cytosporone-b has been researched along with Fibrosis* in 2 studies
2 other study(ies) available for cytosporone-b and Fibrosis
| Article | Year |
|---|---|
NR4A1 is Involved in Fibrogenesis in Ovarian Endometriosis.
Excess fibrosis may lead to chronic pain, scarring, and infertility as endometriosis develops and progresses. The pathogenesis of endometriosis has been linked to transforming growth factor-β (TGF-β), the most potent promoter of fibrosis.. Levels of NR4A1 and P-NR4A1 protein in human endometrial and endometriotic tissue were assessed by western blotting and immunohistochemistry. The expression levels of fibrotic markers in stromal cells were evaluated by real-time PCR. The degree of fibrosis in mouse endometriotic lesions was detected by Masson trichrome and Sirius red staining.. The level of phosphorylated-NR4A1 was higher in ovarian endometriotic tissue than in normal endometrium, and long-term TGF-β1 stimulation phosphorylated NR4A1 in an AKT-dependent manner and then promoted the expression of fibrotic markers. Furthermore, inhibition of NR4A1 in stromal cells increased the TGF-β1-dependent elevated expression of fibrotic markers, and loss of NR4A1 stimulated fibrogenesis in mice with endometriosis. Additionally, Cytosporone B (Csn-B), an NR4A1 agonist, effectively decreased the TGF-β1-dependent elevated expression of fibrotic markers in vitro and significantly inhibited fibrogenesis in vivo.. NR4A1 can regulate fibrosis in endometriosis and may serve as a new target for the treatment of endometriosis. Topics: Adult; Animals; Cells, Cultured; Collagen Type I; Collagen Type I, alpha 1 Chain; Connective Tissue Growth Factor; Disease Models, Animal; Endometriosis; Endometrium; Female; Fibronectins; Fibrosis; Heterocyclic Compounds, 3-Ring; Humans; Mice; Mice, Nude; Microscopy, Fluorescence; Nuclear Receptor Subfamily 4, Group A, Member 1; Phenylacetates; Phosphorylation; Proto-Oncogene Proteins c-akt; RNA Interference; RNA, Small Interfering; Stromal Cells; Transforming Growth Factor beta; Transplantation, Heterologous; Up-Regulation; Young Adult | 2018 |
The effects of cytosporone-B, a novel antifibrotic agent, on vocal fold fibroblasts.
Our laboratory recently described NR4A1 as an endogenous inhibitor of TGF-β-induced vocal fold (VF) fibrosis. Our prior report described the temporal expression of NR4A1 during VF healing in vivo and the effects of NR4A1 knockdown on fibroplastic cell activities in vitro. Based on these findings, we hypothesized that cytosporone-B (Csn-B), an NR4A1 agonist, may hold significant therapeutic potential.. In vitro.. Human VF fibroblasts were exposed to TGF-β1+/-Csn-B. Expression of genes related to fibrosis were quantified. In addition, contraction was assayed as a surrogate for the fibrotic phenotype in our cell line.. TGF-B1 stimulated COL1A1 and ACTA2, as expected. Csn-B significantly downregulated TGF-β1-mediated upregulation of these genes (P = .009, P = .03, respectively). Csn-B had no effect on genes related to TGF-β/Smad signaling. Csn-B also decreased the TGF-β1-mediated contractile phenotype in our cells (P = .004).. NR4A1 is an endogenous inhibitor of fibrosis in the vocal folds and Csn-B, as an NR4A1 agonist, may evolve as an ideal, therapeutic candidate for this challenging condition.. NA Laryngoscope, 128:E425-E428, 2018. Topics: Actins; Cell Differentiation; Cell Line; Collagen; Collagen Type I; Collagen Type I, alpha 1 Chain; Fibroblasts; Fibrosis; Humans; Nuclear Receptor Subfamily 4, Group A, Member 1; Phenylacetates; Transforming Growth Factor beta1; Vocal Cords | 2018 |