Effect of crosstalk between Th17 and Th9 cells on the activation of dermal vascular smooth muscle cells in systemic scleroderma and regulation of tanshinone IIA

Liu, Mengguo

doi:10.1016/j.abd.2021.11.008

Cited by 2 publications

(2 citation statements)

References 22 publications

(24 reference statements)

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“…Our earlier research demonstrated that TAN IIA reduces the endothelial‐to‐mesenchymal transition that bleomycin (BLM) causes in SSc 12 . Additionally, TAN IIA prevented the activation of vascular smooth muscle cells in SSc that were induced by crosstalk between Th17 and Th9 cells in vitro 13 . However, the underlying mechanism of the TAN IIA‐mediated anti‐fibrosis effect is still unclear at present.…”

Section: Introductionmentioning

confidence: 99%

“…12 Additionally, TAN IIA prevented the activation of vascular smooth muscle cells in SSc that were induced by crosstalk between Th17 and Th9 cells in vitro. 13 However, the underlying mechanism of the TAN IIA-mediated anti-fibrosis effect is still unclear at present. To shed light on TAN IIA's impact on skin fibrosis in SSc and further define the underlying mechanism of its anti-fibrotic activity, we designed both in vitro and in vivo research for this article.…”

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confidence: 99%

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Tanshinone IIA ameliorates the development of dermal fibrosis in systemic sclerosis

Jiang,

Hu,

et al. 2023

Clin Exp Pharma Physio

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ObjectivesWe previously revealed the role of tanshinone IIA (TAN IIA) on endothelial cells and the impact of TAN IIA on the endothelial‐to‐mesenchymal transition in systemic sclerosis (SSc). In this study, we sought to further determine whether TAN IIA can directly act on the skin fibroblasts of scleroderma and look into its underlying anti‐fibrotic mechanisms.MethodsBleomycin was used to establish the SSc mouse model. After TAN IIA treatment, dermal thickness, type I collagen and hydroxyproline content were measured. Primary fibroblasts were acquired from SSc patients and cultured in vitro, and the effects of TAN IIA on proliferation, apoptosis and the cell cycle of fibroblasts were detected.ResultsIn a bleomycin‐induced SSc model, we discovered that TAN IIA significantly improved skin thickness and collagen deposition, demonstrating a potent anti‐fibrotic action. TAN IIA inhibits the proliferation of skin fibroblasts derived from SSc patients by causing G2/M cell cycle arrest and promoting apoptosis. Additionally, TAN IIA downregulated extracellular matrix gene transcription and collagen protein expression in skin fibroblasts in a dose‐gradient‐dependent manner. Furthermore, we showed how TAN IIA can reduce the activation of the transforming growth factor‐β (TGF‐β)/Smad and mitogen‐activated protein kinase (MAPK)/extracellular signal‐regulated kinase (ERK) pathways, which are important factors in SSc.ConclusionsIn summary, these data suggest that TAN IIA can reduce SSc‐related skin fibrosis by modulating the TGF‐β/Smad and MAPK/ERK signalling pathways. More importantly, our results imply that TAN IIA can directly act on the skin fibroblasts of SSc, therefore, inhibiting fibrosis.

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Section: Introductionmentioning

confidence: 99%

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confidence: 99%