Regulation of Inflammation-Mediated Endothelial to Mesenchymal Transition with Echinochrome a for Improving Myocardial Dysfunction
Endothelial–mesenchymal transition (EndMT) is a process by which endothelial cells (ECs) transition into mesenchymal cells (e.g., myofibroblasts and smooth muscle cells) and induce fibrosis of cells/tissues, due to ischemic conditions in the heart. Previously, we reported that echinochrome A (EchA)...
| Main Authors: | , , , , , , , , , , , , , , |
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| Format: | Article |
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MDPI AG
2022-11-01
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| Series: | Marine Drugs |
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| Online Access: | https://www.mdpi.com/1660-3397/20/12/756 |
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| author | Byeong-Wook Song Sejin Kim Ran Kim Seongtae Jeong Hanbyeol Moon Hojin Kim Elena A. Vasileva Natalia P. Mishchenko Sergey A. Fedoreyev Valentin A. Stonik Min Young Lee Jongmin Kim Hyoung Kyu Kim Jin Han Woochul Chang |
| author_facet | Byeong-Wook Song Sejin Kim Ran Kim Seongtae Jeong Hanbyeol Moon Hojin Kim Elena A. Vasileva Natalia P. Mishchenko Sergey A. Fedoreyev Valentin A. Stonik Min Young Lee Jongmin Kim Hyoung Kyu Kim Jin Han Woochul Chang |
| author_sort | Byeong-Wook Song |
| collection | DOAJ |
| description | Endothelial–mesenchymal transition (EndMT) is a process by which endothelial cells (ECs) transition into mesenchymal cells (e.g., myofibroblasts and smooth muscle cells) and induce fibrosis of cells/tissues, due to ischemic conditions in the heart. Previously, we reported that echinochrome A (EchA) derived from sea urchin shells can modulate cardiovascular disease by promoting anti-inflammatory and antioxidant activity; however, the mechanism underlying these effects was unclear. We investigated the role of EchA in the EndMT process by treating human umbilical vein ECs (HUVECs) with TGF-β2 and IL-1β, and confirmed the regulation of cell migration, inflammatory, oxidative responses and mitochondrial dysfunction. Moreover, we developed an EndMT-induced myocardial infarction (MI) model to investigate the effect of EchA in vivo. After EchA was administered once a day for a total of 3 days, the histological and functional improvement of the myocardium was investigated to confirm the control of the EndMT. We concluded that EchA negatively regulates early or inflammation-related EndMT and reduces the myofibroblast proportion and fibrosis area, meaning that it may be a potential therapy for cardiac regeneration or cardioprotection from scar formation and cardiac fibrosis due to tissue granulation. Our findings encourage the study of marine bioactive compounds for the discovery of new therapeutics for recovering ischemic cardiac injuries. |
| first_indexed | 2024-03-09T16:09:46Z |
| format | Article |
| id | doaj.art-22fa38c2568f4304aecaf98ceeb0c100 |
| institution | Directory Open Access Journal |
| issn | 1660-3397 |
| language | English |
| last_indexed | 2024-03-09T16:09:46Z |
| publishDate | 2022-11-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Marine Drugs |
| spelling | doaj.art-22fa38c2568f4304aecaf98ceeb0c1002023-11-24T16:19:40ZengMDPI AGMarine Drugs1660-33972022-11-01201275610.3390/md20120756Regulation of Inflammation-Mediated Endothelial to Mesenchymal Transition with Echinochrome a for Improving Myocardial DysfunctionByeong-Wook Song0Sejin Kim1Ran Kim2Seongtae Jeong3Hanbyeol Moon4Hojin Kim5Elena A. Vasileva6Natalia P. Mishchenko7Sergey A. Fedoreyev8Valentin A. Stonik9Min Young Lee10Jongmin Kim11Hyoung Kyu Kim12Jin Han13Woochul Chang14Institute for Bio-Medical Convergence, Catholic Kwandong University International St. Mary’s Hospital, Incheon 22711, Republic of KoreaDepartment of Biology Education, College of Education, Pusan National University, Busan 46241, Republic of KoreaDepartment of Biology Education, College of Education, Pusan National University, Busan 46241, Republic of KoreaInstitute for Bio-Medical Convergence, Catholic Kwandong University International St. Mary’s Hospital, Incheon 22711, Republic of KoreaInstitute for Bio-Medical Convergence, Catholic Kwandong University International St. Mary’s Hospital, Incheon 22711, Republic of KoreaInstitute for Bio-Medical Convergence, Catholic Kwandong University International St. Mary’s Hospital, Incheon 22711, Republic of KoreaG.B. Elyakov Pacific Institute of Bioorganic Chemistry, Far-Eastern Branch of the Russian Academy of Science, 690022 Vladivostok, RussiaG.B. Elyakov Pacific Institute of Bioorganic Chemistry, Far-Eastern Branch of the Russian Academy of Science, 690022 Vladivostok, RussiaG.B. Elyakov Pacific Institute of Bioorganic Chemistry, Far-Eastern Branch of the Russian Academy of Science, 690022 Vladivostok, RussiaG.B. Elyakov Pacific Institute of Bioorganic Chemistry, Far-Eastern Branch of the Russian Academy of Science, 690022 Vladivostok, RussiaDepartment of Molecular Physiology, College of Pharmacy, Kyungpook National University, Daegu 41566, Republic of KoreaDepartment of Life Systems, Sookmyung Women’s University, Seoul 04310, Republic of KoreaDepartment of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, Smart Marine Therapeutic Center, Inje University, Busan 47392, Republic of KoreaDepartment of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, Smart Marine Therapeutic Center, Inje University, Busan 47392, Republic of KoreaDepartment of Biology Education, College of Education, Pusan National University, Busan 46241, Republic of KoreaEndothelial–mesenchymal transition (EndMT) is a process by which endothelial cells (ECs) transition into mesenchymal cells (e.g., myofibroblasts and smooth muscle cells) and induce fibrosis of cells/tissues, due to ischemic conditions in the heart. Previously, we reported that echinochrome A (EchA) derived from sea urchin shells can modulate cardiovascular disease by promoting anti-inflammatory and antioxidant activity; however, the mechanism underlying these effects was unclear. We investigated the role of EchA in the EndMT process by treating human umbilical vein ECs (HUVECs) with TGF-β2 and IL-1β, and confirmed the regulation of cell migration, inflammatory, oxidative responses and mitochondrial dysfunction. Moreover, we developed an EndMT-induced myocardial infarction (MI) model to investigate the effect of EchA in vivo. After EchA was administered once a day for a total of 3 days, the histological and functional improvement of the myocardium was investigated to confirm the control of the EndMT. We concluded that EchA negatively regulates early or inflammation-related EndMT and reduces the myofibroblast proportion and fibrosis area, meaning that it may be a potential therapy for cardiac regeneration or cardioprotection from scar formation and cardiac fibrosis due to tissue granulation. Our findings encourage the study of marine bioactive compounds for the discovery of new therapeutics for recovering ischemic cardiac injuries.https://www.mdpi.com/1660-3397/20/12/756endothelial–mesenchymal transitionechinochrome Amyocardial infarctioncardiac fibrosis |
| spellingShingle | Byeong-Wook Song Sejin Kim Ran Kim Seongtae Jeong Hanbyeol Moon Hojin Kim Elena A. Vasileva Natalia P. Mishchenko Sergey A. Fedoreyev Valentin A. Stonik Min Young Lee Jongmin Kim Hyoung Kyu Kim Jin Han Woochul Chang Regulation of Inflammation-Mediated Endothelial to Mesenchymal Transition with Echinochrome a for Improving Myocardial Dysfunction Marine Drugs endothelial–mesenchymal transition echinochrome A myocardial infarction cardiac fibrosis |
| title | Regulation of Inflammation-Mediated Endothelial to Mesenchymal Transition with Echinochrome a for Improving Myocardial Dysfunction |
| title_full | Regulation of Inflammation-Mediated Endothelial to Mesenchymal Transition with Echinochrome a for Improving Myocardial Dysfunction |
| title_fullStr | Regulation of Inflammation-Mediated Endothelial to Mesenchymal Transition with Echinochrome a for Improving Myocardial Dysfunction |
| title_full_unstemmed | Regulation of Inflammation-Mediated Endothelial to Mesenchymal Transition with Echinochrome a for Improving Myocardial Dysfunction |
| title_short | Regulation of Inflammation-Mediated Endothelial to Mesenchymal Transition with Echinochrome a for Improving Myocardial Dysfunction |
| title_sort | regulation of inflammation mediated endothelial to mesenchymal transition with echinochrome a for improving myocardial dysfunction |
| topic | endothelial–mesenchymal transition echinochrome A myocardial infarction cardiac fibrosis |
| url | https://www.mdpi.com/1660-3397/20/12/756 |
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