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Su1201 The Expression of the 67 kDa Laminin Receptor (LR) or Green Tea Catechin Epigallocatechin-3-Gallate (EGCG) Receptor May Explain the Different Responses to EGCG in the Cell Lines Infected With H. pylori

Su1201 The Expression of the 67 kDa Laminin Receptor (LR) or Green Tea Catechin Epigallocatechin-3-Gallate (EGCG) Receptor May Explain the Different Responses to EGCG in the Cell Lines Infected With H. pylori

Author: Prakitpunthu Tomtitchong and Jean E. Crabtree

Introduction: Epidemiological studies suggest epigallocatechin-3-gallate (EGCG), a natural product from green tea, may have a role in prevention of gastric atrophy and gastric cancer in Asian populations. Anyway, the diversity of results from in vivo studies was observed. Our group reported that EGCG inhibits H. pylori-induced upregulation of COX-2, EGF- related ligand and ADAMs transcripts, ERK phosphorylation and IL-8 activation in gastric and non-gastric epithelial cells. But we have simultaneously observed that EGCG can be a stimulator in some conditions. Recently, an EGCG specific receptor has been identified which is the 67 kDa laminin receptor (LR). We postulate that varying levels of the EGCG receptor, the 67 kDa LR, on different cell lines may modify the in vitro results determining the inhibitory effects of EGCG on cell signaling pathways. Methods: MKN28, MGEC, L5F11 and A431 epithelial cells were incubated with MLuC5 mouse monoclonal IgM before incuba- tion with TRITC-conjugated goat anti-mouse expression of the EGCG receptor. The 67 kDa laminin receptor (LR) or EGCG receptor was evident by immunofluorescence. Expression levels of EGCG receptor were compared with the different responses to EGCG among the four cell lines. Results: Strong expression of the EGCG receptor was evident on MKN28 cells but reduced levels were observed on L5F11 and A431 cells. MGEC cells show no expression of 67 kDa LR. Conclusions: Varying levels of the laminin or EGCG receptor may explain the different responses of the cell lines to EGCG and might explain variation of a role EGCG in prevention of H. pylori-induced gastric carcinogenesis.

 

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