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Characterization of SIS3, a Novel Specific Inhibitor of Smad3, and Its Effect on Transforming Growth Factor-β1-Induced Extracellular Matrix Expression
TLDR
SIS3 completely diminished the constitutive phosphorylation of Smad3 as well as the up-regulated type I collagen expression in scleroderma fibroblasts, suggesting that SIS3 is a useful tool to evaluate the TGF-β-regulated cellular mechanisms via selective inhibition ofSmad3.
Suppressed NFAT-dependent VEGFR1 expression and constitutive VEGFR2 signaling in infantile hemangioma
TLDR
Normalization of the constitutive VEGfr2 signaling in hemECs with soluble VEGFR1 or antibodies that neutralize VEGF or stimulate β1 integrin suggests that local administration of these or similar agents may be effective in hemangioma treatment.
Impaired IL-17 Signaling Pathway Contributes to the Increased Collagen Expression in Scleroderma Fibroblasts
TLDR
IL-17A signaling, not IL-17F, has an antifibrogenic effect via the upregulation of miR-129-5p and the downregulation of connective tissue growth factor and α1(I) collagen, which may lead to a new therapeutic approach for this disease.
Tenascin-C upregulation by transforming growth factor-β in human dermal fibroblasts involves Smad3, Sp1, and Ets1
TLDR
Findings demonstrate the existence of a novel, functional binding element in the proximal region of the TN-C promoter mediating responsiveness to TGF-β involving Smad3/4, Sp1, Ets1, and CBP/p300.
Increased Expression of Integrin αvβ5 Induces the Myofibroblastic Differentiation of Dermal Fibroblasts
TLDR
These data identify a novel mechanism for the establishment of autocrine TGF-β signaling in dermal fibroblasts by the up-regulation of αvβ5 and suggest the possibility of regulating fibrotic disorders, especially scleroderma, by targeting this integrin.
Characterization of monocyte/macrophage subsets in the skin and peripheral blood derived from patients with systemic sclerosis
TLDR
This is the first report indicating CD163+ or CD204+ activated macrophages may be one of the potential fibrogenic regulators in the SSc skin, and suggests a portion of PBMCs in SSc patients abnormally differentiates into CD14brightCD163+CD204+ subset.
The Downregulation of microRNA let-7a Contributes to the Excessive Expression of Type I Collagen in Systemic and Localized Scleroderma
TLDR
It is demonstrated let-7a expression was downregulated in SSc and LSc skin both in vivo and in vitro, compared with normal or keloid skin and it was revealed that the intermittent overexpression of let- 7a in the skin by i.p. miRNA injection improved the skin fibrosis induced by bleomycin in mice.
Clinical and laboratory features of scleroderma patients developing skeletal myopathy
TLDR
It is suggested that the SSc patients with severe internal organ involvement, such as pulmonary fibrosis and heart disease, and some other complications were prone to develop skeletal myopathy during their clinical course of the disease.
Down-Regulation of mir-424 Contributes to the Abnormal Angiogenesis via MEK1 and Cyclin E1 in Senile Hemangioma: Its Implications to Therapy
TLDR
Investigating the mechanism of endothelial proliferation in senile hemangioma and the regulatory mechanisms of angiogenesis by miRNA in the aged skin may lead to new treatments using miRNA by the transfection of siRNA for MEK1 or cyclin E1 to cause abnormal cell proliferation in the tumor.
Kinesin-2 controls development and patterning of the vertebrate skeleton by Hedgehog- and Gli3-dependent mechanisms.
TLDR
It is demonstrated that conditional inactivation of the Kif3a subunit of the kinesin-2 intraflagellar transport motor in mesenchymal skeletal progenitor cells results in severe patterning defects in the craniofacial area, the formation of split sternum and the development of polydactyly.
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