Genetic influences of the intercellular adhesion molecule 1 (ICAM-1) gene polymorphisms in development of Type 1 diabetes and diabetic nephropathy
Aim The intercellular adhesion molecule‐1 (ICAM‐1) gene is located on chromosome 19p13, which is linked to Type 1 diabetes (T1D). ICAM‐1 expression is related to development of T1D and diabetic nephropathy. The present study aims to evaluate the genetic influence of ICAM‐1 gene polymorphisms on the...
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| Published in | Diabetic medicine Vol. 23; no. 10; pp. 1093 - 1099 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford, UK
Blackwell Publishing Ltd
01.10.2006
Blackwell |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0742-3071 1464-5491 1464-5491 |
| DOI | 10.1111/j.1464-5491.2006.01948.x |
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| Abstract | Aim The intercellular adhesion molecule‐1 (ICAM‐1) gene is located on chromosome 19p13, which is linked to Type 1 diabetes (T1D). ICAM‐1 expression is related to development of T1D and diabetic nephropathy. The present study aims to evaluate the genetic influence of ICAM‐1 gene polymorphisms on the development of T1D and diabetic nephropathy.
Methods Five valid single nucleotide polymorphisms (SNPs) were genotyped in 432 T1D patients (196 patients had diabetic nephropathy) and 187 non‐diabetic control subjects by using dynamic allele‐specific hybridization (DASH) and pyrosequencing.
Results SNPs rs281432(C/G) and rs5498 E469K(A/G) had high heterozygous indexes. They were significantly associated with T1D [P = 0.026, OR = 1.644 (95% CI 1.138–2.376) and P < 0.001, OR = 2.456 (1.588–3.8)]. Frequencies of the C allele in SNP rs281432(C/G) and the A allele in SNP rs5498 E469K(A/G) increased stepwise from non‐diabetic control subjects to T1D patients without diabetic nephropathy and T1D patients with diabetic nephropathy. Further analysis for these two SNPs indicated that T1D patients had increased frequency of the common haplotype C‐A, in comparison with non‐diabetic control subjects (38.1 vs. 32.1%, P = 0.035).
Conclusion The present study provided evidence that SNPs rs281432(C/G) and rs5498 E469K(A/G) in the ICAM‐1 gene confer susceptibility to the development of T1D and might also be associated with diabetic nephropathy in Swedish Caucasians. |
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| AbstractList | Aim The intercellular adhesion molecule‐1 (ICAM‐1) gene is located on chromosome 19p13, which is linked to Type 1 diabetes (T1D). ICAM‐1 expression is related to development of T1D and diabetic nephropathy. The present study aims to evaluate the genetic influence of ICAM‐1 gene polymorphisms on the development of T1D and diabetic nephropathy.
Methods Five valid single nucleotide polymorphisms (SNPs) were genotyped in 432 T1D patients (196 patients had diabetic nephropathy) and 187 non‐diabetic control subjects by using dynamic allele‐specific hybridization (DASH) and pyrosequencing.
Results SNPs rs281432(C/G) and rs5498 E469K(A/G) had high heterozygous indexes. They were significantly associated with T1D [P = 0.026, OR = 1.644 (95% CI 1.138–2.376) and P < 0.001, OR = 2.456 (1.588–3.8)]. Frequencies of the C allele in SNP rs281432(C/G) and the A allele in SNP rs5498 E469K(A/G) increased stepwise from non‐diabetic control subjects to T1D patients without diabetic nephropathy and T1D patients with diabetic nephropathy. Further analysis for these two SNPs indicated that T1D patients had increased frequency of the common haplotype C‐A, in comparison with non‐diabetic control subjects (38.1 vs. 32.1%, P = 0.035).
Conclusion The present study provided evidence that SNPs rs281432(C/G) and rs5498 E469K(A/G) in the ICAM‐1 gene confer susceptibility to the development of T1D and might also be associated with diabetic nephropathy in Swedish Caucasians. The intercellular adhesion molecule-1 (ICAM-1) gene is located on chromosome 19p13, which is linked to Type 1 diabetes (T1D). ICAM-1 expression is related to development of T1D and diabetic nephropathy. The present study aims to evaluate the genetic influence of ICAM-1 gene polymorphisms on the development of T1D and diabetic nephropathy. Five valid single nucleotide polymorphisms (SNPs) were genotyped in 432 T1D patients (196 patients had diabetic nephropathy) and 187 non-diabetic control subjects by using dynamic allele-specific hybridization (DASH) and pyrosequencing. SNPs rs281432(C/G) and rs5498 E469K(A/G) had high heterozygous indexes. They were significantly associated with T1D [P = 0.026, OR = 1.644 (95% CI 1.138-2.376) and P < 0.001, OR = 2.456 (1.588-3.8)]. Frequencies of the C allele in SNP rs281432(C/G) and the A allele in SNP rs5498 E469K(A/G) increased stepwise from non-diabetic control subjects to T1D patients without diabetic nephropathy and T1D patients with diabetic nephropathy. Further analysis for these two SNPs indicated that T1D patients had increased frequency of the common haplotype C-A, in comparison with non-diabetic control subjects (38.1 vs. 32.1%, P = 0.035). The present study provided evidence that SNPs rs281432(C/G) and rs5498 E469K(A/G) in the ICAM-1 gene confer susceptibility to the development of T1D and might also be associated with diabetic nephropathy in Swedish Caucasians. AIM: The intercellular adhesion molecule-1 (ICAM-1) gene is located on chromosome 19p13, which is linked to Type 1 diabetes (T1D). ICAM-1 expression is related to development of T1D and diabetic nephropathy. The present study aims to evaluate the genetic influence of ICAM-1 gene polymorphisms on the development of T1D and diabetic nephropathy. METHODS: Five valid single nucleotide polymorphisms (SNPs) were genotyped in 432 T1D patients (196 patients had diabetic nephropathy) and 187 non-diabetic control subjects by using dynamic allele-specific hybridization (DASH) and pyrosequencing. RESULTS: SNPs rs281432(C/G) and rs5498 E469K(A/G) had high heterozygous indexes. They were significantly associated with T1D [P = 0.026, OR = 1.644 (95% CI 1.138-2.376) and P < 0.001, OR = 2.456 (1.588-3.8)]. Frequencies of the C allele in SNP rs281432(C/G) and the A allele in SNP rs5498 E469K(A/G) increased stepwise from non-diabetic control subjects to T1D patients without diabetic nephropathy and T1D patients with diabetic nephropathy. Further analysis for these two SNPs indicated that T1D patients had increased frequency of the common haplotype C-A, in comparison with non-diabetic control subjects (38.1 vs. 32.1%, P = 0.035). CONCLUSION: The present study provided evidence that SNPs rs281432(C/G) and rs5498 E469K(A/G) in the ICAM-1 gene confer susceptibility to the development of T1D and might also be associated with diabetic nephropathy in Swedish Caucasians. The intercellular adhesion molecule-1 (ICAM-1) gene is located on chromosome 19p13, which is linked to Type 1 diabetes (T1D). ICAM-1 expression is related to development of T1D and diabetic nephropathy. The present study aims to evaluate the genetic influence of ICAM-1 gene polymorphisms on the development of T1D and diabetic nephropathy.AIMThe intercellular adhesion molecule-1 (ICAM-1) gene is located on chromosome 19p13, which is linked to Type 1 diabetes (T1D). ICAM-1 expression is related to development of T1D and diabetic nephropathy. The present study aims to evaluate the genetic influence of ICAM-1 gene polymorphisms on the development of T1D and diabetic nephropathy.Five valid single nucleotide polymorphisms (SNPs) were genotyped in 432 T1D patients (196 patients had diabetic nephropathy) and 187 non-diabetic control subjects by using dynamic allele-specific hybridization (DASH) and pyrosequencing.METHODSFive valid single nucleotide polymorphisms (SNPs) were genotyped in 432 T1D patients (196 patients had diabetic nephropathy) and 187 non-diabetic control subjects by using dynamic allele-specific hybridization (DASH) and pyrosequencing.SNPs rs281432(C/G) and rs5498 E469K(A/G) had high heterozygous indexes. They were significantly associated with T1D [P = 0.026, OR = 1.644 (95% CI 1.138-2.376) and P < 0.001, OR = 2.456 (1.588-3.8)]. Frequencies of the C allele in SNP rs281432(C/G) and the A allele in SNP rs5498 E469K(A/G) increased stepwise from non-diabetic control subjects to T1D patients without diabetic nephropathy and T1D patients with diabetic nephropathy. Further analysis for these two SNPs indicated that T1D patients had increased frequency of the common haplotype C-A, in comparison with non-diabetic control subjects (38.1 vs. 32.1%, P = 0.035).RESULTSSNPs rs281432(C/G) and rs5498 E469K(A/G) had high heterozygous indexes. They were significantly associated with T1D [P = 0.026, OR = 1.644 (95% CI 1.138-2.376) and P < 0.001, OR = 2.456 (1.588-3.8)]. Frequencies of the C allele in SNP rs281432(C/G) and the A allele in SNP rs5498 E469K(A/G) increased stepwise from non-diabetic control subjects to T1D patients without diabetic nephropathy and T1D patients with diabetic nephropathy. Further analysis for these two SNPs indicated that T1D patients had increased frequency of the common haplotype C-A, in comparison with non-diabetic control subjects (38.1 vs. 32.1%, P = 0.035).The present study provided evidence that SNPs rs281432(C/G) and rs5498 E469K(A/G) in the ICAM-1 gene confer susceptibility to the development of T1D and might also be associated with diabetic nephropathy in Swedish Caucasians.CONCLUSIONThe present study provided evidence that SNPs rs281432(C/G) and rs5498 E469K(A/G) in the ICAM-1 gene confer susceptibility to the development of T1D and might also be associated with diabetic nephropathy in Swedish Caucasians. Aim The intercellular adhesion molecule‐1 (ICAM‐1) gene is located on chromosome 19p13, which is linked to Type 1 diabetes (T1D). ICAM‐1 expression is related to development of T1D and diabetic nephropathy. The present study aims to evaluate the genetic influence of ICAM‐1 gene polymorphisms on the development of T1D and diabetic nephropathy. Methods Five valid single nucleotide polymorphisms (SNPs) were genotyped in 432 T1D patients (196 patients had diabetic nephropathy) and 187 non‐diabetic control subjects by using dynamic allele‐specific hybridization (DASH) and pyrosequencing. Results SNPs rs281432(C/G) and rs5498 E469K(A/G) had high heterozygous indexes. They were significantly associated with T1D [ P = 0.026, OR = 1.644 (95% CI 1.138–2.376) and P < 0.001, OR = 2.456 (1.588–3.8)]. Frequencies of the C allele in SNP rs281432(C/G) and the A allele in SNP rs5498 E469K(A/G) increased stepwise from non‐diabetic control subjects to T1D patients without diabetic nephropathy and T1D patients with diabetic nephropathy. Further analysis for these two SNPs indicated that T1D patients had increased frequency of the common haplotype C‐A, in comparison with non‐diabetic control subjects (38.1 vs. 32.1%, P = 0.035). Conclusion The present study provided evidence that SNPs rs281432(C/G) and rs5498 E469K(A/G) in the ICAM‐1 gene confer susceptibility to the development of T1D and might also be associated with diabetic nephropathy in Swedish Caucasians. Aim: The intercellular adhesion molecule-1 (ICAM-1) gene is located on chromosome 19p13, which is linked to Type 1 diabetes (T1D). ICAM-1 expression is related to development of T1D and diabetic nephropathy. The present study aims to evaluate the genetic influence of ICAM-1 gene polymorphisms on the development of T1D and diabetic nephropathy. Methods: Five valid single nucleotide polymorphisms (SNPs) were genotyped in 432 T1D patients (196 patients had diabetic nephropathy) and 187 non-diabetic control subjects by using dynamic allele-specific hybridization (DASH) and pyrosequencing. Results: SNPs rs281432(C/G) and rs5498 E469K(A/G) had high heterozygous indexes. They were significantly associated with T1D [P = 0.026, OR = 1.644 (95% CI 1.138-2.376) and P < 0.001, OR = 2.456 (1.588-3.8)]. Frequencies of the C allele in SNP rs281432(C/G) and the A allele in SNP rs5498 E469K(A/G) increased stepwise from non-diabetic control subjects to T1D patients without diabetic nephropathy and T1D patients with diabetic nephropathy. Further analysis for these two SNPs indicated that T1D patients had increased frequency of the common haplotype C-A, in comparison with non-diabetic control subjects (38.1 vs. 32.1%, P = 0.035). Conclusion: The present study provided evidence that SNPs rs281432(C/G) and rs5498 E469K(A/G) in the ICAM-1 gene confer susceptibility to the development of T1D and might also be associated with diabetic nephropathy in Swedish Caucasians. |
| Author | Brismar, K. Dahlquist, G. Möllsten, A. Efendic, S. Prázny, M. Ma, J. Gu, H. F. Falhammar, H. |
| Author_xml | – sequence: 1 givenname: J. surname: Ma fullname: Ma, J. – sequence: 2 givenname: A. surname: Möllsten fullname: Möllsten, A. organization: Diabetes Center Karolinska (DCK), Department of Molecular Medicine and Surgery, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden, Department of Clinical Sciences, Pediatrics, Umeå University, Umeå, Sweden and – sequence: 3 givenname: M. surname: Prázny fullname: Prázny, M. organization: Third Department of Internal Medicine, First Faculty of Medicine, Charles University, Prague, Czech Republic – sequence: 4 givenname: H. surname: Falhammar fullname: Falhammar, H. organization: Diabetes Center Karolinska (DCK), Department of Molecular Medicine and Surgery, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden, Department of Clinical Sciences, Pediatrics, Umeå University, Umeå, Sweden and – sequence: 5 givenname: K. surname: Brismar fullname: Brismar, K. organization: Diabetes Center Karolinska (DCK), Department of Molecular Medicine and Surgery, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden, Department of Clinical Sciences, Pediatrics, Umeå University, Umeå, Sweden and – sequence: 6 givenname: G. surname: Dahlquist fullname: Dahlquist, G. organization: Diabetes Center Karolinska (DCK), Department of Molecular Medicine and Surgery, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden, Department of Clinical Sciences, Pediatrics, Umeå University, Umeå, Sweden and – sequence: 7 givenname: S. surname: Efendic fullname: Efendic, S. organization: Diabetes Center Karolinska (DCK), Department of Molecular Medicine and Surgery, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden, Department of Clinical Sciences, Pediatrics, Umeå University, Umeå, Sweden and – sequence: 8 givenname: H. F. surname: Gu fullname: Gu, H. F. organization: Diabetes Center Karolinska (DCK), Department of Molecular Medicine and Surgery, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden, Department of Clinical Sciences, Pediatrics, Umeå University, Umeå, Sweden and |
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| Keywords | Endocrinopathy Kidney disease Immunopathology Urinary system disease Genetic variability Intercellular adhesion molecule 1 Cell adhesion molecule genetic association Autoimmune disease Genotype Nephropathy Type 1 diabetes Genetics Single nucleotide polymorphism Type 1 diabetes mellitus |
| Language | English |
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| PublicationYear | 2006 |
| Publisher | Blackwell Publishing Ltd Blackwell |
| Publisher_xml | – name: Blackwell Publishing Ltd – name: Blackwell |
| References | Shaw CJ, Lupski JR. Implications of human genome architecture for arrangement-based disorders: the genomic basis of disease. Human Mol Genet 2004; 13: R57-64. Toivonen A, Kulmala P, Rahko J, Ilonen J, Knip M. Soluble adhesion molecules in Finnish schoolchildren with signs of pre-clinical type 1 diabetes. Diabetes Metab Res Rev 2004; 20: 48-54. Park Y. Prediction of the risk of type 1 diabetes from polymorphisms in candidate genes. Diabetes Res Clin Pract 2004; 66: S19-25. Lampeter ER, Kishimoto TK, Rothlein R, Mainolfi EA, Bertrams J, Kolb H et al. Elevated levels of circulating adhesion molecules in IDDM patients and in subjects at risk for IDDM. Diabetes 1992; 41: 1668-1671. Kristiansen OP, Nolsoe RL, Holst H, Reker S, Larsen ZM, Johannesen J et al., Danish Study Group of IDDM in Childhood. The intercellular adhesion molecule-1 K469E polymorphism in type 1 diabetes. Immunogenetics 2000; 52: 107-111. World Health Organization. Diabetes Mellitus. Report of a WHO Study Group, Technical Report Series 727. Geneva: World Health Organization, 1985. Nejentsev S, Laine AP, Simell O, Ilonen J. Intercellular adhesion molecule-1 (ICAM-1) K469E polymorphism: no association with type 1 diabetes among Finns. Tissue Antigens 2000; 55: 568-570. Howell WM, Jobs M, Gyllensten U, Brookes AJ. Dynamic allele-specific hybridisation: a new method for scoring single nucleotide polymorphisms. Nat Biotech 1999; 17: 87-88. Kado S, Wakatsuki T, Yamamoto M, Nagato N. Expression of intercellular adhesion molecule-1 induced by high glucose in human aortic endothelial cells. Life Sci 2001; 68: 727-737. Sugimoto H, Shikata K, Hirata K, Akiyama K, Matsuda M, Kushiro M et al. Increased expression of intercellular adhesion molecule-1 (ICAM-1) in diabetic rat glomeruli. Glomerular hyperfiltration is a potential mechanism of ICAM-1 upregulation. Diabetes 1997; 46: 2075-2081. Martin S, Heidenthal E, Schulte B, Rothe H, Kolb H. Soluble forms of intercellular adhesion molecule-1 inhibit insulitis and onset of autoimmune diabetes. Diabetologia 1998; 41: 1298-1303. Venter JC, Adams MD, Myers EW, Li PW, Mural RJ, Sutton GG et al. The sequence of the human genome. Science 2001; 291: 1304-1351. Nishimura M, Obayashi H, Maruya E, Ohta M, Tegoshi H, Fukui M et al. Association between type 1 diabetes age-at-onset and intercellular adhesion molecule-1 (ICAM-1) gene polymorphism. Hum Immunol 2000; 61: 507-510. Mein CA, Esposito L, Dunn MG, Johnson GC, Timms AE, Goy JV et al. A search for type 1 diabetes susceptibility genes in families from the United Kingdom. Nat Genet 1998; 19: 297-300. Matsui H, Suzuki M, Tsukuda R, Iida K, Miyasaka M, Ikeda H. Expression of ICAM-1 on glomeruli is associated with progression of diabetic nephropathy in a genetically obese diabetic rat, Wistar fatty. Diabetes Res Clin Pract 1996; 32: 1-9. Pollin TI, Hsueh WC, Steinle NI, Snitker S, Shuldiner AR, Mitchell BD. A genome-wide scan of serum lipid levels in the Old Order Amish. Atherosclerosis 2004; 173: 89-96. Staunton DE, Marlin SD, Stratowa C, Dustin ML, Springer TA. Primary structure of ICAM−1 demonstrates interaction between members of the immunoglobulin and integrin supergene families. Cell 1988; 52: 925-933. Mohamed-Ali V, Armstrong L, Clarke D, Bolton CH, Pinkney JH. Evidence for the regulation of levels of plasma adhesion molecules by pro-inflammatory cytokines and their soluble receptors in type 1 diabetes. J Intern Med 2001; 250: 415-421. Joling P, Boom S, Johnson J, Dekker ME, Van Den Tweel JG, Schuurman HJ et al. Domain 5 of the intercellular adhesion molecule-1 (ICAM-1) is involved in adhesion of B-cells and follicular dendritic cells. Adv Exp Med Biol 1994; 355: 131-135. Ronaghi M, Uhlen M, Nyren P. A sequencing method based on real-time pyrophosphate. Science 1998; 281: 363-365. Balasa B, La Cava A, Van Gunst K, Mocnik L, Balakrishna D, Nguyen N et al. A mechanism for IL-10-mediated diabetes in the non-obese diabetic (NOD) mouse: ICAM-1 deficiency blocks accelerated diabetes. J Immunol 2000; 165: 7330-7337. Van De Stolpe A, Van Der Saag PT. Intercellular adhesion molecule-1. J Mol Med 1996; 74: 13-33. Nejentsev S, Guja C, McCormack R, Cooper J, Howson JMM, Nutland S, et al. Association of intercellular adhesion molecule-1 gene with type 1 diabetes. Lancet 2003; 362: 1723-1724. Omi H, Okayama N, Shimizu M, Okouchi M, Ito S, Fukutomi T et al. Participation of high glucose concentrations in neutrophil adhesion and surface expression of adhesion molecules in cultured human endothelial cells: effect of anti-diabetic medicines. J Diabetes Complications 2002; 16: 201-208. Cox NJ, Wapelhorst B, Morrison VA, Johnson L, Pinchuk L, Spielman RS et al. Seven regions of the genome show evidence of linkage to type 1 diabetes in a consensus analysis of 767 multiplex families. Am J Hum Genet 2001; 69: 820-830. Iwao M, Morisaki H, Morisaki T. Single-nucleotide polymorphism g.1548G > A (E469K) in human ICAM-1 gene affects mRNA splicing pattern and TPA-induced apoptosis. Biochem Biophys Res Commun 2004; 7: 729-735. Guja C, Todd JA, Welsh K, Marshall S, Ionescu-Tirgoviste C. Increased transmission of intercellular adhesion-molecule-1, 469E allele in type 1 Romanian diabetic families. 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(e_1_2_8_22_2) 1985 9392499 - Diabetes. 1997 Dec;46(12):2075-81 9705713 - Science. 1998 Jul 17;281(5375):363, 365 11132145 - Immunogenetics. 2000 Nov;52(1-2):107-11 15177127 - Atherosclerosis. 2004 Mar;173(1):89-96 9662409 - Nat Genet. 1998 Jul;19(3):297-300 14737745 - Diabetes Metab Res Rev. 2004 Jan-Feb;20(1):48-54 9920276 - Nat Biotechnol. 1999 Jan;17(1):87-8 14764619 - Hum Mol Genet. 2004 Apr 1;13 Spec No 1:R57-64 11507694 - Am J Hum Genet. 2001 Oct;69(4):820-30 3349522 - Cell. 1988 Mar 25;52(6):925-33 15563974 - Diabetes Res Clin Pract. 2004 Dec;66 Suppl 1:S19-25 11120869 - J Immunol. 2000 Dec 15;165(12):7330-7 9833936 - Diabetologia. 1998 Nov;41(11):1298-303 14643123 - Lancet. 2003 Nov 22;362(9397):1723-4 11205865 - Life Sci. 2001 Jan 5;68(7):727-37 12015189 - J Diabetes Complications. 2002 May-Jun;16(3):201-8 3934850 - World Health Organ Tech Rep Ser. 1985;727:1-113 8803476 - Diabetes Res Clin Pract. 1996 Apr;32(1-2):1-9 11181995 - Science. 2001 Feb 16;291(5507):1304-51 10773353 - Hum Immunol. 2000 May;61(5):507-10 15081401 - Biochem Biophys Res Commun. 2004 May 7;317(3):729-35 11887976 - J Intern Med. 2001 Nov;250(5):415-21 7709811 - Adv Exp Med Biol. 1994;355:131-5 1280239 - Diabetes. 1992 Dec;41(12):1668-71 8834767 - J Mol Med (Berl). 1996 Jan;74(1):13-33 10902613 - Tissue Antigens. 2000 Jun;55(6):568-70 |
| References_xml | – reference: Van De Stolpe A, Van Der Saag PT. Intercellular adhesion molecule-1. J Mol Med 1996; 74: 13-33. – reference: Howell WM, Jobs M, Gyllensten U, Brookes AJ. Dynamic allele-specific hybridisation: a new method for scoring single nucleotide polymorphisms. Nat Biotech 1999; 17: 87-88. – reference: Nishimura M, Obayashi H, Maruya E, Ohta M, Tegoshi H, Fukui M et al. Association between type 1 diabetes age-at-onset and intercellular adhesion molecule-1 (ICAM-1) gene polymorphism. Hum Immunol 2000; 61: 507-510. – reference: Park Y. Prediction of the risk of type 1 diabetes from polymorphisms in candidate genes. Diabetes Res Clin Pract 2004; 66: S19-25. – reference: Toivonen A, Kulmala P, Rahko J, Ilonen J, Knip M. Soluble adhesion molecules in Finnish schoolchildren with signs of pre-clinical type 1 diabetes. Diabetes Metab Res Rev 2004; 20: 48-54. – reference: Nejentsev S, Guja C, McCormack R, Cooper J, Howson JMM, Nutland S, et al. Association of intercellular adhesion molecule-1 gene with type 1 diabetes. Lancet 2003; 362: 1723-1724. – reference: Balasa B, La Cava A, Van Gunst K, Mocnik L, Balakrishna D, Nguyen N et al. A mechanism for IL-10-mediated diabetes in the non-obese diabetic (NOD) mouse: ICAM-1 deficiency blocks accelerated diabetes. J Immunol 2000; 165: 7330-7337. – reference: Kado S, Wakatsuki T, Yamamoto M, Nagato N. Expression of intercellular adhesion molecule-1 induced by high glucose in human aortic endothelial cells. Life Sci 2001; 68: 727-737. – reference: Omi H, Okayama N, Shimizu M, Okouchi M, Ito S, Fukutomi T et al. Participation of high glucose concentrations in neutrophil adhesion and surface expression of adhesion molecules in cultured human endothelial cells: effect of anti-diabetic medicines. J Diabetes Complications 2002; 16: 201-208. – reference: Lampeter ER, Kishimoto TK, Rothlein R, Mainolfi EA, Bertrams J, Kolb H et al. Elevated levels of circulating adhesion molecules in IDDM patients and in subjects at risk for IDDM. Diabetes 1992; 41: 1668-1671. – reference: Ronaghi M, Uhlen M, Nyren P. A sequencing method based on real-time pyrophosphate. Science 1998; 281: 363-365. – reference: World Health Organization. Diabetes Mellitus. Report of a WHO Study Group, Technical Report Series 727. Geneva: World Health Organization, 1985. – reference: Shaw CJ, Lupski JR. Implications of human genome architecture for arrangement-based disorders: the genomic basis of disease. Human Mol Genet 2004; 13: R57-64. – reference: Pollin TI, Hsueh WC, Steinle NI, Snitker S, Shuldiner AR, Mitchell BD. A genome-wide scan of serum lipid levels in the Old Order Amish. Atherosclerosis 2004; 173: 89-96. – reference: Nejentsev S, Laine AP, Simell O, Ilonen J. Intercellular adhesion molecule-1 (ICAM-1) K469E polymorphism: no association with type 1 diabetes among Finns. Tissue Antigens 2000; 55: 568-570. – reference: Mohamed-Ali V, Armstrong L, Clarke D, Bolton CH, Pinkney JH. Evidence for the regulation of levels of plasma adhesion molecules by pro-inflammatory cytokines and their soluble receptors in type 1 diabetes. J Intern Med 2001; 250: 415-421. – reference: Iwao M, Morisaki H, Morisaki T. Single-nucleotide polymorphism g.1548G > A (E469K) in human ICAM-1 gene affects mRNA splicing pattern and TPA-induced apoptosis. Biochem Biophys Res Commun 2004; 7: 729-735. – reference: Matsui H, Suzuki M, Tsukuda R, Iida K, Miyasaka M, Ikeda H. Expression of ICAM-1 on glomeruli is associated with progression of diabetic nephropathy in a genetically obese diabetic rat, Wistar fatty. Diabetes Res Clin Pract 1996; 32: 1-9. – reference: Venter JC, Adams MD, Myers EW, Li PW, Mural RJ, Sutton GG et al. The sequence of the human genome. Science 2001; 291: 1304-1351. – reference: Cox NJ, Wapelhorst B, Morrison VA, Johnson L, Pinchuk L, Spielman RS et al. Seven regions of the genome show evidence of linkage to type 1 diabetes in a consensus analysis of 767 multiplex families. Am J Hum Genet 2001; 69: 820-830. – reference: Guja C, Todd JA, Welsh K, Marshall S, Ionescu-Tirgoviste C. Increased transmission of intercellular adhesion-molecule-1, 469E allele in type 1 Romanian diabetic families. Diabetologia 1999; 42: 327-327. – reference: Kristiansen OP, Nolsoe RL, Holst H, Reker S, Larsen ZM, Johannesen J et al., Danish Study Group of IDDM in Childhood. The intercellular adhesion molecule-1 K469E polymorphism in type 1 diabetes. Immunogenetics 2000; 52: 107-111. – reference: Sugimoto H, Shikata K, Hirata K, Akiyama K, Matsuda M, Kushiro M et al. Increased expression of intercellular adhesion molecule-1 (ICAM-1) in diabetic rat glomeruli. Glomerular hyperfiltration is a potential mechanism of ICAM-1 upregulation. Diabetes 1997; 46: 2075-2081. – reference: Mein CA, Esposito L, Dunn MG, Johnson GC, Timms AE, Goy JV et al. 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| Snippet | Aim The intercellular adhesion molecule‐1 (ICAM‐1) gene is located on chromosome 19p13, which is linked to Type 1 diabetes (T1D). ICAM‐1 expression is related... Aim The intercellular adhesion molecule‐1 (ICAM‐1) gene is located on chromosome 19p13, which is linked to Type 1 diabetes (T1D). ICAM‐1 expression is related... The intercellular adhesion molecule-1 (ICAM-1) gene is located on chromosome 19p13, which is linked to Type 1 diabetes (T1D). ICAM-1 expression is related to... Aim: The intercellular adhesion molecule-1 (ICAM-1) gene is located on chromosome 19p13, which is linked to Type 1 diabetes (T1D). ICAM-1 expression is related... AIM: The intercellular adhesion molecule-1 (ICAM-1) gene is located on chromosome 19p13, which is linked to Type 1 diabetes (T1D). ICAM-1 expression is related... |
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| SubjectTerms | Adult Biological and medical sciences Diabetes Diabetes Mellitus, Type 1 - genetics Diabetes. Impaired glucose tolerance Diabetic Nephropathies - genetics Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female genetic association Genetic Predisposition to Disease - genetics genetics Humans Intercellular Adhesion Molecule-1 - genetics intercellular adhesion molecule 1 Male Medical sciences Middle Aged nephropathy Original Polymorphism, Genetic - genetics single nucleotide polymorphism Sweden Type 1 Type 1 diabetes mellitus |
| Title | Genetic influences of the intercellular adhesion molecule 1 (ICAM-1) gene polymorphisms in development of Type 1 diabetes and diabetic nephropathy |
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