Disease relevance of Ecm1

• The findings of this study will shed a new light into the pathogenesis of cerebral aneurysms and highlight the importance of inflammatory response causing the degeneration of extracellular matrix in the process of this disease [1].
• BACKGROUND: CD26 is a T-cell co-stimulator, and interacts with adenosine deaminase, human immunodeficiency virus (HIV) Tat-1 protein and extracellular matrix [2].
• We have used an animal model of acute mesangial proliferative glomerulonephritis to show that this disease is associated with increased production and activity of transforming growth factor beta 1 (TGF-beta 1), an inducer of extracellular matrix production [3].
• Glomerulonephritis is an inflammation of the kidney characterized by the accumulation of extracellular matrix within the damaged glomeruli, impaired filtration and proteinuria [3].
• Progression of pulmonary hypertension is associated with increased serine elastase activity and the proteinase-dependent deposition of the extracellular matrix smooth muscle cell survival factor tenascin-C (refs. 1,2) [4].

Psychiatry related information on Ecm1

• Such increase in ECM protein expression as well as astrocyte permissiveness to neurite outgrowth was reversed by the specific EGF receptor tyrosine kinase inhibitor, tyrphostin [5].
• A growing amount of evidence indicates the involvement of extracellular matrix components, especially laminins, in the development of Alzheimer's disease, although their role remains unclear [6].
• OBJECTIVE: To observe the extracellular matrix modifications and quantify the structural alterations of the aortic wall in spontaneously hypertensive rats (SHR) submitted to an aerobic physical activity (PA) protocol [7].

High impact information on Ecm1

• We show here that the interaction of integrins with extracellular matrix at the newly formed cell front leads to the activation and polarized recruitment of Cdc42, which in turn recruits and activates a cytoplasmic mPar6/PKCzeta complex [8].
• The phenotypic changes involving both increased adhesion to ECM and inhibition of apoptosis were reversed by sulindac sulfide (a COX inhibitor) [9].
• Transforming growth factor-beta (TGF-beta) increases the steady-state RNA levels of several fibroblast extracellular matrix proteins [10].
• Of the extracellular matrix proteins compared, tenascin is the least effective substrate for attachment of primary mammary tumor cells, but the most effective in promoting cell growth after serum is removed from the culture medium [11].
• The extracellular matrix protein tenascin (previously described as myotendinous antigen) is selectively present in the mesenchyme surrounding fetal rat mammary glands, hair follicles, and teeth, three organ anlagen where the mesenchyme is essential for development [11].

Chemical compound and disease context of Ecm1

• Angiotensin II (AII) is a critical factor in cardiac remodeling which involves hypertrophy, fibroblast proliferation, and extracellular matrix production [12].
• In adult rat brain the extracellular matrix glycoprotein, laminin, is found only in basement membranes, but is transiently expressed by astrocytes after brain injury [13].
• Unlike cultured hepatocytes, the hepatoma cells did not deposit these proteoglycans into an extracellular matrix, and most of the newly synthesized heparan sulfate proteoglycans were secreted into the culture medium [14].
• Cell contact with the extracellular matrix component hyaluronic acid (HA) plays an important role in many developmental, physiological, and pathological processes, although the regulation of this contact is poorly understood [15].
• The prevention of arterial stiffening and cardiac hypertrophy in the absence of changes in collagen and elastin content suggests that the effect of aminoguanidine is related to a decrease in the AGE-induced cross-linking of the extracellular matrix [16].

Biological context of Ecm1

• Carvedilol at doses that inhibited PDGF-induced cell proliferation, inhibited ECM synthesis, cellular ROS, or subsequent MAPK activation [17].
• Adhesion molecules, chemokine, and extracellular matrix gene expression were evaluated by Northern blotting [18].
• Tissue transglutaminase (tTG) is a Ca(2+)-dependent enzyme which stabilizes the extracellular matrix (ECM) through post-translational modification, and may play an important role in the pathogenesis of focal and segmental glomerulosclerosis (FSGS) [19].
• Minocycline inhibits inflammation, apoptosis and extracellular matrix degradation [20].
• Alternative splicing may serve as a mechanism for generating functional diversity in the Ecm1 gene [21].

Anatomical context of Ecm1

• BACKGROUND: Vascular smooth muscle cell (VSMC) proliferation, migration, and extracellular matrix (ECM) synthesis are major pathologic features of chronic allograft vasculopathy [17].
• Accumulation of glomerular macrophages, proliferation of mesangial cells, and deposition of extracellular matrix proteins are pathobiological hallmarks of GN [18].
• As the uterus returns to its prepregnancy state, the involuting uterus undergoes a rapid reduction in size primarily due to the degradation of the extracellular matrix, particularly collagen [22].
• To investigate this we have studied in vitro the interaction of anti-BP effector T lymphocytes with the basement membrane-like extracellular matrix produced by vascular endothelial cells [23].
• Pulmonary artery pressure and muscularization were reduced by myocyte apoptosis and loss of extracellular matrix, specifically elastin and tenascin-C [4].

Associations of Ecm1 with chemical compounds

• The present study was designed to examine the effect of carvedilol on platelet-derived growth factor (PDGF)-induced ECM synthesis in rat VSMCs [17].
• It has been assumed that SMCs derived from the outer medial layer migrate, proliferate and synthesize extracellular matrix components on the luminal side of the vessel [24].
• It contains six C2 domains and also shares three type III domains with the extracellular matrix adhesion molecule fibronectin [25].
• We found that merlin mediates contact inhibition of growth through signals from the extracellular matrix [26].
• We hypothesized that integrin-mediated interactions with extracellular matrix components of the skin and lymph node may regulate LC/DC migration [27].

Physical interactions of Ecm1

• Previous findings have described the reduction in affinity of IGFBP-5 for IGFs that occurs after complexation of the binding protein with heparin or other components of the extracellular matrix (ECM) and have postulated that such an interaction may result in conformational changes in protein structure, affecting subsequent IGF interaction [28].
• Together, these results indicate GATA-2 regulation of the MMP-2 promoter in endothelial cells and that the GATA-2 binding domain is sufficient to drive increased activity of the MMP-2 promoter in response to an extracellular matrix stimulus [29].
• BEHAB (brain-enriched hyaluronan-binding protein)/brevican is the most abundant chondroitin sulfate proteoglycan in the extracellular matrix of the adult rat brain [30].
• The present study tested the hypothesis that matrix vesicle enzymes are also involved in the release of the large latent TGF-beta1 complex stored in the extracellular matrix [31].
• We recently suggested that the transferrin (Tf)-gallium-67 (67Ga) complex dissociated on the surface of the hepatocytes after partial hepatectomy and free 67Ga bound to heparan sulfate in the extracellular matrix [32].

Enzymatic interactions of Ecm1

• In addition, we show that other focal adhesion proteins such as talin and vinculin do not become tyrosine-phosphorylated under the same conditions of cell spreading on extracellular matrix proteins [33].
• The presence of talin and extracellular matrix receptor in podosomes together with the adhesive properties of these actin-containing structures argues against the hypothesis that pp60src affects the interaction of actin with the plasma membrane by phosphorylating the fibronectin receptor and/or other associated proteins [34].
• Lysyl oxidase is an extracellular enzyme that catalyzes cross-linkages of extracellular matrix proteins [35].
• Paxillin is known to be tyrosine phosphorylated following adhesion to the extracellular matrix in many types of cells [36].
• The docking protein p130Cas becomes phosphorylated upon cell adhesion to extracellular matrix proteins, and is thought to play an essential role in cell transformation [37].

Regulatory relationships of Ecm1

• Carvedilol inhibits platelet-derived growth factor-induced extracellular matrix synthesis by inhibiting cellular reactive oxygen species and mitogen-activated protein kinase activation [17].
• In conclusion, Ets-1 promotes degradation of ECM proteins and is critical for integral glomerular reorganization [38].
• CTGF is able to promote VSMC proliferation and migration and influences the composition of extracellular matrix [39].
• Neuritogenesis induced by thyroid hormone-treated astrocytes is mediated by epidermal growth factor/mitogen-activated protein kinase-phosphatidylinositol 3-kinase pathways and involves modulation of extracellular matrix proteins [5].
• BACKGROUND: Transforming growth factor beta (TGF-beta) regulates hepatocyte proliferation and biosynthesis of the extracellular matrix [40].

Other interactions of Ecm1

• In contrast, knockdown of Ets-1 in glomeruli resulted in severe ECM deposition in diseased glomeruli [38].
• In cultures of fetal rat calvarial cells, which form mineralized bonelike nodules, both LTBP and the TGF-beta 1 precursor localized to large fibrillar structures in the extracellular matrix [41].
• Immunoreactivity for both aFGF and bFGF was positive and similar in the cytoplasm, nuclei, and extracellular matrix of cells of neuroectodermal and mesodermal origin, while it was negative in endoderm-derived cells [42].
• Reelin (Reln) is a protein with some structural analogies with other extracellular matrix proteins that functions in the regulation of neuronal migration during the development of cortical laminated structures [43].
• HB-GAM is a secretory, extracellular matrix-associated protein that was isolated by screening for factors that enhance neurite outgrowth in rat brain neurons [44].

Analytical, diagnostic and therapeutic context of Ecm1

• The distribution in the F344 rat liver of two extracellular matrix and basement membrane components, fibronectin and laminin, was studied by immunofluorescence [45].
• Most of the ECM glycoproteins were recovered in the region of 200,000 (200K) on gel chromatography [46].
• RESULTS: Coating of cells with extracellular matrix components before transplantation did not enhance cell engraftment [47].
• Gene expression of ECM proteins was measured by conventional and real-time reverse-transcription polymerase chain reaction (RT-PCR) [48].
• Cellular fibronectin was localized in the cytoplasm and on the surface of cultured fat-storing cells as well as in extracellular matrix fibrils by indirect immunofluorescence [49].

References