Is CCR5-Δ32 mutation associated with diabetic nephropathy in type 2 diabetes?

Arababadi, Mohammad Kazemi; Naghavi, Nima; Hassanshahi, Gholamhossein; Mahmoodi, Mehdi

doi:10.4103/0256-4947.55177

Cited by 20 publications

(10 citation statements)

References 9 publications

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“…In SLE, inflammatory processes starts with lymphocytic infiltration into tissue space, and biodistribution of lymphocytes at the inflammation site can be determined by expression of some chemokine receptors such as CCR5 (24). The CCR5Δ32 reduces expression of the protein and disrupts its function, effects that are crucial in development of autoimmune diseases (25). CCR5 is a chemokine receptor involved in inflammatory responses and could, therefore, trigger autoimmune disease.…”

Section: Resultsmentioning

confidence: 99%

Evaluation of CCR5Δ32 Polymorphism in Patients with Systemic Lupus Erythematosus and Healthy Individuals

et al. 2018

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Background and Objectives: CC chemokine receptor type 5 (CCR5) is a chemokine receptor expressed at high levels on the surface of T-cells. A 32-bp deletion in the coding region of the CCR5 (CCR5Δ32) leads to production of an incomplete protein that is not expressed on the cell surface. CCR5Δ32 may be involved in development of autoimmune disease, such as systemic lupus erythematosus. We investigated frequency of the CCR5Δ32 polymorphism in SLE patients and healthy controls, and evaluated the relationship between the CCR5Δ32 polymorphism and susceptibility to SLE in Golestan Province, Iran. Methods: Whole blood samples were taken from 80 SLE patients admitted to Shahid Sayyad Shirazi hospital and 80 healthy controls (from a blood bank) in the Golestan Province, in 2016. Baseline clinical and laboratorial characteristics were evaluated regarding the CCR5Δ32 genotypes. The CCR5Δ32 polymorphism was determined from genomic DNA by polymerase chain reaction. Result: Genotype frequencies of both groups were in the Hardy-Weinberg equilibrium. The frequencies of the CCR5 and the CCR5Δ32 alleles were 98.13% and 1.88% among the patients, and 98.75% and 1.25% among the controls, respectively. Homozygote CCR5Δ32 was not observed in the subjects. The frequency of heterozygous Δ32 was 3.8% and 2.5% among the SLE patients and controls, respectively (P-value>0.05). There was no significant association between the CCR5 status and clinical signs of SLE (P>0.05). Conclusion: Our data suggest that the CCR5Δ32 polymorphism has no correlation with SLE in our study population. In addition, the frequency of the Δ32 polymorphism in SLE patients and controls does not follow the Hardy-Weinberg equilibrium

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Section: Resultsmentioning

confidence: 99%

Evaluation of CCR5Δ32 Polymorphism in Patients with Systemic Lupus Erythematosus and Healthy Individuals

et al. 2018

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“…188 bp fragment showed a wild type gene without CCR5-D32 mutation, while, the presence of a PCR product with 156 bp confirms CCR5-D32 mutation in the CCR5 gene. Furthermore PCR condition, the sequences of forward and reverse primers and gel electrophoresis were described in our previous studies [11][12][13].…”

Section: Genomic Dna Extraction and Polymorphism Analysismentioning

confidence: 99%

Lack of Correlation Between the CCR5-Δ32 Mutation and Acute Myeloid Leukemia in Iranian Patients

Khorramdelazad

Mortazavi

Momeni

et al. 2014

Indian J Hematol Blood Transfus

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Chemokines and their receptors are crucially important in the pathogenesis of acute myeloblastic leukemia (AML). The CC chemokine receptor 5 (CCR5) is a specific chemokine receptor for CC chemokine ligand 3 (CCL3), CCL4 and CCL5 which all play key roles in identifying cancer properties and localization of leukemia cells. It has been demonstrated that the known mutation in CCR5 gene (CCR5-Δ32) leads to mal-expression of the receptor and affect its function. The aim of this study was to determine the rate of CCR5-Δ32 mutation within Iranian AML patients. In this study, blood samples were obtained from 60 AML patients and 300 healthy controls. The CCR5-Δ32 mutation was evaluated using Gap-PCR technique. Our results showed that CCR5-Δ32 mutation was not found in the patients, while three out of the controls had hetrozygotic form of this mutation. The rest of studied samples had the wild form of the gene. According to these findings, it can probably be concluded that the CCR5-Δ32 is not associated with susceptibility to AML in Iranian patients.

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“…, 2008). Type‐2, sometimes referred to as non‐insulin dependent diabetes mellitus (NIDDM) or adult‐onset diabetes is the most prevalent type of the diabetes (Arababadi et al. , 2009a) and is often caused by decreased insulin production by the pancreas.…”

Section: Introductionmentioning

confidence: 99%

Polymorphisms within exon 9 but not intron 8 of the vitamin D receptor are associated with the nephropathic complication of type‐2 diabetes

Nosratabadi

Arababadi

Salehabad

et al. 2010

Int J Immunogenetics

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The impact of several environmental and genetic factors on diabetes and its complications is well documented but there is an urgent need to understand more about genetic risk factors associated with this disease. The present study was aimed at examining the two single nucleotide polymorphisms (SNP) in intron 8 and exon 9 of the vitamin D receptor (VDR) gene in nephropathic and non-nephropathic type-2 diabetic patients. In this clinical study, peripheral blood samples were obtained from 100 type-2 diabetic patients, 100 nephropathic type-2 diabetic patients and 100 healthy controls. DNA was extracted and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was performed to examine two SNP polymorphisms within the VDR gene. Our results showed a significant difference in the Taq-1 evaluated genotypes of exon 9 in the VDR gene of diabetic individuals with (P=0.012) and without (P ≤ 0.001) nephropathy. Analysis of the Taq-1 evaluated alleles of nephropathic (P=0.917) and non-nephropathic (P=1.000) did not show a significant difference. We also evaluated the intron 8 Apa-1 alleles in patients with (P=0.480) and without nephropathy (P=0.543) and determined there were no differences between these groups. Our results also showed that the frequency of Apa-1 genotypes did not differ in nephropathic (P=0.224) and non-nephropathic (P=0.236) diabetic patients. Based on our results, it can be concluded that VDR and its functional polymorphism in exon 9 may play an important role in pathogenesis of type-2 diabetes and more investigations are required to clarify their role in nephropathy.

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Is CCR5-Δ32 mutation associated with diabetic nephropathy in type 2 diabetes?

Cited by 20 publications

References 9 publications

Evaluation of CCR5Δ32 Polymorphism in Patients with Systemic Lupus Erythematosus and Healthy Individuals

Evaluation of CCR5Δ32 Polymorphism in Patients with Systemic Lupus Erythematosus and Healthy Individuals

Lack of Correlation Between the CCR5-Δ32 Mutation and Acute Myeloid Leukemia in Iranian Patients

Polymorphisms within exon 9 but not intron 8 of the vitamin D receptor are associated with the nephropathic complication of type‐2 diabetes

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