Inhibition of TGF-alpha gene expression by vitamin A in airway epithelium.

Miller, Lisa; Zhao, Yu; Wu, Reen

doi:10.1172/jci118564

Cited by 7 publications

(6 citation statements)

References 47 publications

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“…Previous studies indicated that treatment with ATRA reduced the levels of TGF-␣ and EGFR mRNA in human SCC cell lines by inhibiting the transcription of these two genes (42), and the RXR-selective retinoid LGD1069 also inhibited both TGF-␣ and EGFR expression in human SCC cell lines (43). Furthermore, in bronchial epithelial cells retinol inhibited TGF-␣ promoter activity in the presence of RAR␤ (44). Our results with ACR are also consistent with evidence that this compound decreases TGF-␣ expression in human hepatoma cells (8).…”

Section: Discussionsupporting

confidence: 90%

Effects of Acyclic Retinoid on Growth, Cell Cycle Control, Epidermal Growth Factor Receptor Signaling, and Gene Expression in Human Squamous Cell Carcinoma Cells

Shimizu

Suzui

Deguchi

et al. 2004

Clinical Cancer Research

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Section: Discussionsupporting

confidence: 90%

Effects of Acyclic Retinoid on Growth, Cell Cycle Control, Epidermal Growth Factor Receptor Signaling, and Gene Expression in Human Squamous Cell Carcinoma Cells

Shimizu

Suzui

Deguchi

et al. 2004

Clinical Cancer Research

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“…First, Shao and colleagues used a much lower concentration of retinoic acid in their culture media ‫ف(‬ 3 ϫ 10 Ϫ10 M versus 5 ϫ 10 Ϫ8 M in our cultures). This is likely relevant because TGF-␣ gene expression is induced by these low concentrations of retinoic acid (70,71). We used the concentration that Koo and colleagues (71) found to be necessary to maintain mucous cell differentiation in NHBE cell cultures.…”

Section: Discussionmentioning

confidence: 99%

Epidermal Growth Factor Receptor Activation by Epidermal Growth Factor Mediates Oxidant-Induced Goblet Cell Metaplasia in Human Airway Epithelium

Casalino‐Matsuda

Monzón

Forteza

2006

Am J Respir Cell Mol Biol

144

110

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Mucus overproduction in inflammatory and obstructive airway diseases is associated with goblet cell (GC) metaplasia in airways. Although the mechanisms involved in GC metaplasia and mucus hypersecretion are not completely understood, association with oxidative stress and epidermal growth factor receptor (EGFR) signaling has been reported. To explore the mechanisms involved in oxidative stress-induced GC metaplasia, cultures of differentiated normal human bronchial epithelial cells grown at the air-liquid interface were exposed to reactive oxygen species (ROS) generated by xanthine/xanthine oxidase. EGFR activation and signaling was assessed by measuring EGF and transforming growth factor-alpha release and EGFR and (44/42)MAPK phosphorylation. The GC population was evaluated by confocal microscopy. ROS-induced EGFR activation resulted in GC proliferation and increased MUC5AC gene and protein expression. Signaling was due to pro-EGF processing by tissue kallikrein (TK), which was activated by ROS-induced hyaluronan breakdown. It was inhibited by catalase, a TK inhibitor, and EGF-blocking antibodies. Exposure to recombinant TK mimicked the ROS effects, increasing the expression of MUC5AC and lactoperoxidase. In addition, ROS induced the antiapoptotic factor Bcl-2 in a TK-dependent fashion. In conclusion, ROS-induced GC metaplasia in normal human bronchial epithelial cells is associated with HA depolymerization and EGF processing by TK followed by EGFR signaling, suggesting that increases in TK activity could contribute to GC metaplasia and mucus hypersecretion in diseases such as asthma and chronic bronchitis. The data also suggest that increases in GC population could be sustained by the associated upregulation of Bcl-2 in airway epithelial cells.

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“…The data were analysed with the chi-squared test, Fisher's exact probability test, or one-way analysis of variance with Dunn's multiple comparison (Miller et al, 1966). The data are shown as means ± s.e.…”

Section: Discussionmentioning

confidence: 99%

“…TGF-α has the ability to induce malignant transformation in some epithelial cells (McGeady et al, 1989;Shankar et al, 1989). Miller et al (1996) found that vitamin A suppresses the proliferation of tracheobronchial epithelial cells in culture by inhibiting expression of the TGF-α gene product. They also noted that similar inhibition of the TGF-α mRNA level by retinol was observed in airway explant cultures and in a cell line immortalized from normal human bronchial epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

Attenuation by all-trans-retinoic acid of sodium chloride-enhanced gastric carcinogenesis induced by N-methyl-N ′-nitro-N-nitrosoguanidine in Wistar rats

et al. 1999

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The effect of prolonged administration of all- trans -retinoic acid (RA) on sodium chloride-enhanced gastric carcinogenesis induced by N -methyl- N ′-nitro- N -nitrosoguanidine, and the labelling and apoptotic indices and immunoreactivity of transforming growth factor (TGF) α in the gastric cancers was investigated in Wistar rats. After 25 weeks of carcinogen treatment, the rats were given chow pellets containing 10% sodium chloride and subcutaneous injections of RA at doses of 0.75 or 1.5 mg kg −1 body weight every other day. In week 52, oral supplementation with sodium chloride significantly increased the incidence of gastric cancers compared with the untreated controls. Long-term administration of RA at both doses significantly reduced the incidence of gastric cancers, which was enhanced by oral administration of sodium chloride. RA at both doses significantly decreased the labelling index and TGF-α immunoreactivity of gastric cancers, which were enhanced by administration of sodium chloride, and significantly increased the apoptotic index of cancers, which was lowered by administration of sodium chloride. These findings suggest that RA attenuates gastric carcinogenesis, enhanced by sodium chloride, by increasing apoptosis, decreasing DNA synthesis, and reducing TGF-α expression in gastric cancers. © 1999 Cancer Research Campaign

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Inhibition of TGF-alpha gene expression by vitamin A in airway epithelium.

Abstract: The autocrine/paracrine growth mechanism has been implicated in the regulation of bronchial epithelial cell proliferation. By inhibiting the expression of the transforming growth factor-␣ (TGF- ␣

Cited by 7 publications

References 47 publications

Effects of Acyclic Retinoid on Growth, Cell Cycle Control, Epidermal Growth Factor Receptor Signaling, and Gene Expression in Human Squamous Cell Carcinoma Cells

Effects of Acyclic Retinoid on Growth, Cell Cycle Control, Epidermal Growth Factor Receptor Signaling, and Gene Expression in Human Squamous Cell Carcinoma Cells

Epidermal Growth Factor Receptor Activation by Epidermal Growth Factor Mediates Oxidant-Induced Goblet Cell Metaplasia in Human Airway Epithelium

Attenuation by all-trans-retinoic acid of sodium chloride-enhanced gastric carcinogenesis induced by N-methyl-N ′-nitro-N-nitrosoguanidine in Wistar rats

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