The role of calcium-sensing receptor in ginsenoside Rg1 promoting reendothelialization to inhibit intimal hyperplasia after balloon injury
Calcium-sensing receptor (CaSR) is a G protein-coupled receptor, widely distributed in various tissues, including vascular endothelial cells and smooth muscle cells, which plays an important role in the migration and homing of stem/progenitor cells and the proliferation of tissue cells. Restenosis a...
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| Format: | Article |
| Language: | English |
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Elsevier
2023-07-01
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| Series: | Biomedicine & Pharmacotherapy |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0753332223006339 |
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| author | Shangfu Xu Anling Hu Jiameng Chen Zhiqin Shuai Taotao Liu Jiang Deng Lisheng Li Qihai Gong Zhixu He Limei Yu |
| author_facet | Shangfu Xu Anling Hu Jiameng Chen Zhiqin Shuai Taotao Liu Jiang Deng Lisheng Li Qihai Gong Zhixu He Limei Yu |
| author_sort | Shangfu Xu |
| collection | DOAJ |
| description | Calcium-sensing receptor (CaSR) is a G protein-coupled receptor, widely distributed in various tissues, including vascular endothelial cells and smooth muscle cells, which plays an important role in the migration and homing of stem/progenitor cells and the proliferation of tissue cells. Restenosis after Percutaneous coronary intervention (PCI) seriously affects its prognosis and application. Our previous research has found that ginsenoside Rg1 (GS-Rg1) can inhibit the occurrence of restenosis after balloon injury of the common carotid artery in rats, but the mechanism is still unclear. In this study, it was found that GS-Rg1 (4, 8, 16 mg/kg) inhibited vascular restenosis caused by balloon injury, and mobilize endothelial progenitor cells (EPCs) to promote reendothelialization and inhibit intimal hyperplasia, which significantly reduced after administration of CaSR antagonist NPS 2143. Interestingly, CaSR and its downstream JNK, P38 were highly expressed in the proliferative intima and participated in the abnormal proliferation of vascular smooth muscle cells mediated by smooth muscle progenitor cells (SMPCs). GS-Rg1 inhibited intimal hyperplasia, while it decreased the expression of CaSR, JNK, and P38. This might relate to the distribution of CaSR and the facilitation of GS-Rg1 on the vascular endothelial repair. It is concluded that CaSR plays a key role in GS-Rg1 promoting reendothelialization to inhibit intimal hyperplasia after balloon Injury. |
| first_indexed | 2024-03-13T10:03:07Z |
| format | Article |
| id | doaj.art-63141055328b406e808f6a4e432cc55c |
| institution | Directory Open Access Journal |
| issn | 0753-3322 |
| language | English |
| last_indexed | 2024-03-13T10:03:07Z |
| publishDate | 2023-07-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Biomedicine & Pharmacotherapy |
| spelling | doaj.art-63141055328b406e808f6a4e432cc55c2023-05-23T04:21:16ZengElsevierBiomedicine & Pharmacotherapy0753-33222023-07-01163114843The role of calcium-sensing receptor in ginsenoside Rg1 promoting reendothelialization to inhibit intimal hyperplasia after balloon injuryShangfu Xu0Anling Hu1Jiameng Chen2Zhiqin Shuai3Taotao Liu4Jiang Deng5Lisheng Li6Qihai Gong7Zhixu He8Limei Yu9Key Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou 563000, China; Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563000, China; Collaborative Innovation Center of Chinese Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563000, China; Department of Pharmacology, School of Pharmacy, Zunyi Medical University, Zunyi, Guizhou 563000, China; Corresponding authors at: Key Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou 563000, China.Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563000, China; The Key Laboratory of Chemistry for Natural Products of Guizhou Province and Chinese Academic of Sciences, Guiyang, Guizhou 550014, ChinaKey Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou 563000, China; Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563000, ChinaKey Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou 563000, China; Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563000, ChinaKey Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou 563000, China; Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563000, ChinaKey Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563000, China; Department of Pharmacology, School of Pharmacy, Zunyi Medical University, Zunyi, Guizhou 563000, ChinaKey Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563000, China; Department of Pharmacology, School of Pharmacy, Zunyi Medical University, Zunyi, Guizhou 563000, ChinaKey Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563000, China; Department of Pharmacology, School of Pharmacy, Zunyi Medical University, Zunyi, Guizhou 563000, ChinaKey Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou 563000, China; Collaborative Innovation Center of Chinese Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563000, China; Corresponding authors at: Key Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou 563000, China.Key Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou 563000, China; Collaborative Innovation Center of Chinese Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563000, China; Corresponding authors at: Key Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou 563000, China.Calcium-sensing receptor (CaSR) is a G protein-coupled receptor, widely distributed in various tissues, including vascular endothelial cells and smooth muscle cells, which plays an important role in the migration and homing of stem/progenitor cells and the proliferation of tissue cells. Restenosis after Percutaneous coronary intervention (PCI) seriously affects its prognosis and application. Our previous research has found that ginsenoside Rg1 (GS-Rg1) can inhibit the occurrence of restenosis after balloon injury of the common carotid artery in rats, but the mechanism is still unclear. In this study, it was found that GS-Rg1 (4, 8, 16 mg/kg) inhibited vascular restenosis caused by balloon injury, and mobilize endothelial progenitor cells (EPCs) to promote reendothelialization and inhibit intimal hyperplasia, which significantly reduced after administration of CaSR antagonist NPS 2143. Interestingly, CaSR and its downstream JNK, P38 were highly expressed in the proliferative intima and participated in the abnormal proliferation of vascular smooth muscle cells mediated by smooth muscle progenitor cells (SMPCs). GS-Rg1 inhibited intimal hyperplasia, while it decreased the expression of CaSR, JNK, and P38. This might relate to the distribution of CaSR and the facilitation of GS-Rg1 on the vascular endothelial repair. It is concluded that CaSR plays a key role in GS-Rg1 promoting reendothelialization to inhibit intimal hyperplasia after balloon Injury.http://www.sciencedirect.com/science/article/pii/S0753332223006339Calcium-sensing receptorGinsenoside Rg1RestenosisEndothelial progenitor cellsReendothelialization |
| spellingShingle | Shangfu Xu Anling Hu Jiameng Chen Zhiqin Shuai Taotao Liu Jiang Deng Lisheng Li Qihai Gong Zhixu He Limei Yu The role of calcium-sensing receptor in ginsenoside Rg1 promoting reendothelialization to inhibit intimal hyperplasia after balloon injury Biomedicine & Pharmacotherapy Calcium-sensing receptor Ginsenoside Rg1 Restenosis Endothelial progenitor cells Reendothelialization |
| title | The role of calcium-sensing receptor in ginsenoside Rg1 promoting reendothelialization to inhibit intimal hyperplasia after balloon injury |
| title_full | The role of calcium-sensing receptor in ginsenoside Rg1 promoting reendothelialization to inhibit intimal hyperplasia after balloon injury |
| title_fullStr | The role of calcium-sensing receptor in ginsenoside Rg1 promoting reendothelialization to inhibit intimal hyperplasia after balloon injury |
| title_full_unstemmed | The role of calcium-sensing receptor in ginsenoside Rg1 promoting reendothelialization to inhibit intimal hyperplasia after balloon injury |
| title_short | The role of calcium-sensing receptor in ginsenoside Rg1 promoting reendothelialization to inhibit intimal hyperplasia after balloon injury |
| title_sort | role of calcium sensing receptor in ginsenoside rg1 promoting reendothelialization to inhibit intimal hyperplasia after balloon injury |
| topic | Calcium-sensing receptor Ginsenoside Rg1 Restenosis Endothelial progenitor cells Reendothelialization |
| url | http://www.sciencedirect.com/science/article/pii/S0753332223006339 |
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