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the absence of TIMP-3 leads to a more pro-angiogenic microenvironment, playing a key role in choroidal neovascularization formation by positively modulating M2 polarization.
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the aim of this study was to determine whether Acanthamoeba spp. may affect the levels of matrix metalloproteinases (MMP-2,-9), their tissue inhibitors (TIMP-1,-3) and MMP-9/TIMP-1, MMP-2/TIMP-3 ratios in the cerebral cortex and hippocampus, in relation to the host's immunological status.
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The data indicate that hepatic TIMP3 expression can slow the progression of nonalcoholic fatty liver disease and tumorigenesis, at least in part, through the regulation of ADAM17 activity.
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Loss of Timp3 enhanced the susceptibility to iron overload-mediated heart and liver injury, suggesting that Timp3 is a key protective molecule against iron-mediated pathology.
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Loss of TIMP3 is associated with germinal matrix hemorrhage-intraventricular hemorrhage.
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altered cortical and trabecular bone mineralization and increased compositional heterogeneity were found in Timp-3 (-/-) bone, all being indicative of high bone remodeling
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In a clinically relevant CADASIL mouse model, we show that exogenous ADAM17 or HB-EGF restores cerebral arterial tone and blood flow responses, and identify upregulated voltage-dependent potassium channel (KV) number in cerebral arterial myocytes as a heretofore-unrecognized downstream effector of TIMP3-induced deficits.
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TIMP3 promotes normal microvascular endothelial cell barrier function, at least partially, through inhibition of metalloproteinase-dependent disruption of adherens junctions, and septic downregulation of TIMP3 may contribute to septic MVEC barrier dysfunction.
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data strongly suggest that TIMP3 has direct neuroprotective effects that can mitigate the deleterious effects associated with TBI, an area with few if any therapeutic options.
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Elevated levels of TIMP3 and vitronectin, acting downstream of Notch3(ECD) deposition, play a role in CADASIL, producing divergent influences on early CBF deficits and later white matter lesions.
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4-Hydroxyisoleucine improved insulin resistant-like state in 3T3-L1 adipocytes by targeting TACE/TIMP3 and the insulin signaling pathway.
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In a mouse model of prostate cancer, increased tumor growth, proliferation index, increased microvascular density, and invasion was observed in Pten(-/-), Timp3(-/-) prostate tumors compared to Pten(-/-), Timp3(+/+) tumors.
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Timp3 status determines p53, p38 and Notch coactivation to instruct hepatic cell fate and transformation.
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TIMP2 and TIMP3 play fundamental and differential roles in mediating pathological remodelling, independent from their MMP-inhibitory function
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Expansion of stem cells counteracts age-related mammary regression in compound Timp1/Timp3-deficient mice.
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lack of TIMP3 increases inflammation and polarizes macrophages towards a more inflammatory phenotype resulting in increased atherosclerosis.
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TIMP-3 KO mice exhibit enhanced metabolism, as reflected by a higher body temperature than WT mice, possibly due to increased mitochondrial activity.
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TIMP3 protects kidney from damage
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TIMP3 reduction is due, at least in part, to increased expression of certain TIMP3-targeting microRNAs in diabetic kidneys compared to healthy controls.
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Demonstrate a critical role for TIMP3, among all TIMPs, in preserving arterial remodelling in response to Ang II-induced hypertension.