NCBI Summary:
Proteins of the matrix metalloproteinase (MMP) family are involved in the breakdown of extracellular matrix in normal physiological processes, such as embryonic development, reproduction, and tissue remodeling, as well as in disease processes, such as arthritis and metastasis. Most MMP's are secreted as inactive proproteins which are activated when cleaved by extracellular proteinases. The encoded protein degrades type IV collagen, fibronectin, fibrinogen, casein, vitronectin, alpha 1-antitrypsin, alpha 2-macroglobulin, and insulin-like growth factor-binding protein 1, and activates MMP9 by cleavage. The protein differs from most MMP family members in that it lacks a conserved C-terminal protein domain. [provided by RefSeq, Jul 2008]
General function
Enzyme
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Cellular localization
Secreted
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Microarray evaluation of endometrial receptivity in Chinese women with polycystic ovary syndrome. Qiao J et al. (2008) Patients with polycystic ovary syndrome (PCOS) have lower pregnancy and higher miscarriage rates, possibly due to decreased endometrial receptivity. In this study, endometrium was processed for RNA extraction and hybridization of chemically fragmented, biotinylated, complementary RNA on high-density oligonucleotide microarrays, and screened for 21,571 genes. Real-time polymerase chain reaction (PCR) was used to verify the result. Genes found to be down-regulated in the endometrium during the implantation window in PCOS patients included those whose activity was integral to membrane function, adhesion, invasive growth and the cytoskeleton. Among these genes, some have previously been associated with endometrial receptivity (by microarray research or other methods) and some have never previously been associated with endometrial receptivity. Using real-time PCR, expression of transmembrane 4 superfamily member 4 (TM4SF4) and matrix metalloproteinase 26 (MMP26) was found to be significantly decreased during the implantation window in patients with PCOS (P= 0.003). TM4SF4 has been demonstrated to be associated with adhesion; MMP26 has been shown to be related to degradation of extracellular matrix. It is suggested the down-regulated gene expression during the implantation window in patients with PCOS indicates differential gene expression in the endometrium between PCOS and normal women during the implantation window. This might affect endometrial receptivity.//////////////////
Ovarian function
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Expression regulated by
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Ovarian localization
Theca, Luteal cells
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Expression of matrix metalloproteinase-26 and tissue inhibitors of metalloproteinase-3 and -4 in normal ovary and ovarian carcinoma. Ripley D et al. The objective of this study was to determine the spatial expression of matrix metalloproteinases (MMPs) and their physiologic inhibitors, the tissue inhibitor of MMP (TIMP)-3 and TIMP-4, in ovarian carcinoma compared to normal ovaries. Immunohistochemistry was carried out in this study. Tissue sections prepared from normal ovarian tissues from throughout the menstrual cycle (N= 20) and ovarian carcinomas (N= 45) characterized as stage I (N= 5), stage III/IV (N= 40) were immunostained using polyclonal antibodies to the latent and the active form of MMP-26, TIMP-3, and a monoclonal antibody to TIMP-4. Immunoreactive MMP-26, TIMP-3, and TIMP-4 were detected in all the ovarian cell types in normal and tumor tissues. In normal ovarian tissues, theca externa and luteal cells immunostained with high intensity for MMP-26 and TIMPs while theca/granulosa cell staining intensity increased as lutenization progressed. There was low immunostaining of the ovarian stromal and surface epithelial cells for MMP-26, with moderate staining for TIMPs. In the carcinoma specimens, cancer cells and vascular endothelial cells displayed the highest staining intensity compared to adjacent nontumor areas. The immunostaining intensity of MMP-26 and TIMP-3 increased with stage of tumor with the invading tumor cells displaying the strongest immunostaining. MMP-26, TIMP-3, and TIMP-4 are expressed in normal ovarian as well as ovarian tumors with elevated expression in the invasive tumor cells suggesting a potential role for MMP-26 in normal ovary and ovarian cancer biologic function.