Unexpected functional consequences of xenogeneic transgene expression in β-cells of NOD mice

Diabetes, Obesity and Metabolism

Volumn 9, Issue SUPPL. 2, 2007, Pages 14-22

  Leiter, Edward H ^a   Reifsnyder, P ^a   Driver, J ^a   Kamdar, S ^a   Choisy Rossi, C ^a   Serreze, D V ^a   Hara, M ^b   Chervonsky, A ^b  

^a JACKSON LABORATORY   (United States)

^b UNIVERSITY OF CHICAGO   (United States)

Author keywords

Cre recombinase; Diabetes; Green flourescent protein; NOD mice; Transgenes; Cells

Indexed keywords

CRE RECOMBINASE; GREEN FLUORESCENT PROTEIN; INSULIN; OXIDIZED LOW DENSITY LIPOPROTEIN RECEPTOR; OXIDIZED LOW DENSITY LIPOPROTEIN RECEPTOR P; UNCLASSIFIED DRUG;

BACTERIOPHAGE P1; CONFERENCE PAPER; GENE EXPRESSION; HISTOPATHOLOGY; HOMOZYGOSITY; IMPAIRED GLUCOSE TOLERANCE; INSULIN BLOOD LEVEL; INSULIN DEPENDENT DIABETES MELLITUS; INSULITIS; JUVENILE DIABETES MELLITUS; NONHUMAN; NONOBESE DIABETIC MOUSE; PANCREAS ISLET BETA CELL; PERINATAL PERIOD; PROMOTER REGION; PROTEIN EXPRESSION; TRANSGENIC MOUSE;

EID: 35148866180     PISSN: 14628902     EISSN: 14631326     Source Type: Journal    
DOI: 10.1111/j.1463-1326.2007.00770.x     Document Type: Conference Paper

References (24)

1. Lee JY, Ristow M, Lin X et al. RIP-Cre revisited, evidence for impairments of pancreatic β-cell function. J Biol Chem 2006; 281: 2649-2653.
2. Magnuson M, Burlison J. Caveats and considerations for performing pancreas-specific gene manipulations in the mouse. Diabetes Obes Metab 2007; 9 (Suppl. 2): 5-13.
3. Efrat S, Fleischer N, Hanahan D. Diabetes induced in male transgenic mice by expression of human H-ras oncoprotein in pancreatic β cells. Mol Cell Biol 1990; 10: 1779-1783.
4. Pujol-Borrell R, Bottazzo GF. Puzzling diabetic transgenic mice. Immunol Today 1988; 9: 303-306.
5. Epstein PN, Ribar TJ, Decker GL et al. Elevated β-cell calmodulin produces a unique insulin secretory defect in transgenic mice. Endocrinology 1992; 130: 1387-1393.
6. Martin L, Keller GA, Liggitt D et al. Male-specific β-cell dysfunction and diabetes resulting from increased expression of a syngeneic MHC class I protein in the pancreata of transgenic mice. New Biol 1990; 2: 1101-1110.
7. Allison J, Campbell IL, Morahan G et al. Diabetes in transgenic mice resulting from over-expression of class I histocompatibility molecules in pancreatic β cells. Nature 1988; 333: 529-533.
8. Allison J, Malcolm L, Culvenor J et al. Overexpression of β2-microglobulin in transgenic mouse islet β cells results in defective insulin secretion. Proc Natl Acad Sci U S A 1991; 88: 2070-2074.
9. Leiter EH. Nonobese diabetic mice and the genetics of diabetes susceptibility. Curr Diab Rep 2005; 5: 141-148.
10. Atkinson MA, Leiter EH. The NOD mouse model of type 1 diabetes: As good as it gets? Nat Med 1999; 5: 601-604.
11. Serreze DV, Leiter EH. Genes and cellular requirements for autoimmune diabetes susceptibility in nonobese diabetic mice. Curr Dir Autoimmun 2001; 4: 31-67.
12. Moriyama H, Abiru N, Paronen J et al. Evidence for a primary islet autoantigen (preproinsulin 1) for insulitis and diabetes in the nonobese diabetic mouse. Proc Natl Acad Sci U S A 2003; 100: 10376-10381.
13. Thebault-Baumont K, Dubois-Laforgue D, Krief P et al. Acceleration of type 1 diabetes mellitus in proinsulin 2-deficient NOD mice. J Clin Invest 2003; 111: 851-857.
14. Pugliese A. The insulin gene in type 1 diabetes. IUBMB Life 2005; 57: 463-468.
15. Hara M, Wang X, Kawamura T et al. Transgenic mice with green fluorescent protein-labeled pancreatic β-cells. Am J Physiol Endocrinol Metab 2003; 284: E177-E183.
16. Chen J, Chen YG, Reifsnyder PC et al. Targeted disruption of CD38 accelerates autoimmune diabetes in NOD/Lt mice by enhancing autoimmunity in an ADP-ribosyltransferase 2-dependent fashion. J Immunol 2006; 176: 4590-4599.
17. DiLorenzo TP, Lieberman SM, Takaki T et al. During the early prediabetic period in NOD mice, the pathogenic CD8(+) T-cell population comprises multiple antigenic specificities. Clin Immunol 2002; 105: 332-341.
18. Verdaguer J, Schmidt D, Averill N et al. Spontaneous autoimmune diabetes in monoclonal T-cell nonobese diabetic mice. J Exp Med 1997; 186: 1663-1676.
19. Leiter EH. Mice with targeted gene disruptions or gene insertions for diabetes research: Problems, pitfalls, and potential solutions. Diabetologia 2002; 45: 296-308.
20. Larger E, Becourt C, Bach JF et al. Pancreatic islet β cells drive T cell-immune responses in the nonobese diabetic mouse model. J Exp Med 1995; 181: 1635-1642.
21. Jansen A, Rosmalen JGM, Homodelarche F et al. Effect of prophylactic insulin treatment on the number of ER-MP23(+) macrophages in the pancreas of NOD mice. Is the prevention of diabetes based on β-cell rest? J Autoimmun 1996; 9: 341-348.
22. Schmidt EE, Taylor DS, Prigge JR et al. Illegitimate Cre-dependent chromosome rearrangements in transgenic mouse spermatids. Proc Natl Acad Sci U S A 2000; 97: 13702-13707.
23. Loonstra A, Vooijs M, Beverloo HB et al. Growth inhibition and DNA damage induced by Cre recombinase in mammalian cells. Proc Natl Acad Sci U S A 2001; 98: 9209-9214.
24. Semprini S, Troup TJ, Kotelevtseva N et al. Cryptic loxP sites in mammalian genomes: Genome-wide distribution and relevance for the efficiency of BAC/PAC recombineering techniques. Nucleic Acids Res 2007; 35: 1402-1410.