Inhibition of transforming growth factor-β-induced liver fibrosis by a retinoic acid derivative via the suppression of Col 1A2 promoter activity

Yang, Kun; Chang, Wen Teng; Hung, Kuo Chen; Li, Eric I.C.; Chuang, Chia Chang

doi:10.1016/j.bbrc.2008.05.192

Cited by 21 publications

(19 citation statements)

References 30 publications

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“…Col1A2 is one of the major components of the extracellular matrix (47), whereas SM22␣ is a marker of myofibroblast differentiation (33). As expected, treatment with TGF-␤ alone for 12 h caused a 2.3-fold induction of Col1A2 mRNA expression compared with control; butyrate treatment induced Col1A2 mRNA expression to a similar magnitude as TGF-␤ treatment; the combined treatment of butyrate and TGF-␤ induced Col1A2 expression in a similar level as either treatment alone.…”

Section: Pectin Feeding Increases Smad3 Expression and Activation In supporting

confidence: 61%

Dietary fiber enhances TGF-β signaling and growth inhibition in the gut

Cao¹,

Gao²,

Zhang³

et al. 2011

American Journal of Physiology-Gastrointestinal and Liver Physi

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Dietary fiber intake links to decreased risk of colorectal cancers. The underlying mechanisms remain unclear. Recently, we found that butyrate, a short-chain fatty acid produced in gut by bacterial fermentation of dietary fiber, enhances TGF-β signaling in rat intestinal epithelial cells (RIE-1). Furthermore, TGF-β represses inhibitors of differentiation (Ids), leading to apoptosis. We hypothesized that dietary fiber enhances TGF-β's growth inhibitory effects on gut epithelium via inhibition of Id2. In this study, Balb/c and DBA/2N mice were fed with a regular rodent chow or supplemented with a dietary fiber (20% pectin) and Smad3 level in gut epithelium was measured. In vitro, RIE-1 cells were treated with butyrate and TGF-β1, and cell functions were evaluated. Furthermore, the role of Ids in butyrate- and TGF-β-induced growth inhibition was investigated. We found that pectin feeding increased Smad3 protein levels in the jejunum (1.47 ± 0.26-fold, P = 0.045, in Balb/c mice; 1.49 ± 0.19-fold, P = 0.016, in DBA/2N mice), and phospho-Smad3 levels (1.92 ± 0.27-fold, P = 0.009, in Balb/c mice; 1.83 ± 0.28-fold, P = 0.022, in DBA/2N mice). Butyrate or TGF-β alone inhibited cell growth and induced cell cycle arrest. The combined treatment of butyrate and TGF-β synergistically induced cell cycle arrest and apoptosis in RIE-1 cells and repressed Id2 and Id3 levels. Furthermore, knockdown of Id2 gene expression by use of small interfering RNA caused cell cycle arrest and apoptosis. We conclude that dietary fiber pectin enhanced Smad3 expression and activation in the gut. Butyrate and TGF-β induced cell cycle arrest and apoptosis, which may be mediated by repression of Id2. Our results implicate a novel mechanism of dietary fiber in reducing the risk of colorectal cancer development.

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Section: Pectin Feeding Increases Smad3 Expression and Activation In supporting

confidence: 61%

Dietary fiber enhances TGF-β signaling and growth inhibition in the gut

Cao¹,

Gao²,

Zhang³

et al. 2011

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…For cardiac cells, Ca 2+ is either a critical mediator of excitation-contraction coupling or an important second messenger for Ca 2+ -dependent signaling that regulates vital cell functions and cardiac functions (Bers, 2008;Houser, 2009). Previous studies have demonstrated that [Ca 2+ ] i entry plays an essential role in TGF-␤ signaling regulating cellular functions (Chu et al, 2011;Deng et al, 2001;Yang et al, 2008), and is associated with numerous pathological stimuli, including hypoxia and other stresses (Chaudhari et al, 2014;Ventura-Clapier and Vassort, 1983). Moreover, [Ca 2+ ] i overload has been demonstrated to participate in hypoxia-mediated CF apoptosis (Chu et al, 2011;Yang et al, 2014).…”

Section: Discussionmentioning

confidence: 97%