gillham Road, Kansas 64108, USA

    • Corresponding author: Sitang Gong, sitangg@126.com
    • Received Date: 05 May 2014
      Accepted Date: 18 July 2014
      Published Date: 30 July 2014
      Available online: 01 August 2014
    • Rotavirus diarrhea is a major worldwide cause of infantile gastroenteritis; however, the mechanism responsible for intestinal fluid loss remains unclear. Water transfer across the intestinal epithelial membrane seems to occur because of aquaporins (AQPs). Accumulating evidence indicates that alterations in AQPs may play an important role in pathogenesis. Here, we focus on changes in AQPs in a mouse model of rotavirus diarrhea. In the present study, 32 of 35 mice developed diarrhea and mild dehydration within 24 hours after infection with rotavirus strain SA11. Intestinal epithelial cells demonstrated cytoplasmic vacuolation, malaligned villi, and atrophy. AQP1 expression was significantly attenuated in the ileum and colon in comparison with controls; likewise, AQP4 and-8 protein expression were significantly decreased in the colon of rotavirus diarrhea-infected mice. In contrast, AQP3 protein expression was significantly increased in the colon of rotavirus-infected mice in comparison with controls. These results indicate that rotavirus diarrhea is associated with the downregulation of AQP1,-4, and-8 expression. Therefore, AQPs play an important role in rotavirus diarrhea.
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      2. Chen H, Gong S T, Ou W J. 2009. Expression of Aquaporins in Rotavirus Enteritis Treatment by Drug. Progr Modern Biomed.17: 3258-3261. (In Chinese)

      3. Guttman J A, Samji F N, Li Y, Deng W, Lin A, Finlay B B. 2007.Aquaporins contribute to diarrhoea caused by attaching and effacingbacterial pathogens. Cell Microbiol, 9: 131-141.
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      4. Hardin J A, Wallace L E, Wong J F, O'Loughlin E V, Urbanski SJ, Gall D G. 2004. Aquaporin expression is downregulated in a murine model of colitis and in patients with ulcerative colitis, Crohn's disease and infectious colitis, Crohn's disease and infectious colitis. Cell Tissue Res, 318:313-323.
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      5. Hodges K, Gill R. 2010. Infectious diarrhea: Cellular and molecular mechanisms. Gut Microbes, 1: 4-21.
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      6. Ikarashi N, Baba K, Ushiki T, Kon R, Mimura A, Toda T. 2011.The laxative effect of bisacodyl is attributable to decreased aquaporin-3 expression in the colon induced by increased PGE2 secretion from macrophages. Am J Physiol Gastrointest Liver Physiol, 301: G887-G895.
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      7. Ikarashi N, Ushiki T, Mochizuki T, Toda T, Kudo T, Baba K. 2011.Effects of magnesium sulphate administration on aquaporin 3 in rat gastrointestinal tract. Biol Pharm Bull, 34: 238-242.
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      8. Ishihara E, Nagahama M, Naruse S, Semba R, Miura T, Usami M.2008. Neuropathological alteration of aquaporin 1 immunoreactive enteric neurons in the streptozotocin-induced diabetic rats. Auton Neurosci, 138: 31-40.
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      9. King L S, Kozono D, Agre P. 2004. From structure to disease: the evolving tale of aquaporin biology. Nat Rev Mol Cell Biol, 5:687-698.
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      10. Knipping K, McNeal M M, Crienen A, van Amerongen G, GarssenJ, Van't Land B. 2011. A gastrointestinal rotavirus infectionmouse model for immune modulation studies. Virol J, 8: 109.
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      12. Laforenza U, Cova E, Gastaldi G, Tritto S, Grazioli M, LaRusso NF. 2005. Aquaporin-8 is involved in water transport in isolated superficial colonocytes from rat proximal colon. J Nutr, 135:2329-2336.

      13. Ma T, Jayaraman S, Wang K S, Song Y, Yang B, Li J. 2001.Defective dietary fat processing in transgenic mice lacking aquaporin-1 water channels. Am J Physiol Cell Physiol, 280:C126-C134.

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      Involvement of aquaporins in a mouse model of rotavirus diarrhea

        Corresponding author: Sitang Gong, sitangg@126.com
      • 1. Department of Gastroenterology, Guangzhou Women and Children's Medical Center, Guangzhou 510623, China
      • 2. Department of Gastroenterology, Children's Mercy Hospital, University of Missouri Kansas City School of Medicine, 2401 Gillham Road, Kansas 64108, USA
      • Received Date: 05 May 2014
      • Accepted Date: 18 July 2014
      • Published Date: 30 July 2014

      Abstract: Rotavirus diarrhea is a major worldwide cause of infantile gastroenteritis; however, the mechanism responsible for intestinal fluid loss remains unclear. Water transfer across the intestinal epithelial membrane seems to occur because of aquaporins (AQPs). Accumulating evidence indicates that alterations in AQPs may play an important role in pathogenesis. Here, we focus on changes in AQPs in a mouse model of rotavirus diarrhea. In the present study, 32 of 35 mice developed diarrhea and mild dehydration within 24 hours after infection with rotavirus strain SA11. Intestinal epithelial cells demonstrated cytoplasmic vacuolation, malaligned villi, and atrophy. AQP1 expression was significantly attenuated in the ileum and colon in comparison with controls; likewise, AQP4 and-8 protein expression were significantly decreased in the colon of rotavirus diarrhea-infected mice. In contrast, AQP3 protein expression was significantly increased in the colon of rotavirus-infected mice in comparison with controls. These results indicate that rotavirus diarrhea is associated with the downregulation of AQP1,-4, and-8 expression. Therefore, AQPs play an important role in rotavirus diarrhea.

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