EGCG-rich green tea extract stimulates sRAGE secretion to inhibit S100A12-RAGE axis through ADAM10-mediated ectodomain shedding of extracellular RAGE in type 2 diabetes

Shang Ming Huang, Yin Hsuan Chang, Ya Chan Chao, Jer An Lin, Chi Hao Wu, Ching Yi Lai, Kung Chi Chan, Shih Ting Tseng, Gow Chin Yen

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

The receptor for advanced glycation of end products (RAGE) plays a critical role in the progression of type 2 diabetes (T2D). Soluble RAGE (sRAGE) is one of the RAGE variants, which acts as a decoy domain receptor and competes with RAGE, thus contributing to prevention of T2D. In this study, we conducted clinical trials of (-)-epigallocatechin-3-gallate (EGCG) rich green tea extract (300-900 mg/day) to investigate the effect of EGCG on relationship between S100A12 RAGE ligand and diverse sRAGE in T2D. Moreover, mechanism of sRAGE production also confirmed in vitro. Our data indicated that EGCG could stimulate sRAGE circulation but inhibited RAGE ligand in T2D, and ADAM10-mediated ectodomain shedding of extracellular RAGE was mainly involved in EGCG-stimulated sRAGE circulation. The present evidence indicates that EGCG has a potential to block S100A12-RAGE axis by stimulating sRAGE production through ADAM10-mediated ectodomain shedding of extracellular RAGE. Therefore, EGCG contributes to nutritional strategies for diabetes, not only because of its efficient antioxidant activity to scavenge free radicals, but also because of its ability stimulating sRAGE release in the circulation. Additionally, ADAM10-induced ectodomain shedding of extracellular RAGE leading to sRAGE circulation should be a potential of passive mechanism of sRAGE production to block S100A12-RAGE axis-related pathogenesis of proinflammation and diabetes.

Original languageEnglish
Pages (from-to)2264-2268
Number of pages5
JournalMolecular Nutrition and Food Research
Volume57
Issue number12
DOIs
Publication statusPublished - Dec 2013

Fingerprint

epigallocatechin
green tea
Tea
noninsulin-dependent diabetes mellitus
Type 2 Diabetes Mellitus
secretion
receptors
extracts
diabetes
advanced glycation end products
Advanced Glycosylation End Product-Specific Receptor
S100A12 Protein
epigallocatechin gallate
Ligands
Free Radicals
clinical trials
Antioxidants
Clinical Trials
pathogenesis
antioxidant activity

Keywords

  • ADAM10
  • EGCG
  • RAGE
  • S100A12
  • SRAGE

ASJC Scopus subject areas

  • Food Science
  • Biotechnology

Cite this

EGCG-rich green tea extract stimulates sRAGE secretion to inhibit S100A12-RAGE axis through ADAM10-mediated ectodomain shedding of extracellular RAGE in type 2 diabetes. / Huang, Shang Ming; Chang, Yin Hsuan; Chao, Ya Chan; Lin, Jer An; Wu, Chi Hao; Lai, Ching Yi; Chan, Kung Chi; Tseng, Shih Ting; Yen, Gow Chin.

In: Molecular Nutrition and Food Research, Vol. 57, No. 12, 12.2013, p. 2264-2268.

Research output: Contribution to journalArticle

Huang, Shang Ming ; Chang, Yin Hsuan ; Chao, Ya Chan ; Lin, Jer An ; Wu, Chi Hao ; Lai, Ching Yi ; Chan, Kung Chi ; Tseng, Shih Ting ; Yen, Gow Chin. / EGCG-rich green tea extract stimulates sRAGE secretion to inhibit S100A12-RAGE axis through ADAM10-mediated ectodomain shedding of extracellular RAGE in type 2 diabetes. In: Molecular Nutrition and Food Research. 2013 ; Vol. 57, No. 12. pp. 2264-2268.
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AU - Huang, Shang Ming

AU - Chang, Yin Hsuan

AU - Chao, Ya Chan

AU - Lin, Jer An

AU - Wu, Chi Hao

AU - Lai, Ching Yi

AU - Chan, Kung Chi

AU - Tseng, Shih Ting

AU - Yen, Gow Chin

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AB - The receptor for advanced glycation of end products (RAGE) plays a critical role in the progression of type 2 diabetes (T2D). Soluble RAGE (sRAGE) is one of the RAGE variants, which acts as a decoy domain receptor and competes with RAGE, thus contributing to prevention of T2D. In this study, we conducted clinical trials of (-)-epigallocatechin-3-gallate (EGCG) rich green tea extract (300-900 mg/day) to investigate the effect of EGCG on relationship between S100A12 RAGE ligand and diverse sRAGE in T2D. Moreover, mechanism of sRAGE production also confirmed in vitro. Our data indicated that EGCG could stimulate sRAGE circulation but inhibited RAGE ligand in T2D, and ADAM10-mediated ectodomain shedding of extracellular RAGE was mainly involved in EGCG-stimulated sRAGE circulation. The present evidence indicates that EGCG has a potential to block S100A12-RAGE axis by stimulating sRAGE production through ADAM10-mediated ectodomain shedding of extracellular RAGE. Therefore, EGCG contributes to nutritional strategies for diabetes, not only because of its efficient antioxidant activity to scavenge free radicals, but also because of its ability stimulating sRAGE release in the circulation. Additionally, ADAM10-induced ectodomain shedding of extracellular RAGE leading to sRAGE circulation should be a potential of passive mechanism of sRAGE production to block S100A12-RAGE axis-related pathogenesis of proinflammation and diabetes.

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