Increased Expression of TGF-β1 by 4-hexylresorcinol Is Mediated by Endoplasmic Reticulum and Mitochondrial Stress in Human Umbilical Endothelial Vein Cells
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 re...
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2021-09-01
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| author | Jwa-Young Kim Dae-Won Kim Suk Keun Lee Je-Yong Choi Xiangguo Che Seong-Gon Kim Umberto Garagiola |
| author_facet | Jwa-Young Kim Dae-Won Kim Suk Keun Lee Je-Yong Choi Xiangguo Che Seong-Gon Kim Umberto Garagiola |
| author_sort | Jwa-Young Kim |
| collection | DOAJ |
| description | 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. |
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| institution | Directory Open Access Journal |
| issn | 2076-3417 |
| language | English |
| last_indexed | 2024-03-10T07:06:03Z |
| publishDate | 2021-09-01 |
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| spelling | doaj.art-c1ba3c9bae2541ee881b545ac14a1db62023-11-22T15:48:11ZengMDPI AGApplied Sciences2076-34172021-09-011119912810.3390/app11199128Increased Expression of TGF-β1 by 4-hexylresorcinol Is Mediated by Endoplasmic Reticulum and Mitochondrial Stress in Human Umbilical Endothelial Vein CellsJwa-Young Kim0Dae-Won Kim1Suk Keun Lee2Je-Yong Choi3Xiangguo Che4Seong-Gon Kim5Umberto Garagiola6Hallym University Kangnam Sacred Heart Hospital, Hallym University Medical Center, 1, Singil-ro, Yeongdeungpo-gu, Seoul 07441, KoreaDepartment of Oral Biochemistry, College of Dentistry, Gangneung-Wonju National University, Gangneung 28644, KoreaInstitution of Hydrogen Magnetic Reaction Gene Regulation, Daejeon 34140, KoreaDepartment of Biochemistry and Cell Biology, Cell and Matrix Research Institute, Skeletal Diseases Analysis Center, Korea Mouse Phenotyping Center (KMPC), School of Medicine, Kyungpook National University, Daegu 41944, KoreaDepartment of Biochemistry and Cell Biology, Cell and Matrix Research Institute, Skeletal Diseases Analysis Center, Korea Mouse Phenotyping Center (KMPC), School of Medicine, Kyungpook National University, Daegu 41944, KoreaDepartment of Oral and Maxillofacial Surgery, College of Dentistry, Gangneung-Wonju National University, Gangneung 28644, KoreaBiomedical, Surgical and Oral Sciences Department, Maxillofacial and Dental Unit, School of Dentistry, University of Milan, 20122 Milan, ItalyIn 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.https://www.mdpi.com/2076-3417/11/19/91284-hexylresorcinolTGF-β1endoplasmic reticulummitochondriaATP |
| spellingShingle | Jwa-Young Kim Dae-Won Kim Suk Keun Lee Je-Yong Choi Xiangguo Che Seong-Gon Kim Umberto Garagiola Increased Expression of TGF-β1 by 4-hexylresorcinol Is Mediated by Endoplasmic Reticulum and Mitochondrial Stress in Human Umbilical Endothelial Vein Cells Applied Sciences 4-hexylresorcinol TGF-β1 endoplasmic reticulum mitochondria ATP |
| title | Increased Expression of TGF-β1 by 4-hexylresorcinol Is Mediated by Endoplasmic Reticulum and Mitochondrial Stress in Human Umbilical Endothelial Vein Cells |
| title_full | Increased Expression of TGF-β1 by 4-hexylresorcinol Is Mediated by Endoplasmic Reticulum and Mitochondrial Stress in Human Umbilical Endothelial Vein Cells |
| title_fullStr | Increased Expression of TGF-β1 by 4-hexylresorcinol Is Mediated by Endoplasmic Reticulum and Mitochondrial Stress in Human Umbilical Endothelial Vein Cells |
| title_full_unstemmed | Increased Expression of TGF-β1 by 4-hexylresorcinol Is Mediated by Endoplasmic Reticulum and Mitochondrial Stress in Human Umbilical Endothelial Vein Cells |
| title_short | Increased Expression of TGF-β1 by 4-hexylresorcinol Is Mediated by Endoplasmic Reticulum and Mitochondrial Stress in Human Umbilical Endothelial Vein Cells |
| title_sort | increased expression of tgf β1 by 4 hexylresorcinol is mediated by endoplasmic reticulum and mitochondrial stress in human umbilical endothelial vein cells |
| topic | 4-hexylresorcinol TGF-β1 endoplasmic reticulum mitochondria ATP |
| url | https://www.mdpi.com/2076-3417/11/19/9128 |
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