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While identifying the cellular pathologic mechanisms underlying the murine mutant (MT)-COMP model of pseudoachondroplasia, increased midline-1 (MID1) expression and mammalian target of rapamycin complex 1 (mTORC1) signaling was found.
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COMP N-terminus directly interacted with the EGF11-12 domain of Notch1 and activated Notch1 signaling, as evidenced by co-immunoprecipitation and mammalian two-hybrid assay. In conclusion, COMP served as a potential ligand of Notch1, thereby driving embryonic stem cell (ESC)-vascular smooth muscle cells (VSMCs) differentiation.
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presents the expression levels of ADAMTS-7 and COMP in the decidual tissues of mice and humans suffering from SA.
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Of the six biomarkers, only COMP and DPP4 showed high and SPP1 moderate correlation with the spinal muscular atrophy phenotype. PLS3 overexpression neither influenced the SMN level nor the six biomarkers, supporting the hypothesis that PLS3 acts as an independent protective modifier.
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Study describes a novel mechanism by which the deleterious consequences of mutant COMP retention results in upregulation of miR-223 disturbing the adipogenesis - osteogenesis balance. This results in reduction in bone mineral density, bone quality, mechanical strength and subchondral bone thickness which align with the pseudoachondroplasia phenotype.
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COMP could normally have a protective role against PASMC phenotype switching
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these findings revealed the essential role of COMP in retarding the development of vascular aging and vascular smooth muscle cell senescence.
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COMP deficiency drove macrophages toward the atherogenic phenotype and thereby aggravated atherosclerotic calcification.
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COMP forms a complex with collagens intracellularly that is a prerequisite for collagen secretion.
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The accumulation and thereby the functionality of thrombospondin in extracellular matrix is controlled by concentration-dependent, intermolecular "matrix trapping" mechanism.
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COMP-Ang1 can enhance BMP2-induced cranial bone regeneration with increased pericyte recruitment. Combined delivery of the proteins might be a therapeutic strategy to repair cranial bone damage.
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COMP deficiency shortened tail-bleeding and clotting time and accelerated ferric-chloride-induced thrombosis. COMP specifically inhibited thrombin-induced platelet aggregation, activation, and retraction and the thrombin-mediated cleavage of fibrinogen.
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COMP immunoreactivity was observed in about half of the investigated plaques from the ApoE null mice, mainly located along the intima-medial border. Plaques in the brachiocephalic artery from ApoE mice lacking COMP were increased in size with 54%.
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study will facilitate better awareness of the differential diagnoses that might be associated with the PSACH/MED spectrum and subsequent care of PSACH/MED patients
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The lack of arthritis, together with high levels of COMP-specific antibodies, in COMP-deficient mice indicates that susceptibility to arthritis is COMP specific and that endogenous expression of COMP in wild-type mice tolerizes B cells in vivo.
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results imply that COMP is not a key upstream mediator of the anabolic effects of ML on the skeleton.
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Lack of COMP and matrilin 3 leads to increased deposition of TIMP-3, which causes partial inactivation of matrix metalloproteinases in bone, including MMP-13.
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A novel form of chondrocyte stress triggered by the expression of a human-like mutation in COMP is central to the pathogenesis of pseudoachondroplasia.
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reducing steady state levels of COMP mRNA alleviates intracellular retention of other extracellular matrix proteins associated with the pseudoachondroplasia cellular pathology
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Data show that cartilage oligomeric matrix protein (COMP) promotes cell attachment via independent mechanisms involving cell surface CD47 and alphaVbeta3 integrin and that cell attachment to COMP induces formation of fascin-stabilized actin microspikes.