Activin A inhibits activities of lipopolysaccharide-activated macrophages via TLR4, not of TLR2

Li, Nan; Cui, Xueling; Ge, Jingyan; Li, Jiru; Niu, Liman; Liu, Haiyan; Qi, Yan; Liu, Zhonghui; Wang, Yinan

doi:10.1016/j.bbrc.2013.04.077

Cited by 23 publications

(27 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To our surprise, TLR4 , MyD88 , IRF3 and IRF7 mRNA in the liver tissues of HFHFr diet‐fed mice showed a trend toward decreased expression at Week 16 compared with Week 8, similar to expression of TLR4 and MyD88 protein. Recently, it has been shown that LPS induces the release of activin A, a member of the multifunctional TGF‐ β superfamily, from activated Kupffer cells and HSC through the TLR4 pathway and that activin A inhibits the activity of LPS‐activated macrophages via TLR4 . In the present study, we found that both the protein and mRNA expression of activin A increased markedly in the liver with progression from NASH to hepatic fibrosis, suggesting that activin A is released upon activation of TLR4 and that, in turn, the increased activin A may inhibit TLR4 expression.…”

Section: Discussionsupporting

confidence: 60%

“…Activation of TLR4 not only potentiates the production of various chemokines, thereby inducing chemotaxis of Kupffer cells, but also mediates the development of liver fibrosis by inhibiting the transforming growth factor (TGF)‐ β pseudoreceptor Bambi, which can sensitize hepatic stellate cells (HSC) to TGF‐ β signals . A recent study showed that a multifunctional growth and differentiation factor of the TGF‐ β superfamily reduced expression of TLR4 mRNA and protein in LPS‐induced RAW264.7 cells . The transient and consistent activation and inhibition of the TLR4 pathway could promote the evolution of NAFLD.…”

Section: Introductionmentioning

confidence: 99%

“…12 A recent study showed that a multifunctional growth and differentiation factor of the TGF-b superfamily reduced expression of TLR4 mRNA and protein in LPS-induced RAW264.7 cells. 13 The transient and consistent activation and inhibition of the TLR4 pathway could promote the evolution of NAFLD.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Toll‐like receptor‐4 signalling in the progression of non‐alcoholic fatty liver disease induced by high‐fat and high‐fructose diet in mice

Liu

Zhuang

Bian

et al. 2014

Clin Exp Pharma Physio

View full text Add to dashboard Cite

The aim of the present study was to investigate Toll-like receptor-4 (TLR4) signalling at different stages of non-alcoholic fatty liver disease (NAFLD) induced by a high-fat, high-fructose (HFHFr) diet in mice. Both TLR4 wild-type (WT) and mutant (TLR4(mut) ) mice were fed either standard chow (SC) or the HFHFr diet for different periods of time from 4 to 16 weeks. Pathological characteristics and function of the liver were assessed. Simple steatosis, steatohepatitis and hepatic fibrosis occurred sequentially in Week 4, 8 and 16 in WT mice fed with the HFHFr. Expression of TLR4, myeloid differentiation factor 88 (MyD88), interferon regulatory factor (IRF) 3 and IRF7 started to increase at Week 4, peaked at Week 8 and then declined to basal levels at Week 16. This pattern was consistent with changes in inflammation in the liver revealed by haematoxylin and eosin staining. However, lipid accumulation, inflammation and fibrosis in livers of TLR4(mut) mice fed the HFHFr diet were significantly alleviated. In addition, the expression of activin A in WT mice fed the HFHFr diet increased at Week 16. The data suggest that TLR4 signalling mediates non-alcoholic steatohepatitis before fibrosis and that activin A is subsequently involved in NAFLD.

show abstract

Section: Discussionsupporting

confidence: 60%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Toll‐like receptor‐4 signalling in the progression of non‐alcoholic fatty liver disease induced by high‐fat and high‐fructose diet in mice

Liu

Zhuang

Bian

et al. 2014

Clin Exp Pharma Physio

View full text Add to dashboard Cite

show abstract

“…Activin A is also associated with the maintenance of neuron survival, induction of hepatocyte apoptosis, promotion of erythroid differentiation and dual regulation of macrophage activation (14)(15)(16)(17). The involvement of activin A in the process of tumor genesis and progression has been previously reported (18), and a significant increase of activin A in the serum of certain patients with colorectal adenocarcinoma has been observed (19).…”

Section: Discussionmentioning

confidence: 89%

Activin A induces apoptosis of mouse myeloma cells via the mitochondrial pathway

Zhang

Zhao

et al. 2017

Oncol Lett

Self Cite

View full text Add to dashboard Cite

Abstract. Activin A is a pleiotropic cytokine belonging to the transforming growth factor β superfamily. Abnormal expression of activin A is associated with tumorigenesis. Multiple myeloma is characterized by the development of osteolytic disease, which ultimately leads to cachexia. However, the involvement of activin A in myeloma cell viability and apoptosis remains to be fully elucidated. For this purpose, mouse myeloma NS-1 cells were treated with activin A, and subsequently subjected to 5-bromo-2'-deoxyuridine analysis, Hoechst 33342 staining, flow cytometry and western blot analysis. The results revealed that activin A significantly suppressed NS-1 cell viability, and induced NS-1 cell apoptosis. In addition, activin A-induced promotion of NS-1 cell apoptosis was accompanied by upregulated expression of BCL2 associated X, apoptosis regulator (Bax), but downregulated expression of B cell lymphoma-2 (Bcl-2), resulting in an increase of the Bax/Bcl-2 ratio. Furthermore, cytochrome c and caspase-3 protein expression also increased following treatment with activin A. These data suggest that activin A induces apoptosis in mouse myeloma NS-1 cells via the mitochondrial pathway, providing a novel insight into multiple myeloma treatment.

show abstract

“…Based on our data, the overall balance would be turned toward a proinflammatory environment and potential damage because the AF follistatin levels remained unchanged. Interestingly, in vitro, activin-A inhibits LPS action on macrophages via suppressing TLR-4 expression (37). If during AF infection, this anti-inflammatory effect is exercised in human fetal membranes, remains to be determined.…”

Section: Discussionmentioning

confidence: 98%

Imbalance of Amniotic Fluid Activin-A and Follistatin in Intraamniotic Infection, Inflammation, and Preterm Birth

Hardy

Buhimschi

McCarthy

et al. 2016

The Journal of Clinical Endocrinology &Amp; Metabolism

View full text Add to dashboard Cite

show abstract

Activin A inhibits activities of lipopolysaccharide-activated macrophages via TLR4, not of TLR2

Cited by 23 publications

References 30 publications

Toll‐like receptor‐4 signalling in the progression of non‐alcoholic fatty liver disease induced by high‐fat and high‐fructose diet in mice

Toll‐like receptor‐4 signalling in the progression of non‐alcoholic fatty liver disease induced by high‐fat and high‐fructose diet in mice

Activin A induces apoptosis of mouse myeloma cells via the mitochondrial pathway

Imbalance of Amniotic Fluid Activin-A and Follistatin in Intraamniotic Infection, Inflammation, and Preterm Birth

Contact Info

Product

Resources

About