Anti-MMP25 polyclonal antibody

Objective: Endogenous activation of matrix metalloproteinase (MMP) in human fetal membranes is hypothesized to contribute to membrane weakening leading to early rupture and is also involved in the initiation of labor. Our laboratory and several others have studied the source and action of some of these MMPs. The objective of this study is to document the expression pattern of most of the MMPs cloned and sequenced so far in amniochorion during preterm premature rupture of membranes (pPROM), at term not in labor and during term labor. Materials and Methods: Placentas were collected from women with PROM, term not in labor after C-sections and from women after term vaginal delivery. Membranes were separated from the placenta and a section away from the rupture site was selected. Amniochorion were separated from the placenta. RT-PCR was performed to study the expression pattern of MMP15 (MT2-MMP), MMP16 (MT3-MMP), MMP17 (MT4-MMP), MMP18, MMP20, MMP23, MMP24 (MT5-MMP), MMP25 (MT6-MMP), and MMP 26 using specific primers. Results: A differential pattern of expression was noted for some of the novel MMPs screened in this study in human fetal membranes. mRNA for most of the MMPs were expressed by amniochorion. MMP16 [membrane type metalloproteinase 3], MMP20 [enamelysin], and MMP26 [matrilysin] were not expressed. Conclusion: Amniochorion expresses several of the MMP genes at the time of pPROM, term not in labor and during active labor. We have previously reported the expression pattern of other MMPs and their inhibitors and their potential role in PROM. These findings support our hypothesis that amniochorion has a fully functional MMP system.

Bronchopulmonary dysplasia (BPD) is a complex disorder resulting from interactions between genes and the environment. The accurate molecular etiology of BPD remains largely unclear. This study aimed to identify key BPD-associated genes and pathways functionally enriched using weighted gene co-expression network analysis (WGCNA). We analyzed microarray data of 62 pre-term patients with BPD and 38 pre-term patients without BPD from Gene Expression Omnibus (GEO). WGCNA was used to construct a gene expression network, and genes were classified into definite modules. In addition, the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses of BPD-related hub genes were performed. Firstly, we constructed a weighted gene co-expression network, and genes were divided into 10 modules. Among the modules, the yellow module was related to BPD progression and severity and included the following hub genes:MMP25,MMP9,SIRPA,CKAP4,SLCO4C1, andSLC2A3; and the red module included some co-expression molecules that displayed a continuous decline in expression with BPD progression and included the following hub genes:LEF1,ITK,CD6,RASGRP1,IL7R,SKAP1,CD3E, andICOS. GO and KEGG analyses showed that high expression of inflammatory response-related genes and low expression of T cell receptor activation-related genes are significantly correlated with BPD progression. The present WGCNA-based study thus provides an overall perspective of BPD and lays the foundation for identifying potential pathways and hub genes that contribute to the development of BPD.