ArticleActa pharmacologica Sinica2014
Selective α1B- and α1D-adrenoceptor antagonists suppress noradrenaline-induced activation, proliferation and ECM secretion of rat hepatic stellate cells in vitro.
Article in Acta pharmacologica Sinica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 35 citations in OpenAlex.
- Review
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- Pathophysiologic Role of Neurotransmitters in Digestive Diseases.Frontiers in physiology · 2021Review
- β-arrestin2 regulating β2-adrenergic receptor signaling in hepatic stellate cells contributes to hepatocellular carcinoma progression.Journal of Cancer · 2021Article
- Norepinephrine-stimulated HSCs secrete sFRP1 to promote HCC progression following chronic stress via augmentation of a Wnt16B/β-catenin positive feedback loop.Journal of experimental & clinical cancer research : CR · 2020Article
- Curcumin andJournal of immunology research · 2019Article
- Evidence for a direct effect of the autonomic nervous system on intestinal epithelial stem cell proliferation.Physiological reports · 2018Article
- Interaction of dendritic cells and T lymphocytes for the therapeutic effect of Dangguiliuhuang decoction to autoimmune diabetes.Scientific reports · 2015Article
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4 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
aimTo explore the effects of noradrenaline (NA) on hepatic stellate cells (HSCs) in vitro and to determine the adrenoceptor (AR) subtypes and underlying mechanisms.
methodsThe distribution and expressions of α1A-, α1B-, and α1D-ARs in HSC-T6 cells were analyzed using immunocytochemistry and RT-PCR. Cell proliferation was evaluated with MTT assay. The expression of HSC activation factors [transforming factor-β1 (TGF-β1) and α-smooth muscle actin (α-SMA)], extracellular matrix (ECM) secretion factors [tissue inhibitor of metalloproteinase-1 (TIMP-1) and collagen-Ι (ColΙ)] and PKC-PI3K-AKT signaling components (PKC, PI3K, and AKT) in the cells were detected by Western blotting and RT-PCR.
resultsBoth α1B- and α1D-AR were expressed in the membrane of HSC-T6 cells, whereas α1A-AR was not detected. Treatment of the cells with NA concentration-dependently increased cell proliferation (EC50=277 nmol/L), which was suppressed by the α1B-AR antagonist CEC or by the α1D-AR antagonist BMY7378. Furthermore, NA (0.001, 0.1, and 10 μmol/L) concentration-dependently increased the expression of TGF-β1, α-SMA, TIMP-1 and ColΙ, PKC and PI3K, and phosphorylation of AKT in HSC-T6 cells, which were suppressed by CEC or BMY7378, or by pertussis toxin (PT), RO-32-0432 (PKC antagonist), LY294002 (PI3K antagonist) or GSK690693 (AKT antagonist).
conclusionNA promotes HSC-T6 cell activation, proliferation and secretion of ECM in vitro via activation of Gα-coupled α1B-AR and α1D-AR and the PKC-PI3K-AKT signaling pathway.
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