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Exp Clin Endocrinol Diabetes 2017; 125(08): 530-537
DOI: 10.1055/s-0043-103966
Article
© Georg Thieme Verlag KG Stuttgart · New York

Transcriptional Coactivator p300 and Silent Information Regulator 1 (SIRT1) Gene Polymorphism Associated with Diabetic Kidney Disease in a Chinese Cohort

Kang Tang
1   Department of Endocrinology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, P.R. China
,
Mingfang Sun
1   Department of Endocrinology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, P.R. China
,
Jing Shen
,
Bo Zhou
› Author Affiliations
Further Information

Publication History

received 22 November 2016
revised 04 February 2017

accepted 14 February 2017

Publication Date:
25 April 2017 (online)

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Abstract

Objective

One of the most serious complications of diabetes mellitus, which could lead to end-stage renal disease across all demographics, is ‘diabetic kidney disease’. However, how diabetic kidney disease develops remains unclear. Studies conducted thus far suggest that a major factor in the origination and development of the disease occurs through histone acetylation modifications. This study aims to examine the probable relationship in Chinese patients suffering from type 2 diabetes.

Method

A case–control study was conducted in the Chongqing region of China on the Chinese Han population. Patients suffering from type 2 diabetes mellitus were selected between March 2014 and Dec 2014 from the Department of Endocrinology, which is the First Affiliated Hospital of Chongqing Medical University. TaqMan probes were employed to perform an allelic discrimination assay for genotyping p300 and the SIRT1 (Silent Information Regulator 1) polymorphism. The risk factors diabetic kidney disease were determined by statistical analysis.

Results

The dispersion of the p300 genotype frequencies and SIRT1 gene polymorphism adheres to the Hardy-Weinberg equilibrium. The DKD group had a greater allele G frequency distribution, and allele G patients have a higher probability of diabetic kidney disease. Female patients, patients younger than 65 years of age, and those with the AG or GG genotype are more likely to develop diabetic kidney disease than patients with the AA phenotype. Patients with the AG or GG genotype are more likely to suffer from a severe diabetic kidney disease than patients with the AA genotype, particularly if the patients are older than 65 years of age. The SIRT1 rs4746720 allele C is a risk factor for urinary Alb/Cr. Allele G and the TC genotype patients are more likely to develop diabetic kidney disease, while allele G and TT genotype patients are more likely develop a severe diabetic kidney disease.

Conclusion

Transcriptional coactivator p300 gene polymorphism correlates with the development and advancement of diabetic kidney disease. Additionally, the SIRT1 gene collaborates with the p300 gene and participates in promoting albuminuria in type 2 diabetes mellitus patients.

Key words

Single nucleotide polymorphism - p300 gene - SIRT1 gene - diabetic kidney disease
 

  • References

  • 1 Burke JP, Williams K, Gaskill SP. et al. Rapid rise in the incidence of type 2 diabetes from 1987 to 1996: Results from the San Antonio Heart Study. Arch Intern Med 1999; 159: 1450-1456
    CrossrefPubMedGoogle Scholar
  • 2 Mokdad AH, Ford ES, Bowman BA. et al Diabetes Trends in the U.S.: 1990–1998. Diabetes Care 2000; 23: 1278-1283
    CrossrefPubMedGoogle Scholar
  • 3 Harris MI, Flegal KM, Cowie CC. et al Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in US adults: The third national health and nutrition examination survey, 1988–1994. Diabetes Care 1998; 21: 518-524
    CrossrefPubMedGoogle Scholar
  • 4 Gross JL, de Azevedo MJ, Silveiro SP. et al. Diabetic nephropathy: Diagnosis, prevention, and treatment. Diabetes Care 2005; 28: 164-176
    CrossrefPubMedGoogle Scholar
  • 5 Coresh J, Selvin E, Stevens LA. et al Prevalence of chronic kidney disease in the United States. JAMA 2007; 298: 2038-2047
    CrossrefPubMedGoogle Scholar
  • 6 Decleves AE, Sharma K. New pharmacological treatments for improving renal outcomes in diabetes. Nat Rev Nephrol 2010; 6: 371-380
    CrossrefPubMedGoogle Scholar
  • 7 Tan AL, Forbes JM, Cooper ME. AGE, RAGE, and ROS in diabetic nephropathy. Semin Nephrol 2007; 27: 130-143
    CrossrefPubMedGoogle Scholar
  • 8 Putta S, Lanting L, Sun G. et al. Inhibiting microRNA-192 ameliorates renal fibrosis in diabetic nephropathy. J Am Soc Nephrol 2012; 23: 458-469
    CrossrefPubMedGoogle Scholar
  • 9 Kato M, Natarajan R. microRNA cascade in diabetic kidney disease: Big impact initiated by a small RNA. Cell Cycle 2009; 8: 3613-3614
    CrossrefPubMedGoogle Scholar
  • 10 Kurashige M, Imamura M, Araki S. et al. The influence of a single nucleotide polymorphism within CNDP1 on susceptibility to diabetic nephropathy in Japanese women with type 2 diabetes. PLoS One 2013; 8: e54064
    CrossrefPubMedGoogle Scholar
  • 11 Tonna S, El-Osta A, Cooper ME. et al. Metabolic memory and diabetic nephropathy: potential role for epigenetic mechanisms. Nat Rev Nephrol 2010; 6: 332-341
    CrossrefPubMedGoogle Scholar
  • 12 Ihnat MA, Thorpe JE, Ceriello A. Hypothesis: the ‘metabolic memory’, the new challenge of diabetes. Diabet Med 2007; 24: 582-586
    CrossrefPubMedGoogle Scholar
  • 13 El-Osta A, Brasacchio D, Yao D. et al Transient high glucose causes persistent epigenetic changes and altered gene expression during subsequent normoglycemia. J Exp Med 2008; 205: 2409-2417
    CrossrefPubMedGoogle Scholar
  • 14 Strahl BD, Allis CD. The language of covalent histone modifications. Nature 2000; 403: 41-45
    CrossrefPubMedGoogle Scholar
  • 15 Fischle W, Wang Y, Allis CD. Histone and chromatin cross-talk. Curr Opin Cell Biol 2003; 15: 172-183
    CrossrefPubMedGoogle Scholar
  • 16 Gupta J, Kumar S, Li J. et al. Histone H3 lysine 4 monomethylation (H3K4me1) and H3 lysine 9 monomethylation (H3K9me1): Distribution and their association in regulating gene expression under hyperglycaemic/hyperinsulinemic conditions in 3T3 cells. Biochimie 2012; 94: 2656-2664
    CrossrefPubMedGoogle Scholar
  • 17 Zhong Q, Kowluru RA. Role of histone acetylation in the development of diabetic retinopathy and the metabolic memory phenomenon. J Cell Biochem 2010; 110: 1306-1313
    CrossrefPubMedGoogle Scholar
  • 18 Wilson CB. RESM: Epigenetic control of T-helper-cell differentiation. Nature Reviews Immunology 2009; 2: 91-105
    PubMedGoogle Scholar
  • 19 Villeneuve LM, Reddy MA, Lanting LL. et al. Epigenetic histone H3 lysine 9 methylation in metabolic memory and inflammatory phenotype of vascular smooth muscle cells in diabetes. Proc Natl Acad Sci USA 2008; 105: 9047-9052
    CrossrefPubMedGoogle Scholar
  • 20 Sayyed SG, Gaikwad AB, Lichtnekert J. et al Progressive glomerulosclerosis in type 2 diabetes is associated with renal histone H3K9 and H3K23 acetylation,H3K4 dimethylation and phosphorylation at serine 10. Nephrol Dial Transplant 2010; 25: 1811-1817
    CrossrefPubMedGoogle Scholar
  • 21 Struhl K. Histone acetylation and transcriptional regulatory mechanisms. Genes Dev 1998; 12: 599-606
    CrossrefPubMedGoogle Scholar
  • 22 Ghosh AK, Varga J. The Transcriptional Coactivator and acetyltransferase p300 in fibroblast biolgy and fibrosis. J Cell Physiol 2007; 213: 663-671
    CrossrefPubMedGoogle Scholar
  • 23 Chen S, Feng B, George B. et al. Transcriptional coactivator p300 regulates glucose-induced gene expression in endothelial cells. Am J Physiol Endocrinol Metab 2010; 298: E127-E137
    CrossrefPubMedGoogle Scholar
  • 24 Xu B, Chiu J, Feng B. et al. PARP activation and the alteration of vasoactive factors and extracellular matrix protein in retina and kidney in diabetes. Diabetes Metab Res Rev 2008; 24: 404-412
    CrossrefPubMedGoogle Scholar
  • 25 Akil A, Ezzikouri S, El Feydi AE. et al. Associations of genetic variants in the transcriptional coactivators EP300 and PCAF with hepatocellular carcinoma. Cancer Epidemiol 2012; 36: e300-e305
    CrossrefPubMedGoogle Scholar
  • 26 Baur JA. Biochemical effects of SIRT1 activators. Biochim Biophys Acta 2010; 1804: 1626-1634
    CrossrefPubMedGoogle Scholar
  • 27 Kume S, Uzu T, Kashiwagi A. et al. SIRT1, a calorie restriction mimetic, in a new therapeutic approach for type 2 diabetes mellitus and diabetic vascular complications. Endocr Metab Immune Disord Drug Targets 2010; 10: 16-24
    CrossrefPubMedGoogle Scholar
  • 28 Imai S, Guarente L. Ten years of NAD-dependent SIR2 family deacetylases: implications for metabolic diseases. Trends Pharmacol Sci 2010; 31: 212-220
    CrossrefPubMedGoogle Scholar
  • 29 Polak-Jonkisz D, Laszki-Szczachor K, Rehan L. et al. Nephroprotective action of sirtuin 1 (SIRT1). J Physiol Biochem 2013; 69: 957-961
    CrossrefPubMedGoogle Scholar
  • 30 Maeda S, Koya D, Araki S. et al. Association between single nucleotide polymorphisms within genes encoding sirtuin families and diabetic nephropathy in Japanese subjects with type 2 diabetes. Clin Exp Nephrol 2011; 15: 381-390
    CrossrefPubMedGoogle Scholar
  • 31 KDOQI clinical practice guidelines and clinical practice recommendations for diabetes and chronic kidney disease. Am J Kidney Dis 2007; 49 (Suppl. 02) S12-S154
    CrossrefPubMedGoogle Scholar
  • 32 Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl 2013; 3: 1-150
    CrossrefPubMedGoogle Scholar
  • 33 Larmour KE, Maxwell AP, Courtney AE. Improving early detection of chronic kidney disease. Practitioner 2015; 259: 19-23 2-3
    PubMedGoogle Scholar
  • 34 Fotheringham J, Odudu A, McKane W. et al. Modification of the relationship between blood pressure and renal albumin permeability by impaired excretory function and diabetes. Hypertension 2015; 65: 510-516
    CrossrefPubMedGoogle Scholar
  • 35 Krolewski AS, Poznik GD, Placha G. et al. A genome-wide linkage scan for genes controlling variation in urinary albumin excretion in type II diabetes. Kidney Int 2006; 69: 129-136
    CrossrefPubMedGoogle Scholar
  • 36 Ahlqvist E, van Zuydam NR, Groop LC. et al. The genetics of diabetic complications. Nat Rev Nephrol 2015; 11: 277-287
    CrossrefPubMedGoogle Scholar
  • 37 Palmer ND, Ng MC, Hicks PJ. et al. Evaluation of candidate nephropathy susceptibility genes in a genome-wide association study of African American diabetic kidney disease. PLoS One 2014; 9: e88273
    CrossrefPubMedGoogle Scholar
  • 38 Cooke BJ, Palmer ND, Ng MC. et al. Analysis of coding variants identified from exome sequencing resources for association with diabetic and non-diabetic nephropathy in African Americans. Hum Genet 2014; 133: 769-779
    CrossrefPubMedGoogle Scholar
  • 39 McDonough CW, Palmer ND, Hicks PJ. et al. A genome-wide association study for diabetic nephropathy genes in African Americans. Kidney Int 2011; 79: 563-572
    CrossrefPubMedGoogle Scholar
  • 40 Sun YM, Su Y, Li J. et al. Recent advances in understanding the biochemical and molecular mechanism of diabetic nephropathy. Biochem Biophys Res Commun 2013; 433: 359-361
    CrossrefPubMedGoogle Scholar
  • 41 Chiu J, Khan ZA, Farhangkhoee H. et al. Curcumin prevents diabetes-associated abnormalities in the kidneys by inhibiting p300 and nuclear factor-kappaB. Nutrition 2009; 25: 964-972
    CrossrefPubMedGoogle Scholar
  • 42 Yuan H, Reddy MA, Sun G. et al. Involvement of p300/CBP and epigenetic histone acetylation in TGF-beta1-mediated gene transcription in mesangial cells. Am J Physiol Renal Physiol 2013; 304: F601-F613
    CrossrefPubMedGoogle Scholar
  • 43 Chuang PY, Dai Y, Liu R. et al. Alteration of forkhead box O (foxo4) acetylation mediates apoptosis of podocytes in diabetes mellitus. PLoS One 2011; 6: e23566
    CrossrefPubMedGoogle Scholar
  • 44 Mortuza R, Chen S, Feng B. et al. High glucose induced alteration of SIRTs in endothelial cells causes rapid aging in a p300 and FOXO regulated pathway. PLoS One 2013; 8: e54514
    CrossrefPubMedGoogle Scholar
  • 45 Khajehdehi P, Pakfetrat M, Javidnia K. et al. Oral supplementation of turmeric attenuates proteinuria, transforming growth factor-beta and interleukin-8 levels in patients with overt type 2 diabetic nephropathy: A randomized, double-blind and placebo-controlled study. Scand J Urol Nephrol 2011; 45: 365-370
    CrossrefPubMedGoogle Scholar
  • 46 Dekker FJ, Haisma HJ. Histone acetyl transferases as emerging drug targets. Drug Discov Today 2009; 14: 942-948
    CrossrefPubMedGoogle Scholar
  • 47 Robert J. Gene polymorphisms. Bull Cancer 2010; 97: 1253-1264
    PubMedGoogle Scholar