Rabbit Tissue inhibitors of metalloproteinase 4 ELISA Kit

BACKGROUND: This study was aimed at evaluating the gene expression levels of 4 genes in the intracranial aneurysm wall and comparing them with extracranial arteries. The analysis was done using real-time polymerase chain reaction (RT-PCR) and immunohistochemistry (IHC). Also, a correlation of the differential genetic expression was done with various patient clinical and radiologic factors. METHODS: The quantitative assessment of ribonucleic acid levels was done with RT-PCR and was validated with IHC. The genes studied were collagen 1A2 (COL1A2), tissue inhibitor of metalloproteinase 4 (TIMP4), cathepsin B (CTSB), and alpha-1 antitrypsin (alpha-1 AT). The analysis was done on 24 aneurysm sacs and superficial temporal/occipital artery samples from patients undergoing surgical clipping. RESULTS: The mean fold change of COL1A2 in the aneurysm sample was 8.89, that of TIMP4 was 10.16, that of CTSB was 1.02, and that of alpha-1 ATwas 1.46 when compared with normal control vessel on PCR. On semiquantitative IHC, COL1A2 was 94.44%, alpha-1 AT was 77.8% overexpressed, CTSB was positive in 50%, and the expression of TIMP4 was 94.4% underexpressed in aneurysmal walls. There was no statistically significant correlation between patient profile and gene expression. CONCLUSIONS: On RT-PCR and IHC analysis, COL1A2and alpha-1 AT were overexpressed, CTSB was marginally overexpressed, and TIMP4 had equivocal expression in the aneurysmal sac when compared with the normal extracranial vessel. This is the first study of its kind in the Indian population with the largest sample size on live human patients.

Neuroinflammation can damage the brain and plays a critical role in the pathophysiology of epilepsy. Tissue inhibitor of metalloproteinase 4 (TIMP4) is an inflammation-induced apoptosis and matrix turnover factor involved in several neuronal disorders and inflammatory diseases. Evidence has shown linkage disequilibrium between rs3755724 (-55C/F) of this gene with synapsin 2 (SYN2) rs3773364 and peroxisome proliferator-activated G receptor (PPARG) rs2920502 loci, which contribute to epilepsy in Caucasians. The aim of this study was to examine the association of these loci alone or their haplotypes with the risk of epilepsy in the Malaysian population. Genomic DNA of 1241 Malaysian Chinese, Indian, and Malay subjects (670 patients with epilepsy and 571 healthy individuals) was genotyped for the candidate loci by using the Sequenom MassArray method. Allele and genotype association of rs3755724 with susceptibility to epilepsy was significant in the Malaysian Chinese with focal epilepsy under codominant and dominant models (C vs. T: 1.5 (1.1-2.0), p = 0.02; CT vs. TF: 1.8 (1.2-2.8),p = 0.007 and 1.8 (1.2-2.7),p = 0.006, respectively). The T allele and the TT genotype were more common in patients than in controls. No significant association was found between rs2920502 and rs3773364-rs3755724-rs2920502 haplotypes for susceptibility to epilepsy in each ethnicity. This study provides evidence that the promoter TIMP4 rs3755724 is a new focal epilepsy susceptibility variant that is plausibly involved in inflammation-induced seizures in Malaysian Chinese. (C) 2014 Elsevier B.V. All rights reserved.