Functional polymorphisms in matrix metalloproteinase-1 and monocyte chemoattractant protein-1 and rheumatoid arthritis

Abstract

The aim of this study is to investigate whether the functional polymorphisms in the promoter of matrix metalloproteinase-1 (MMP-1) and in the regulatory region of the monocyte chemoattractant protein-1 (MCP-1) gene are associated with susceptibility to rheumatoid arthritis (RA) and its clinical features. The MMP-1 1G/2G polymorphism and the MCP-1 promoter A/G polymorphism were determined by polymerase chain reaction-restriction fragment length polymorphism in 117 RA patients and 97 healthy controls. The genotype distribution of the MMP-1 promoter did not differ between RA patients and control subjects. However, in the 2G/2G genotype, ESR and Plat were higher than the 1G/1G genotype. The genotype distribution of the MCP-1 promoter did not differ between the RA and control groups. Clinically there was no significant difference among RA patients according to the MCP-1 promoter genotypes. Our data show that the functional promoter polymorphism in the MMP-1 promoter may not play an important role in the susceptibility of RA, but the polymorphism may be related to clinical phenotypes.

Pro‐inflammatory genetic profiles in subjects with peripheral arterial occlusive disease and critical limb ischemia

“…Likewise, the E‐sel Ser128Arg gene polymorphism can functionally alter leukocyte‐endothelial interactions [13, 17]. These important biological effects have, not surprisingly, relevant clinical consequences, as indicated by the effects that these gene polymorphisms may exert on the onset and severity of several clinical pathologic conditions, including CVDs [17, 23–27].…”

“…DNA was extracted from peripheral blood and assayed by PCR–RFLP for the detection of the CRP 1059 G/C, IL‐6 ‐174 G/C, MIF ‐173 G/C, MCP‐1 –2518 A/G, E‐Sel Ser128Arg, ICAM‐1 469 E/K, MMP‐1 ‐1607 1G/2G, MMP‐3 ‐1171 5A/6A, and MMP‐9 ‐1563 C/T gene polymorphisms, as previously described [20–28].…”

Identification of a potential proinflammatory genetic profile influencing carotid plaque vulnerability

“…DNA was extracted from peripheral blood and assayed by polymerase chain reaction-restriction fragment length polymorphism to detect the CRP (-1059 G/C), IL-6 (-174 G/C), IL-1b (-31 T/C), TNF-a (-308 G/A), MIF (-173 G/C), CCL2 (-2518 A/G), CCL3 (-906 T/A), SELE (Ser128Arg), ICAM-1 (469 E/K), MMP-3 (-1171 5 A/6A), and MMP-9 (-1562 C/T) gene polymorphisms, as previously reported. [19][20][21][22][23][24][25][26][27] Histologic assays. After endarterectomy, carotid plaque was briefly rinsed in saline solution, immersed in buffered 10% formalin fixative and then in formic acid (a decalcifying solution), and subsequently sectioned.…”

Effect of Proinflammatory Gene Polymorphisms on the Risk of Alzheimer's Disease

“…DNA was extracted from peripheral blood and assayed by PCR-RFLP for the detection of the CRP 1059 G/C, IL6 -174 G/C, IL1B -31 T/C, TNF-α -308 G/A, MIF -173 G/C, CCL2 -2518 A/G, CCL3 -906 T/A, SELE Ser128Arg, ICAM1 469 E/K, MMP3 -1171 5A/6A, and MMP9 -1562 C/T gene polymorphisms, as previously described [15,16,17,18,19,20,21,22,23]. …”