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Knockout results provide evidence that decorin and biglycan are necessary for maintaining collagen fibril structure, fiber realignment, and mechanical properties of mature tendons.
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A novel biological pathway has been discovered of soluble biglycan inducing HIF-2alpha protein stabilization and Epo production presumably in an oxygen-independent manner, ultimately giving rise to secondary polycythemia.
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Results show that Bgn plays a role in the process of angiogenesis during fracture healing, and that effect appears to be partially mediated through endostatin suppression.
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Asporin deficiency changes skin glycosaminoglycan composition, and decorin and biglycan content, which may explain the changes in skin mechanical properties.
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Biglycan plays a protective role during the progression of atherosclerosis in ApoE-deficient mice by inhibiting thrombin generation.
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These genes were concordantly induced by TAC in WT but not in biglycan KO mice. CONCLUSIONS: Left ventricular pressure overload induces biglycan expression in cardiac fibroblasts. Ablation of biglycan improves cardiac function and attenuates left ventricular hypertrophy and fibrosis after long-term pressure overload.
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Importance of biglycan and decorin as targets for the manipulation of fetal membrane extracellular matrix stability in the context of inflammation.
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Biglycan deficiency leads to loosely packed aortic collagen fibers, increased susceptibility of aortic elastin fibers to angII-induced stress, and up-regulation of vascular perlecan content.
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Biglycan signaling supported fetal membrane remodeling during early gestation in the absence of concomitant changes in TGFbeta levels.
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Lumican and biglycan influence corneal keratocyte lamellipodia organization and are critical in the regulation of stromal collagen fibrillogenesis.
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Biglycan-triggered TLR-2- and TLR-4-signaling exacerbates the pathophysiology of ischemic acute kidney injury.
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De novo expression of circulating biglycan evokes an innate inflammatory tissue response via MyD88/TRIF pathways.
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Early stage patellar tendon healing was inferior in biglycan-null and decorin-null mice as compared to wild type.
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This suggests that biglycan and decorin may have sequential roles in the tendon response to injury.
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Mast cell chymase degrades the alarmins heat shock protein 70, biglycan, HMGB1, and interleukin-33 (IL-33) and limits danger-induced inflammation.
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extracellular matrix biglycan mediates breast cancer normalization induced by embryonic mesenchyme
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Biglycan plays a role in tendon viscoelasticity that cannot be completely explained by its role in collagen fibrillogenesis.
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Biglycan deletion alters adiponectin expression in murine adipose tissue and 3T3-L1 adipocytes.
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The glycosaminoglycans chains of biglycan (BGN) promote BGN-assisted BMP-4 function.
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Bgn inhibits the major properties of HER-2/neu-transformed cells, which is inversely modulated by the PKC signaling cascade.
