Pin1 and secondary hyperparathyroidism of chronic kidney disease: gene polymorphisms and protein levels. (1st January 2017)

• Record Type: Journal Article
• Authors: Zhao, Yu; Zhang, Li-Li; Ding, Fa-Xian; Cao, Ping; Qi, Yuan-Yuan; Wang, Jing
• Is Part Of: Renal failure. Volume 39:Number 1(2017)
• Page Start: 159
• Page End: 165
• Publication Date: 2017-01-01
• Subjects: Chronic kidney disease -- secondary hyperparathyroidism -- peptidyl-prolyl cis/trans isomerase NIMA-interacting 1 -- single nucleotide polymorphism; Chronic renal failure -- Periodicals; Acute renal failure -- Periodicals; Uremia -- Periodicals; 616.614005
• DOI: 10.1080/0886022X.2016.1256310
• Languages: English
• ISSNs: 0886-022X

Abstract

Abstract: Background: Peptidyl-prolyl cis/trans isomerase NIMA-interacting 1 (Pin1) is a key regulator of PTH mRNA stability. Secondary hyperparathyroidism (SHPT), which is characterized by elevated serum PTH levels, is a common complication of CKD. We investigated the possible associations between CKD with SHPT (CKD SHPT) and single-nucleotide polymorphisms of the Pin1 gene and compared the levels of the Pin1 protein in the CKD SHPT patients with those of the controls. Methods: The study group included 251 CKD SHPT patients and 61 controls. One putative functional SNP (single nucleotide polymorphism) in the Pin1 promoter (rs2233679C > T: c.−667C > T) is the main object. Genotyping was performed on purified DNA using polymerase chain reaction-restriction (PCR) and restriction fragment length polymorphisms (RFLP). The levels of Pin1 were measured in serum using an enzyme-linked immunosorbent assay. Results: Genotyping showed that CT + TT in the Pin1 promoter was significantly more common in the CKD SHPT group than in the control group ( p <.05). The correlation analysis demonstrated that a significant difference in the C to T transition in the Pin1 promoter contributed to CKD SHPT ( χ 2 =12.47, p <.05; Odds ratios (OR) = 1.26, 95% confidence (CI) intervals =1.06–1.49). The multivariate logistic regression analysis reported that the OR and 95% CI were 12.693 and 2.029–75.819 ( p <.05), respectively, in the Pin1 gene promoter −667T variant genotypes (CT + TT) after adjusting for other factors, and those values in Pin1 were 0.310 and 0.122–0.792 ( p <.05). Conclusion: The −667T genetic variants in the Pin1 promoter contribute to an increased risk of CKD SHPT and may be biomarkers of susceptibility to CKD SHPT.