Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.17 (MMP-3)
 3,419 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent gene targeting studies indicate that the plasminogen system is implicated in cell migration and matrix degradation during arterial neointima formation and atherosclerotic aneurysm formation. This study examined whether plasmin proteolysis is involved in accelerated posttransplant arteriosclerosis (graft arterial disease). Donor carotid arteries from wild-type B10.A2R mice were transplanted into either plasminogen wild-type (Plg+/+) or homozygous plasminogen-deficient (Plg-/-) recipient mice with a genetic background of 75% C57BL/6 and 25% 129. Within 15 d after allograft transplantation, leukocytes and macrophages infiltrated the graft intima in Plg+/+ and Plg-/- recipient mice to a similar extent. In Plg+/+ recipients, the elastic laminae in the transplant media exhibited breaks through which macrophages infiltrated before smooth muscle cell proliferation, whereas in Plg-/- recipients, macrophages failed to infiltrate the transplant media which remained structurally more intact. After 45 d of transplantation, a multilayered smooth muscle cell-rich transplant neointima developed in Plg+/+ hosts, in contrast to Plg-/- recipients, in which the transplants contained a smaller intima, predominantly consisting of leukocytes, macrophages, and thrombus. Media necrosis, fragmentation of the elastic laminae, and adventitial remodeling were more pronounced in Plg+/+ than in Plg-/- recipient mice. Expression of the plasminogen activators (PA), urokinase-type PA (u-PA) and tissue-type PA (t-PA), and expression of the matrix metalloproteinases (MMPs), MMP-3, MMP-9, MMP-12, and MMP-13, were significantly increased within 15 d of transplantation when cells actively migrate. These data indicate that plasmin proteolysis plays a major role in allograft arteriosclerosis by mediating elastin degradation, macrophage infiltration, media remodeling, medial smooth muscle cell migration, and formation of a neointima.
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PMID:Reduced transplant arteriosclerosis in plasminogen-deficient mice. 981 64

Increased synthesis and secretion of the matrix metalloproteinase has been associated with the acquisition of the invasive properties of malignant cells. In a rat malignant anaplastic cell line (T952/F7) sporadic expression of mRNA for collagenase-3 against a background of high transin-l mRNA has been shown. Sporadic induction of either metalloproteinase was not found in the benign precursor cells (A5P/B10) of T952/F7 cells, but a coordinate mRNA induction profile for these two genes could be induced by the addition of 12-O-tetradecanoylphorbol-13-acetate. In a different uncloned neoplastic epithelial cell line (BCl) fluctuations in the levels of collagenase and transin appeared coordinately, but coordinate expression was not a feature in cloned lines derived from BCl. The loss of coordinate regulation of the two matrix metalloproteinases may relate to the variability in metastatic potential seen in clonal cell lines.
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PMID:Non-coexpression of collagenase and transin in malignant epithelial cells. 2153 21