VDBP and VDR Mutations May Cause In-Stent Restenosis

Objective: In-stent restenosis (ISR) is the narrowing of a stented coronary artery lesion. A considerable number of patients undergoing percutaneous coronary intervention (PCI) are affected by ISR. The predominant mechanism in the development of ISR is an inflammatory response to vessel wall injury during PCI. Vitamin D is reported to have anti-inflammatory properties, so it may also be related with ISR. Therefore, in this study the relationship between vitamin D receptor (VDR), vitamin D binding protein (VDBP) gene variations and ISR were investigated. Methods: Fifty-eight ISR patients who have chest pain, underwent angiography and were found to have restenosis in the previously inserted stent were included in the patient group and thirty-five patients who have chest pain and were not found to have restenosis in their previous stent in coronary angiography were included in the control group. rs7041 and rs4588 variations in VDBP; rs1544410 and rs2228570 variations in VDR were investigated by real-time polymerase chain reaction (RT-PCR). Results were evaluated statistically. Results: The CC genotype of rs2228570 variation of VDR and the CA genotype of rs4588 variation of VDBP were found statistically high in patient group. rs7041 variation was found statistically high in patients who had myocardial infarction history before stent implantation. Additionally, it was demonstrated that vitamin D deficiency (vitamin D level

Anahtar Kelime: ISR VDR VDBP RT-PCR

Belge Türü: Makale Makale Türü: Araştırma Makalesi Erişim Türü: Erişime Açık

[1] Dai X, Wiernek S, Evans JP, Runge MS. Genetics of coronary artery disease and myocardial infarction. World J Cardiol. 2016;8:1-23.
[2] Schaffer A, Verdoia M, Barbieri L, Cassetti E, Suryapranata H, De Luca G. Impact of diabetes on homocysteine levels and ıts relationship with coronary artery disease: A single-centre cohort study. Ann Nutr Metab. 2016;68:180-188.
[3] Huang NF, Kurpinski K, Fang Q, Lee RJ, Li S. Proteomic identification of biomarkers of vascular injury. Am J Transl Res. 2011;3:139-418.
[4] Hamid H, Coltart J. ‘Miracle stents’—a future without restenosis. Mcgill J Med. 2007;10:105-111.
[5] Looser PM, Kim LK, Feldman DN. In-Stent Restenosis: Pathophysiology and treatment. Curr Treat Options Cardiovasc Med. 2016;18:10.
[6] Ferrante G, Niccoli G, Biasucci LM, Liuzzo G, Burzotta F, Galiuto L, Trani C, Rebuzzi AG, Crea F. Association between C-reactive protein and angiographic restenosis after bare metal stents: An updated and comprehensive meta-analysis of 2747 patients. Cardiovasc Revasc Med. 2008;9:156-165.
[7] Al Mheid I, Patel R, Murrow J, Pires NM, Pols HA, Zwinderman AH, de Maat MP, Doevendans PA, DeWinter RJ, Tio RA, Waltenberger J, Frants RR, Quax PH, van der Laarse A, van der Wall EE, Uitterlinden AG, Jukema JW. Vitamin D status is associated with arterial stiffness and vascular dysfunction in healthy humans. J Am Coll Cardiol. 2011;58:186-192.
[8] Monraats PS, Fang Y, Pons D, Pires NM, Pols HA, Zwinderman AH, de Maat MP, Doevendans PA, DeWinter RJ, Tio RA, Waltenberger J, Frants RR, Quax PH, van der Laarse A, van der Wall EE, Uitterlinden AG, Jukema JW. Vitamin D receptor: a new risk marker for clinical restenosis after percutaneous coronary intervention. Expert Opin Ther Targets. 2010;14:243- 251.
[9] Sen F, Yilmaz S, Balci KG, Sen Ö, Gül M, Çay S, Topaloglu S, Aydogdu S. The relationship between vitamin D levels and saphenous vein graft patency. Coron Artery Dis. 2015;26:328- 332.
[10] Young KA, Snell-Bergeon JK, Naik RG, Hokanson JE, Tarullo D, Gottlieb PA, Garg SK, Rewers M. Vitamin D deficiency and coronary artery calcification in subjects with type 1 diabetes. Diabetes Care. 2011;34:454-458.
[11] Gupta GK, Agrawal T, Del Core MG, Hunter WJ 3rd, Agrawal DK. Decreased expression of vitamin D receptors in neointimal lesions following coronary artery angioplasty in atherosclerotic swine. PLoS One. 2012;7:e42789.
[12] Verschuren JJ, Trompet S, Sampietro ML, Heijmans BT, Koch W, Kastrati A, Houwing-Duistermaat JJ, Slagboom PE, Quax PH, Jukema JW. Pathway analysis using genome-wide association study data for coronary restenosis—a potential role for the PARVB gene. PLoS One. 2013;8:e70676.
[13] Pan XM, Li DR, Yang L, Wang EY, Chen TY, Liu YJ, Liu M, Liao ZG. No association between vitamin D receptor polymorphisms and coronary artery disease in a Chinese population. DNA Cell Biol. 2009;28:521-525.
[14] He L, Wang M. Association of vitamin D receptor-a gene polymorphisms with coronary heart disease in Han Chinese. Int J Clin Exp Med. 2015;8:6224-6229.
[15] Jorde R, Schirmer H, Wilsgaard T, Joakimsen RM, Mathiesen EB, Njølstad I, Løchen ML, Figenschau Y, Berg JP, Svartberg J, Grimnes G. Polymorphisms related to the serum 25-hydroxyvitamin D level and risk of myocardial infarction, diabetes, cancer and mortality. The Tromso Study. PLoS One. 2012;7:e37295.
[16] Abu El Maaty MA, Hassanein SI, Gad MZ. Genetic variation in vitamin D receptor gene (Fok1:rs2228570) is associated with risk of coronary artery disease. Biomarkers. 2016;21:68-72.
[17] Laczmanski L, Milewicz A, Lwow F, Puzianowska-Kuznicka M, Pawlak M, Kolackov K, Jedrzejuk D, Krzyzanowska-Swiniarska B, Bar-Andziak E, Chudek J, Mossakowska M. Vitamin D receptor gene polymorphism and cardiovascular risk variables in elderly polish subjects. Gynecol Endocrinol. 2013;29:268- 272.
[18] Stakisaitis D, Lesauskaite V, Girdauskaite M, Janulionis E, Ulys A, Benetis R. Investigation of vitamin D-binding protein polymorphism impact on coronary artery disease and relationship with longevity: own data and a review. Int J Endocrinol. 2016;8347379:1-7.
[19] Lafi ZM, Irshaid YM, El-Khateeb M, Ajlouni KM, Hyassat D. Association of rs7041 and rs4588 polymorphisms of the vitamin D binding protein and the rs10741657 polymorphism of CYP2R1 with vitamin D status among jordanian patients. Genet Test Mol Biomarkers. 2015;19:629-636.
[20] Pilz S, Tomaschitz A, Ritz E, Pieber TR. Vitamin D status and arterial hypertension: A systematic review. Nat Rev Cardiol. 2009;6:621-630.
[21] Dhibar DP, Sharma YP, Bhadada SK, Sachdeva N, Sahu KK. Association of vitamin D deficiency with coronary artery disease. J Clin Diagn Res. 2016;10:OC24-OC28.
[22] Gupta GK, Agrawal T, Rai V, Del Core MG, Hunter WJ, Agrawal DK. Vitamin D supplementation reduces intimal hyperplasia and restenosis following coronary intervention in atherosclerotic swine. PLoS One. 2016;11:e0156857.
[23] Chen WR, Qian YA, Chen YD, Shi Y, Yin DW, Wang H, Zhu P, Liu HW, Sha Y. The effects of low vitamin D on coronary artery disease. Heart Lung Circ. 2014;23:314-319.
[24] Li DY, Zhang YC, Philips MI, Sawamura T, Mehta JL. Upregulation of endothelial receptor for oxidized low-density lipoprotein (LOX-1) in cultured human coronary artery endothelial cells by angiotensin II type 1 receptor activation. Circ Res. 1999;84:1043-1049.
[25] Krause R, Buhring M, Hopfenmuller W, Holick MF, Sharma AM. Ultraviolet B and blood pressure. Lancet. 1998;352:709-710.
[26] Pleva L, Kovarova P, Faldynova L, Plevova P, Hilscherova S, Zapletalova J, Kusnierova P, Kukla P. The rs1803274 polymorphism of the BCHE gene is associated with an increased risk of coronary in-stent restenosis. BMC Cardiovasc Disord. 2015;15:135.
[27] Giovannucci E, Liu Y, Hollis BW, Rimm EB. 25-hydroxyvitamin D and risk of myocardial infarction in men: a prospective study. Arch Intern Med 2008;168:1174-1180.
[28] Jorde R, Schirmer H, Wilsgaard T, Bøgeberg Mathiesen E, Njølstad I, Løchen ML, Joakimsen RM, Grimnes G. The DBP Phenotype Gc-1f/Gc-1f is associated with reduced risk of cancer. The tromso study. PLoS One. 2015;10:e0126359.
[29] Zheng SZ, Zhang DG, Wu H, Jiang LJ, Jin J, Lin XQ, Ding R, Jiang Y. The association between vitamin D receptor polymorphisms and serum 25-hydroxyvitamin D levels with ulcerative colitis in chinese han population. Clin Res Hepatol Gastroenterol. 2017;41:110-117.
[30] Xia SL, Yu LQ, Chen H, Hu DY, Shao XX, Guo MD, Jiang LJ, Lin XX, Lin XQ, Jiang Y. Association of vitamin D receptor gene polymorphisms with the susceptibility to ulcerative colitis in patients from southeast china. J Recept Signal Transduct Res. 2015;35:530-535.

APA	Kirac D, Erdem Yaman A, Gezmis H, YESİLCİMEN K, Avcılar T, Güney A, Keleş E, Koc G, Akkanat R, İŞBİR T (2022). VDBP and VDR Mutations May Cause In-Stent Restenosis. , 602 - 606. 10.33808/clinexphealthsci.953893
Chicago	Kirac Deniz,Erdem Yaman Aysun,Gezmis Hazal,YESİLCİMEN KEMAL,Avcılar Tuba,Güney Ahmet İlter,Keleş Elif Çiğdem,Koc Gulsah,Akkanat Rabican,İŞBİR Turgay VDBP and VDR Mutations May Cause In-Stent Restenosis. (2022): 602 - 606. 10.33808/clinexphealthsci.953893
MLA	Kirac Deniz,Erdem Yaman Aysun,Gezmis Hazal,YESİLCİMEN KEMAL,Avcılar Tuba,Güney Ahmet İlter,Keleş Elif Çiğdem,Koc Gulsah,Akkanat Rabican,İŞBİR Turgay VDBP and VDR Mutations May Cause In-Stent Restenosis. , 2022, ss.602 - 606. 10.33808/clinexphealthsci.953893
AMA	Kirac D,Erdem Yaman A,Gezmis H,YESİLCİMEN K,Avcılar T,Güney A,Keleş E,Koc G,Akkanat R,İŞBİR T VDBP and VDR Mutations May Cause In-Stent Restenosis. . 2022; 602 - 606. 10.33808/clinexphealthsci.953893
Vancouver	Kirac D,Erdem Yaman A,Gezmis H,YESİLCİMEN K,Avcılar T,Güney A,Keleş E,Koc G,Akkanat R,İŞBİR T VDBP and VDR Mutations May Cause In-Stent Restenosis. . 2022; 602 - 606. 10.33808/clinexphealthsci.953893
IEEE	Kirac D,Erdem Yaman A,Gezmis H,YESİLCİMEN K,Avcılar T,Güney A,Keleş E,Koc G,Akkanat R,İŞBİR T "VDBP and VDR Mutations May Cause In-Stent Restenosis." , ss.602 - 606, 2022. 10.33808/clinexphealthsci.953893
ISNAD	Kirac, Deniz vd. "VDBP and VDR Mutations May Cause In-Stent Restenosis". (2022), 602-606. https://doi.org/10.33808/clinexphealthsci.953893

APA	Kirac D, Erdem Yaman A, Gezmis H, YESİLCİMEN K, Avcılar T, Güney A, Keleş E, Koc G, Akkanat R, İŞBİR T (2022). VDBP and VDR Mutations May Cause In-Stent Restenosis. Clinical and Experimental Health Sciences, 12(3), 602 - 606. 10.33808/clinexphealthsci.953893
Chicago	Kirac Deniz,Erdem Yaman Aysun,Gezmis Hazal,YESİLCİMEN KEMAL,Avcılar Tuba,Güney Ahmet İlter,Keleş Elif Çiğdem,Koc Gulsah,Akkanat Rabican,İŞBİR Turgay VDBP and VDR Mutations May Cause In-Stent Restenosis. Clinical and Experimental Health Sciences 12, no.3 (2022): 602 - 606. 10.33808/clinexphealthsci.953893
MLA	Kirac Deniz,Erdem Yaman Aysun,Gezmis Hazal,YESİLCİMEN KEMAL,Avcılar Tuba,Güney Ahmet İlter,Keleş Elif Çiğdem,Koc Gulsah,Akkanat Rabican,İŞBİR Turgay VDBP and VDR Mutations May Cause In-Stent Restenosis. Clinical and Experimental Health Sciences, vol.12, no.3, 2022, ss.602 - 606. 10.33808/clinexphealthsci.953893
AMA	Kirac D,Erdem Yaman A,Gezmis H,YESİLCİMEN K,Avcılar T,Güney A,Keleş E,Koc G,Akkanat R,İŞBİR T VDBP and VDR Mutations May Cause In-Stent Restenosis. Clinical and Experimental Health Sciences. 2022; 12(3): 602 - 606. 10.33808/clinexphealthsci.953893
Vancouver	Kirac D,Erdem Yaman A,Gezmis H,YESİLCİMEN K,Avcılar T,Güney A,Keleş E,Koc G,Akkanat R,İŞBİR T VDBP and VDR Mutations May Cause In-Stent Restenosis. Clinical and Experimental Health Sciences. 2022; 12(3): 602 - 606. 10.33808/clinexphealthsci.953893
IEEE	Kirac D,Erdem Yaman A,Gezmis H,YESİLCİMEN K,Avcılar T,Güney A,Keleş E,Koc G,Akkanat R,İŞBİR T "VDBP and VDR Mutations May Cause In-Stent Restenosis." Clinical and Experimental Health Sciences, 12, ss.602 - 606, 2022. 10.33808/clinexphealthsci.953893
ISNAD	Kirac, Deniz vd. "VDBP and VDR Mutations May Cause In-Stent Restenosis". Clinical and Experimental Health Sciences 12/3 (2022), 602-606. https://doi.org/10.33808/clinexphealthsci.953893