Loss of lysosomal membrane protein NCU-G1 in mice results in spontaneous liver fibrosis with accumulation of lipofuscin and iron in Kupffer cells
Kong XY, Nesset CK, Damme M, Loeberg E-M, Lübke T, Maehlen J, Andersson KB, Roos N, Thoresen GH, Rustan AC, Kase ET, et al. (2014)
Disease Models & Mechanisms 7(3): 351-362.
Zeitschriftenaufsatz
| Veröffentlicht | Englisch
Autor*in
Kong, Xiang Yi;
Nesset, Cecilie K.;
Damme, MarkusUniBi;
Loeberg, Else-Marit;
Lübke, TorbenUniBi ;
Maehlen, Jan;
Andersson, Kristin B.;
Roos, Norbert;
Thoresen, G. Hege;
Rustan, Arild C.;
Kase, Eili T.;
Eskild, Winnie
Alle
Alle
Einrichtung
Abstract / Bemerkung
Human kidney predominant protein, NCU-G1, is a highly conserved protein with an unknown biological function. Initially described as a nuclear protein, it was later shown to be a bona fide lysosomal integral membrane protein. To gain insight into the physiological function of NCU-G1, mice with no detectable expression of this gene were created using a gene-trap strategy, and Ncu-g1gt/gt mice were successfully characterized. Lysosomal disorders are mainly caused by lack of or malfunctioning of proteins in the endosomal-lysosomal pathway. The clinical symptoms vary, but often include liver dysfunction. Persistent liver damage activates fibrogenesis and, if unremedied, eventually leads to liver fibrosis/cirrhosis and death. We demonstrate that the disruption of Ncu-g1 results in spontaneous liver fibrosis in mice as the predominant phenotype. Evidence for an increased rate of hepatic cell death, oxidative stress and active fibrogenesis were detected in Ncu-g1gt/gt liver. In addition to collagen deposition, microscopic examination of liver sections revealed accumulation of autofluorescent lipofuscin and iron in Ncu-g1gt/gt Kupffer cells. Because only a few transgenic mouse models have been identified with chronic liver injury and spontaneous liver fibrosis development, we propose that the Ncu-g1gt/gt mouse could be a valuable new tool in the development of novel treatments for the attenuation of fibrosis due to chronic liver damage.
Stichworte
NCU-G1;
Fibrosis;
Lysosome
Erscheinungsjahr
2014
Zeitschriftentitel
Disease Models & Mechanisms
Band
7
Ausgabe
3
Seite(n)
351-362
ISSN
1754-8403
eISSN
1754-8411
Page URI
https://pub.uni-bielefeld.de/record/2658538
Zitieren
Kong XY, Nesset CK, Damme M, et al. Loss of lysosomal membrane protein NCU-G1 in mice results in spontaneous liver fibrosis with accumulation of lipofuscin and iron in Kupffer cells. Disease Models & Mechanisms. 2014;7(3):351-362.
Kong, X. Y., Nesset, C. K., Damme, M., Loeberg, E. - M., Lübke, T., Maehlen, J., Andersson, K. B., et al. (2014). Loss of lysosomal membrane protein NCU-G1 in mice results in spontaneous liver fibrosis with accumulation of lipofuscin and iron in Kupffer cells. Disease Models & Mechanisms, 7(3), 351-362. doi:10.1242/dmm.014050
Kong, Xiang Yi, Nesset, Cecilie K., Damme, Markus, Loeberg, Else-Marit, Lübke, Torben, Maehlen, Jan, Andersson, Kristin B., et al. 2014. “Loss of lysosomal membrane protein NCU-G1 in mice results in spontaneous liver fibrosis with accumulation of lipofuscin and iron in Kupffer cells”. Disease Models & Mechanisms 7 (3): 351-362.
Kong, X. Y., Nesset, C. K., Damme, M., Loeberg, E. - M., Lübke, T., Maehlen, J., Andersson, K. B., Roos, N., Thoresen, G. H., Rustan, A. C., et al. (2014). Loss of lysosomal membrane protein NCU-G1 in mice results in spontaneous liver fibrosis with accumulation of lipofuscin and iron in Kupffer cells. Disease Models & Mechanisms 7, 351-362.
Kong, X.Y., et al., 2014. Loss of lysosomal membrane protein NCU-G1 in mice results in spontaneous liver fibrosis with accumulation of lipofuscin and iron in Kupffer cells. Disease Models & Mechanisms, 7(3), p 351-362.
X.Y. Kong, et al., “Loss of lysosomal membrane protein NCU-G1 in mice results in spontaneous liver fibrosis with accumulation of lipofuscin and iron in Kupffer cells”, Disease Models & Mechanisms, vol. 7, 2014, pp. 351-362.
Kong, X.Y., Nesset, C.K., Damme, M., Loeberg, E.-M., Lübke, T., Maehlen, J., Andersson, K.B., Roos, N., Thoresen, G.H., Rustan, A.C., Kase, E.T., Eskild, W.: Loss of lysosomal membrane protein NCU-G1 in mice results in spontaneous liver fibrosis with accumulation of lipofuscin and iron in Kupffer cells. Disease Models & Mechanisms. 7, 351-362 (2014).
Kong, Xiang Yi, Nesset, Cecilie K., Damme, Markus, Loeberg, Else-Marit, Lübke, Torben, Maehlen, Jan, Andersson, Kristin B., Roos, Norbert, Thoresen, G. Hege, Rustan, Arild C., Kase, Eili T., and Eskild, Winnie. “Loss of lysosomal membrane protein NCU-G1 in mice results in spontaneous liver fibrosis with accumulation of lipofuscin and iron in Kupffer cells”. Disease Models & Mechanisms 7.3 (2014): 351-362.
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