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The present work was designed to assess nine putative functional non-coding <jats:italic>SELP<\/jats:italic> variants in relation to sP-selectin levels and arterial stiffness in T2DM.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>The genetic distribution of rs3917655, rs3917657, rs3917739, rs2235302, rs3917843 was determined by restriction fragment length polymorphism\u2013polymerase chain reaction (RFLP-PCR). Genotyping of rs3917779 was performed by tetra primer amplification-refractory mutation system (ARMS)- PCR. Three SNPs i.e. rs3917853, rs3917854, rs3917855 were genotyped by Sanger sequencing. Construction of haplotypes was performed using PHASE software. The data thus obtained was analyzed by appropriate statistical tools.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>Two non-coding variants i.e. rs3917657 and rs3917854 of <jats:italic>SELP<\/jats:italic> were found to be associated with 2 and 1.7 -fold risk of disease development respectively. However, one non-coding variant rs2235302 was found to provide protection against disease development. Furthermore, variant allele of rs3917854 in T2DM patients was found to be associated with 2.07-fold very high vascular risk. Non-coding haplotype GCAGGCCGC was conferring 4.14-fold risk of disease development. Furthermore, overall sP-selectin levels were higher in T2DM patients when segregated according to genotypes as well as haplotypes. Significant genotype- phenotype correlation was observed for rs3917655 as well as rs3917739 variant in patients and for rs3917854 in controls. In vascular risk categories, a significant genotype- phenotype correlation was observed for rs3917655 and rs2235302. Furthermore, patients with CCGGGCCGC haplotype in high risk category were observed with higher levels of sP-selectin as compared to other haplotypes (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05).<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusions<\/jats:title>\n                <jats:p>Non-coding <jats:italic>SELP<\/jats:italic> variants may significantly modulate sP-selectin levels, vascular risk and T2DM susceptibility.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s12902-020-00548-x","type":"journal-article","created":{"date-parts":[[2020,5,19]],"date-time":"2020-05-19T09:02:53Z","timestamp":1589878973000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Putative functional non-coding polymorphisms in SELP significantly modulate sP-selectin levels, arterial stiffness and type 2 diabetes mellitus susceptibility"],"prefix":"10.1186","volume":"20","author":[{"given":"Raminderjit","family":"Kaur","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jatinder","family":"Singh","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rohit","family":"Kapoor","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Manpreet","family":"Kaur","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2020,5,19]]},"reference":[{"key":"548_CR1","doi-asserted-by":"publisher","first-page":"2134","DOI":"10.1001\/jama.2008.623","volume":"300","author":"H Ogawa","year":"2008","unstructured":"Ogawa H, Nakayama M, Morimoto T, et al. 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