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biglycan is a novel high-affinity ligand for CD14, a well-known GPI-anchored co-receptor for TLRs.
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Transcriptomic profiling of hypothalamus, hippocampus, and liver supported the regulatory action of Bgn on key molecular pathways involved in metabolism, immune response, and neuronal plasticity. Overall results underscore the tissue-specific role of the extracellular matrix in the regulation of metabolism and brain function, and support Bgn as a key modulator for the impact of fructose across body and brain.
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our data indicates that Bgn and Fmod expressed by the bone forming cells, are novel coupling ECM components that control bone mass through sequestration of TNFalpha and/or RANKL, thereby adjusting their bioavailability in order to regulate osteoclastogenesis.
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Bgn deficiency led to abrogation of contact hypersensitivity responses.
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The increased atherosclerosis in biglycan deficient mice does not appear to be due to elevations in TGF-beta.
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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.