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PDGFR alpha beta and PDGFR beta beta dimers were strong inducers of random and directionally-persistent migration in mouse skin fibroblast, respectively, that was sustained for up to 24 h.
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PDGFRbeta was activated around the injury site after experimental traumatic brain injury (TBI), and primarily expressed in astrocytes, microglia, OPC and leukocytes in the boundary of the lesion site, suggesting PDGFRbeta was involved in glial scar formation. Then the PDGFR inhibitor (AG1296) was administered following TBI. Reactive astrocytes were significantly inhibited in AG1296-treated mice.
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Increasing the adipogenic capacity of Pdgfrbeta(+) precursors through Pparg overexpression results in healthy visceral white adipose tissue expansion in obesity and adiponectin-dependent improvements in glucose homeostasis.
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PDGFRalpha/PDGFRbeta signaling balance determines progenitor commitment to beige (PDGFRalpha) or white (PDGFRbeta) adipogenesis.
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The data of this study revealed an acute accumulation of PDGFRbeta+ BBB-related cells in degenerating brain areas, which can be long lasting, suggesting an active role for PDGFRbeta-signaling in blood vessel and post-injury tissue recovery.
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Ltbp4 regulates Pdgfrb expression via TGFbeta-dependent modulation of Nrf2 transcription factor function.
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Beta platelet-derived growth factor is induced in hepatic stellate cells (HSCs) following surgical partial hepatectomy, and its deletion in HSCs leads to prolonged liver injury in mice. However, there is no significant difference in liver regeneration.
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The results provide functional evidence that elevated PDGFRbeta signaling causes tissue wasting or overgrowth reminiscent of human genetic syndromes and that the STAT1 pathway is a crucial modulator of this phenotypic spectrum.
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Identify PDGFRbeta as a driver in activating Akt/mTORC1 nexus for high glucose-mediated expression of collagen I (alpha2) in proximal tubular epithelial cells, which contributes to tubulointerstitial fibrosis in diabetic nephropathy.
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Data show that three platelet-derived growth factor receptor beta (PDGFRB) mutants (R561C, P660T and N666K) were able to transform NIH3T3 and Ba/F3 cells to different extents.
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data therefore collectively suggest that upon TGFbeta stimulation, SP1 recruits SMAD2 to the promoter of Pdgfrb to up-regulate its expression and thus Pdgfrb is a direct downstream target of the TGFbeta/SMAD2 signaling
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PdgfrbetaF7/F7 mice between 4-6 and 36-48 weeks of age developed a region-dependent loss in pericyte coverage (22-46, 24-44 and 4-31%) and cell numbers (36-49, 34-64 and 11-36%), reduction in capillary length (20-39, 13-46 and 1-30%), and an increase in extravascular fibrinogen-derived deposits (3.4-5.2, 2.8-4.1 and 0-3.6-fold) demonstrating BBB breakdown in the cortex, hippocampus and thalamus, respectively.
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PDGF-B-PDGFRbeta signaling plays a significant role in the development of adipose tissue neovascularization.
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there is great possibility that EPCs overexpressing PDGFR-beta enhanc VSMC apoptosis and suppress VSMC migration by competitive consumption of PDGF-BB in the early phase after carotid artery injury in mice.
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PDGFRalpha and PDGFRbeta are coexpressed in the craniofacial mesenchyme of mid-gestation mouse embryos and that ablation of Pdgfrb in the neural crest lineage results in increased nasal septum width, delayed palatal shelf development, and subepidermal blebbing.
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The results from this study indicate that PDGF signaling is required for fiber hypertrophy, extracellular matrix production, and angiogenesis that occur during muscle growth.
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Data show that oligodendrocyte transcription factor 2 (Olig2) deletion causes platelet-derived growth factor receptor (PDGFR) downregulation and reciprocal epidermal growth factor receptor (EGFR) upregulation.
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Decreased expression of PDGFR-beta in vascular smooth muscle cells was associated with thrombosis in vivo.
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Our results highlight the need for careful interpretation of lineage tracing using constitutive Cre lines that cannot discriminate active from historical expression. The early vascular targeting by the Pdgfrb-Cre also warrants consideration for its use in studies of mural cells
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Pdgfrbeta(+) cells do not significantly contribute to the initial cold-induced recruitment of beige adipocytes in WAT; it is only after prolonged cold exposure that these cells differentiate into beige adipocytes.
