Cross talk between toll-like receptor-4 signaling and angiotensin-II in liver fibrosis development in the rat model of non-alcoholic steatohepatitis
Background and Aim The innate immune system, including toll‐like receptor‐4 (TLR4) signaling cascade and angiotensin‐II (AT‐II) play important roles in the progression of liver fibrosis development; the cross talk between TLR4 and AT‐II has not been elucidated yet. The aim of the current study was t...
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Published in | Journal of gastroenterology and hepatology Vol. 28; no. 4; pp. 723 - 730 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Australia
Blackwell Publishing Ltd
01.04.2013
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Subjects | |
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Abstract | Background and Aim
The innate immune system, including toll‐like receptor‐4 (TLR4) signaling cascade and angiotensin‐II (AT‐II) play important roles in the progression of liver fibrosis development; the cross talk between TLR4 and AT‐II has not been elucidated yet. The aim of the current study was to elucidate the effect of AT‐II type 1 receptor blocker (ARB), on the liver fibrosis development, especially in conjunction with the interaction of TLR4 and AT‐II in the rat model of non‐alcoholic steatohepatitis.
Methods
Fischer 344 rats were fed a choline‐deficient, l‐amino‐acid‐defined diet for 8 weeks and the effects of losartan were elucidated in conjunction with activated hepatic stellate cells (Ac‐HSC) activation, TLR4, nuclear factor‐κB (NF‐κB), and transforming growth factor‐β (TGF‐β) expressions. In vitro study was carried out to elucidate the effect of AT‐II on several indices including TLR4, myeloid differentiation factor 88, NF‐κB, and TGF‐β expressions in the rat HSC.
Results
ARB markedly inhibited liver fibrosis development along with suppression of the number of Ac‐HSC and TGF‐β. These inhibitory effects of ARB were almost in parallel with suppression of the hepatic TLR4 and NF‐κB expressions. This in vitro study showed that AT‐II significantly augmented the TLR4 expression in a dose‐ and time‐dependent manner via AT‐II type 1 receptor in the Ac‐HSC. AT‐II also augmented the lipopolysaccharide‐induced myeloid differentiation factor 88 (MyD88), NF‐κB, and TGF‐β and these increments were attenuated by treatment with ARB.
Conclusions
These studies indicated that the cross talk between TLR4 signaling cascade and AT‐II plays a pivotal role in liver fibrosis development in non‐alcoholic steatohepatitis. |
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AbstractList | BACKGROUND AND AIMThe innate immune system, including toll-like receptor-4 (TLR4) signaling cascade and angiotensin-II (AT-II) play important roles in the progression of liver fibrosis development; the cross talk between TLR4 and AT-II has not been elucidated yet. The aim of the current study was to elucidate the effect of AT-II type 1 receptor blocker (ARB), on the liver fibrosis development, especially in conjunction with the interaction of TLR4 and AT-II in the rat model of non-alcoholic steatohepatitis.METHODSFischer 344 rats were fed a choline-deficient, L-amino-acid-defined diet for 8 weeks and the effects of losartan were elucidated in conjunction with activated hepatic stellate cells (Ac-HSC) activation, TLR4, nuclear factor-κB (NF-κB), and transforming growth factor-β (TGF-β) expressions. In vitro study was carried out to elucidate the effect of AT-II on several indices including TLR4, myeloid differentiation factor 88, NF-κB, and TGF-β expressions in the rat HSC.RESULTSARB markedly inhibited liver fibrosis development along with suppression of the number of Ac-HSC and TGF-β. These inhibitory effects of ARB were almost in parallel with suppression of the hepatic TLR4 and NF-κB expressions. This in vitro study showed that AT-II significantly augmented the TLR4 expression in a dose- and time-dependent manner via AT-II type 1 receptor in the Ac-HSC. AT-II also augmented the lipopolysaccharide-induced myeloid differentiation factor 88 (MyD88), NF-κB, and TGF-β and these increments were attenuated by treatment with ARB.CONCLUSIONSThese studies indicated that the cross talk between TLR4 signaling cascade and AT-II plays a pivotal role in liver fibrosis development in non-alcoholic steatohepatitis. The innate immune system, including toll-like receptor-4 (TLR4) signaling cascade and angiotensin-II (AT-II) play important roles in the progression of liver fibrosis development; the cross talk between TLR4 and AT-II has not been elucidated yet. The aim of the current study was to elucidate the effect of AT-II type 1 receptor blocker (ARB), on the liver fibrosis development, especially in conjunction with the interaction of TLR4 and AT-II in the rat model of non-alcoholic steatohepatitis. Fischer 344 rats were fed a choline-deficient, L-amino-acid-defined diet for 8 weeks and the effects of losartan were elucidated in conjunction with activated hepatic stellate cells (Ac-HSC) activation, TLR4, nuclear factor-κB (NF-κB), and transforming growth factor-β (TGF-β) expressions. In vitro study was carried out to elucidate the effect of AT-II on several indices including TLR4, myeloid differentiation factor 88, NF-κB, and TGF-β expressions in the rat HSC. ARB markedly inhibited liver fibrosis development along with suppression of the number of Ac-HSC and TGF-β. These inhibitory effects of ARB were almost in parallel with suppression of the hepatic TLR4 and NF-κB expressions. This in vitro study showed that AT-II significantly augmented the TLR4 expression in a dose- and time-dependent manner via AT-II type 1 receptor in the Ac-HSC. AT-II also augmented the lipopolysaccharide-induced myeloid differentiation factor 88 (MyD88), NF-κB, and TGF-β and these increments were attenuated by treatment with ARB. These studies indicated that the cross talk between TLR4 signaling cascade and AT-II plays a pivotal role in liver fibrosis development in non-alcoholic steatohepatitis. The innate immune system, including toll-like receptor-4 (TLR4) signaling cascade and angiotensin-II (AT-II) play important roles in the progression of liver fibrosis development; the cross talk between TLR4 and AT-II has not been elucidated yet. The aim of the current study was to elucidate the effect of AT-II type 1 receptor blocker (ARB), on the liver fibrosis development, especially in conjunction with the interaction of TLR4 and AT-II in the rat model of non-alcoholic steatohepatitis. Fischer 344 rats were fed a choline-deficient, l-amino-acid-defined diet for 8 weeks and the effects of losartan were elucidated in conjunction with activated hepatic stellate cells (Ac-HSC) activation, TLR4, nuclear factor- Kappa B (NF- Kappa B), and transforming growth factor- beta (TGF- beta ) expressions. In vitro study was carried out to elucidate the effect of AT-II on several indices including TLR4, myeloid differentiation factor 88, NF- Kappa B, and TGF- beta expressions in the rat HSC. ARB markedly inhibited liver fibrosis development along with suppression of the number of Ac-HSC and TGF- beta . These inhibitory effects of ARB were almost in parallel with suppression of the hepatic TLR4 and NF- Kappa B expressions. This in vitro study showed that AT-II significantly augmented the TLR4 expression in a dose- and time-dependent manner via AT-II type 1 receptor in the Ac-HSC. AT-II also augmented the lipopolysaccharide-induced myeloid differentiation factor 88 (MyD88), NF- Kappa B, and TGF- beta and these increments were attenuated by treatment with ARB. These studies indicated that the cross talk between TLR4 signaling cascade and AT-II plays a pivotal role in liver fibrosis development in non-alcoholic steatohepatitis. Abstract Background and Aim The innate immune system, including toll‐like receptor‐4 ( TLR 4) signaling cascade and angiotensin‐ II ( AT ‐ II ) play important roles in the progression of liver fibrosis development; the cross talk between TLR 4 and AT‐II has not been elucidated yet. The aim of the current study was to elucidate the effect of AT‐II type 1 receptor blocker ( ARB ), on the liver fibrosis development, especially in conjunction with the interaction of TLR 4 and AT‐II in the rat model of non‐alcoholic steatohepatitis. Methods Fischer 344 rats were fed a choline‐deficient, l ‐amino‐acid‐defined diet for 8 weeks and the effects of losartan were elucidated in conjunction with activated hepatic stellate cells ( Ac ‐ HSC ) activation, TLR 4, nuclear factor‐κ B ( NF ‐κ B ), and transforming growth factor‐β ( TGF ‐β) expressions. In vitro study was carried out to elucidate the effect of AT ‐ II on several indices including TLR 4, myeloid differentiation factor 88, NF ‐κ B , and TGF ‐β expressions in the rat HSC . Results ARB markedly inhibited liver fibrosis development along with suppression of the number of Ac ‐ HSC and TGF ‐β. These inhibitory effects of ARB were almost in parallel with suppression of the hepatic TLR 4 and NF ‐κ B expressions. This in vitro study showed that AT ‐ II significantly augmented the TLR 4 expression in a dose‐ and time‐dependent manner via AT‐II type 1 receptor in the Ac ‐ HSC . AT ‐ II also augmented the lipopolysaccharide‐induced myeloid differentiation factor 88 (MyD88), NF ‐κ B , and TGF ‐β and these increments were attenuated by treatment with ARB . Conclusions These studies indicated that the cross talk between TLR 4 signaling cascade and AT ‐ II plays a pivotal role in liver fibrosis development in non‐alcoholic steatohepatitis. Background and Aim The innate immune system, including toll‐like receptor‐4 (TLR4) signaling cascade and angiotensin‐II (AT‐II) play important roles in the progression of liver fibrosis development; the cross talk between TLR4 and AT‐II has not been elucidated yet. The aim of the current study was to elucidate the effect of AT‐II type 1 receptor blocker (ARB), on the liver fibrosis development, especially in conjunction with the interaction of TLR4 and AT‐II in the rat model of non‐alcoholic steatohepatitis. Methods Fischer 344 rats were fed a choline‐deficient, l‐amino‐acid‐defined diet for 8 weeks and the effects of losartan were elucidated in conjunction with activated hepatic stellate cells (Ac‐HSC) activation, TLR4, nuclear factor‐κB (NF‐κB), and transforming growth factor‐β (TGF‐β) expressions. In vitro study was carried out to elucidate the effect of AT‐II on several indices including TLR4, myeloid differentiation factor 88, NF‐κB, and TGF‐β expressions in the rat HSC. Results ARB markedly inhibited liver fibrosis development along with suppression of the number of Ac‐HSC and TGF‐β. These inhibitory effects of ARB were almost in parallel with suppression of the hepatic TLR4 and NF‐κB expressions. This in vitro study showed that AT‐II significantly augmented the TLR4 expression in a dose‐ and time‐dependent manner via AT‐II type 1 receptor in the Ac‐HSC. AT‐II also augmented the lipopolysaccharide‐induced myeloid differentiation factor 88 (MyD88), NF‐κB, and TGF‐β and these increments were attenuated by treatment with ARB. Conclusions These studies indicated that the cross talk between TLR4 signaling cascade and AT‐II plays a pivotal role in liver fibrosis development in non‐alcoholic steatohepatitis. |
Author | Douhara, Akitoshi Moriya, Kei Noguchi, Ryuichi Kawaratani, Hideto Shirai, Yusaku Yoshiji, Hitoshi Aihara, Yosuke Namisaki, Tadashi Kaji, Kosuke Fukui, Hiroshi |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23301938$$D View this record in MEDLINE/PubMed |
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Snippet | Background and Aim
The innate immune system, including toll‐like receptor‐4 (TLR4) signaling cascade and angiotensin‐II (AT‐II) play important roles in the... The innate immune system, including toll-like receptor-4 (TLR4) signaling cascade and angiotensin-II (AT-II) play important roles in the progression of liver... Abstract Background and Aim The innate immune system, including toll‐like receptor‐4 ( TLR 4) signaling cascade and angiotensin‐ II ( AT ‐ II ) play important... BACKGROUND AND AIMThe innate immune system, including toll-like receptor-4 (TLR4) signaling cascade and angiotensin-II (AT-II) play important roles in the... |
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SubjectTerms | Angiotensin II - metabolism Angiotensin II Type 1 Receptor Blockers - pharmacology angiotensin-II Animals Cell Communication - drug effects Disease Models, Animal Disease Progression DNA Primers - chemistry Dose-Response Relationship, Drug Fatty Liver - metabolism Fatty Liver - prevention & control Gene Expression - drug effects Hepatic Stellate Cells - drug effects Hepatic Stellate Cells - metabolism lipopolysaccharide Liver Cirrhosis - metabolism Liver Cirrhosis - prevention & control liver fibrosis Losartan - pharmacology Male NF-kappa B - metabolism Non-alcoholic Fatty Liver Disease non-alcoholic steatohepatitis Rats Rats, Inbred F344 Real-Time Polymerase Chain Reaction RNA, Messenger - metabolism Signal Transduction - physiology Time Factors Toll-Like Receptor 4 - metabolism toll-like receptor-4 Transforming Growth Factor beta - metabolism |
Title | Cross talk between toll-like receptor-4 signaling and angiotensin-II in liver fibrosis development in the rat model of non-alcoholic steatohepatitis |
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