Increased Expression of TGF-β1 by 4-hexylresorcinol Is Mediated by Endoplasmic Reticulum and Mitochondrial Stress in Human Umbilical Endothelial Vein Cells

Jwa-Young Kim,Dae-Won Kim,Suk Keun Lee,Je-Yong Choi,Seong-Gon Kim,Umberto Garagiola,Xiangguo Che

doi:10.3390/app11199128

Abstract

In our previous study, 4-hexylresorcinol (4HR) increased the expression level of vascular endothelial growth factor in human umbilical vein endothelial cells (HUVECs) via the transforming growth factor-β1 (TGF-β1)-mediated pathway. Endoplasmic reticulum (ER) and mitochondrial stress is a positive regulator of cellular differentiation. As TGF-β1 is a master regulator for cellular differentiation, 4HR treatment may increase TGF-β1 expression via ER stress. In this study, HUVECs were treated using 4HR (1–100 μM) for 24 h. The 4HR treatment increased ER stress-associated markers and mitochondrial stress. Increased TGF-β1 expression by 4HR administration was alleviated by tauroursodeoxycholate (ER stress inhibitor) treatment. Combining these activities with the elevated acetylation level of histone 3 (H3) by 4HR treatment, TGF-β1 expression was increased in HUVECs. Overall, 4HR increased TGF-β1 expression through upregulation of the stress response of ER as well as H3 acetylation in HUVECs.

Highlights

Some phenolic compounds such as resorcinolic lipids can bind to proteins and change their conformation [1]
The aim of this study was to clarify the cellular mechanism of transforming growth factor-β1 (TGF-β1) expression after
Sometomicroorganisms their metabolic rate and enter a stateand of dormancy administration μM 4HR did lead to apoptosis induction

Summary

Introduction

Some phenolic compounds such as resorcinolic lipids can bind to proteins and change their conformation [1]. The administration of resorcinolic lipids suppresses microbial growth and induces dormancy [2]. It is hard to define dormancy as a biochemical aspect, a life in dormancy shows decreased metabolism with resistance to environmental stress [2,3]. Resorcinolic lipids can be considered chemical chaperones. Resorcinolic lipids can be produced by cells or synthesized chemically [1]. When a chemical chaperone is applied from outside, most active proliferating microorganisms will die [3]

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