# Real Time Monitoring of Inhibition of Adipogenesis and Angiogenesis by (−)-Epigallocatechin-3-Gallate in 3T3-L1 Adipocytes and Human Umbilical Vein Endothelial Cells

**Authors:** Wenjing Tang, Huanlei Song, Wei Cai, Xiuhua Shen

PMC · DOI: 10.3390/nu7105437 · 2015-10-27

## TL;DR

This study shows that EGCG reduces VEGF in fat cells, which may help prevent blood vessel growth linked to obesity and related diseases.

## Contribution

The study is the first to show EGCG's effect on angiogenesis in adipocytes by inhibiting VEGF expression and secretion.

## Key findings

- EGCG treatment reduced VEGF mRNA, protein, and secretion in 3T3-L1 adipocytes.
- Conditioned media from EGCG-treated adipocytes inhibited tube formation in HUVECs.
- PPARγ and C/EBPα expression in adipocytes was decreased by EGCG treatment.

## Abstract

Little is known about the effect of (−)-epigallocatechin-3-gallate (EGCG) on angiogenesis in adipocytes. We aimed to test the effect of EGCG on the expression of vascular endothelial growth factor (VEGF) in adipocytes. The levels of VEGF secretion, the expression of VEGF message ribonucleic acid (mRNA) and VEGF protein in 3T3-L1 cells were measured by enzyme linked immunosorbent assay (ELISA), real time polymerase chain reaction (PCR), and immunofluorescence staining, respectively. The xCELLigence real time cell analysis system was used to study the growth and differentiation of 3T3-L1 preadipocytes. A coculture system was used to test the effects of 3T3-L1 cells on proliferation of human umbilical vein endothelial cells (HUVECs). The conditioned media derived from 3T3-L1 cells treated with or without EGCG was used to culture the HUVECs for a tube formation assay. Peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer binding protein α (C/EBPα), two transcription factors related to both adipogenesis and angiogenesis, were examined to explore the potential mechanism. We found that all the three measurements of VEGF expression in adipocytes (mRNA, protein and secretion in media) were reduced after EGCG treatment. The growth of HUVECs co-cultured with 3T3-L1 cells was significantly increased and the conditioned media from EGCG treated 3T3-L1 adipocytes inhibited tube formation in HUVECs. Both PPARγ and C/EBPα expression in adipocytes were decreased with EGCG treatment. In conclusion, findings from this study suggest that EGCG may inhibit angiogenesis by regulating VEGF expression and secretion in adipocytes.

## Linked entities

- **Genes:** VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422], PPARG (peroxisome proliferator activated receptor gamma) [NCBI Gene 5468], CEBPA (CCAAT enhancer binding protein alpha) [NCBI Gene 1050]
- **Proteins:** VEGFA (vascular endothelial growth factor A), PPARG (peroxisome proliferator activated receptor gamma), CEBPA (CCAAT enhancer binding protein alpha)
- **Chemicals:** (−)-epigallocatechin-3-gallate (PubChem CID 65064), EGCG (PubChem CID 65064)

## Full-text entities

- **Genes:** Lep (leptin) [NCBI Gene 16846] {aka ob, obese}, CEBPA (CCAAT enhancer binding protein alpha) [NCBI Gene 1050] {aka C/EBP-alpha, CEBP}, Il6 (interleukin 6) [NCBI Gene 16193] {aka Il-6}, Actb (actin, beta) [NCBI Gene 11461] {aka Actx, E430023M04Rik, beta-actin}, VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}, Pgf (placental growth factor) [NCBI Gene 18654] {aka PIGF, Plgf}, Cebpa (CCAAT/enhancer binding protein alpha) [NCBI Gene 12606] {aka C/ebpalpha, CBF-A, Cebp}, Pdia4 (protein disulfide isomerase associated 4) [NCBI Gene 12304] {aka Cai, ERp-72, Erp72}, Pparg (peroxisome proliferator activated receptor gamma) [NCBI Gene 19016] {aka Nr1c3, PPAR-gamma, PPAR-gamma2, PPARgamma, PPARgamma2}, Tnf (tumor necrosis factor) [NCBI Gene 21926] {aka DIF, TNF-a, TNF-alpha, TNFSF2, TNFalpha, Tnfa}, Vegfa (vascular endothelial growth factor A) [NCBI Gene 22339] {aka L-VEGF, Vegf, Vpf}, PPARG (peroxisome proliferator activated receptor gamma) [NCBI Gene 5468] {aka CIMT1, FPLD3, GLM1, NR1C3, PPARG1, PPARG2}
- **Diseases:** hypoxia (MESH:D000860), chronic diseases (MESH:D002908), fat (MESH:D004620), obese (MESH:D009765), visceral fat (MESH:D007418), hypoxic (MESH:D002534), tumor (MESH:D009369), inflammation (MESH:D007249), Wenjing Tang (MESH:C536897)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]
- **Cell lines:** 3T3-L1 — Mus musculus (Mouse), Spontaneously immortalized cell line (CVCL_0123)

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC4632457/full.md

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Source: https://tomesphere.com/paper/PMC4632457