Degraded products generated by iron stent inhibit the vascular smooth muscle cell proliferation by downregulating AP-1
Abstract In-stent restenosis (ISR) following interventional therapy is a fatal clinical complication. Current evidence indicates that neointimal hyperplasia driven by uncontrolled proliferation of vascular smooth muscle cells (VSMC) is a major cause of restenosis. This implies that inhibiting VSMC p...
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2025-01-01
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Series: | Journal of Materials Science: Materials in Medicine |
Online Access: | https://doi.org/10.1007/s10856-024-06854-3 |
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author | Jiabing Huang Bingjian Liu Chunguang Zhao Jing Li Dongxu Qiu |
author_facet | Jiabing Huang Bingjian Liu Chunguang Zhao Jing Li Dongxu Qiu |
author_sort | Jiabing Huang |
collection | DOAJ |
description | Abstract In-stent restenosis (ISR) following interventional therapy is a fatal clinical complication. Current evidence indicates that neointimal hyperplasia driven by uncontrolled proliferation of vascular smooth muscle cells (VSMC) is a major cause of restenosis. This implies that inhibiting VSMC proliferation may be an attractive approach for preventing in-stent restenosis. In our previous study, we found that the iron stent reduced the neointimal hyperplasia in an atherosclerotic artery stenosis model, and the iron corroded granules generated by the iron stent inhibited neointimal hyperplasia by suppressing the proliferation of VSMCs. However, this observation needs to be validated through in vitro experimentation. In this study, co-culture experiments and flow cytometer assays were performed to qualitatively investigate the effects of iron stent degradation on VSMCs. Moreover, the degraded products resulting generated by the iron stent were collected and used to elucidate the suppressive effect of the iron stents. The underlying mechanism was explored through molecular biology assays. The major findings are as follows: 1) The degraded iron stent inhibited the proliferation of VSMCs; 2) The degraded products of the iron stent downregulated the expression of AP-1. In summary, this study demonstrates the inhibitory effect of degraded iron products on VSMC proliferation, implying that such products have the potential to mitigate in-stent restenosis. Graphical Abstract degraded products generated from iron stent inhibit the vascular smooth muscle cell proliferation by downregulating AP-1. |
format | Article |
id | doaj-art-bd2954608e6e4b74a0827416f1d02370 |
institution | Kabale University |
issn | 1573-4838 |
language | English |
publishDate | 2025-01-01 |
publisher | Springer |
record_format | Article |
series | Journal of Materials Science: Materials in Medicine |
spelling | doaj-art-bd2954608e6e4b74a0827416f1d023702025-01-19T12:08:12ZengSpringerJournal of Materials Science: Materials in Medicine1573-48382025-01-0136111010.1007/s10856-024-06854-3Degraded products generated by iron stent inhibit the vascular smooth muscle cell proliferation by downregulating AP-1Jiabing Huang0Bingjian Liu1Chunguang Zhao2Jing Li3Dongxu Qiu4Department of Cardiology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang UniversityDepartment of Neurology, Wuhan Hospital of Traditional Chinese and Western Medicine, Tongji Medical College, Huazhong University of Science and TechnologyGeneral ICU/Department of Critical Care Medicine, Xiangya Hospital, Central South UniversityDepartment of Neurology, Xiangya Hospital, Central South UniversityDepartment of Neurology, Xiangya Hospital, Central South UniversityAbstract In-stent restenosis (ISR) following interventional therapy is a fatal clinical complication. Current evidence indicates that neointimal hyperplasia driven by uncontrolled proliferation of vascular smooth muscle cells (VSMC) is a major cause of restenosis. This implies that inhibiting VSMC proliferation may be an attractive approach for preventing in-stent restenosis. In our previous study, we found that the iron stent reduced the neointimal hyperplasia in an atherosclerotic artery stenosis model, and the iron corroded granules generated by the iron stent inhibited neointimal hyperplasia by suppressing the proliferation of VSMCs. However, this observation needs to be validated through in vitro experimentation. In this study, co-culture experiments and flow cytometer assays were performed to qualitatively investigate the effects of iron stent degradation on VSMCs. Moreover, the degraded products resulting generated by the iron stent were collected and used to elucidate the suppressive effect of the iron stents. The underlying mechanism was explored through molecular biology assays. The major findings are as follows: 1) The degraded iron stent inhibited the proliferation of VSMCs; 2) The degraded products of the iron stent downregulated the expression of AP-1. In summary, this study demonstrates the inhibitory effect of degraded iron products on VSMC proliferation, implying that such products have the potential to mitigate in-stent restenosis. Graphical Abstract degraded products generated from iron stent inhibit the vascular smooth muscle cell proliferation by downregulating AP-1.https://doi.org/10.1007/s10856-024-06854-3 |
spellingShingle | Jiabing Huang Bingjian Liu Chunguang Zhao Jing Li Dongxu Qiu Degraded products generated by iron stent inhibit the vascular smooth muscle cell proliferation by downregulating AP-1 Journal of Materials Science: Materials in Medicine |
title | Degraded products generated by iron stent inhibit the vascular smooth muscle cell proliferation by downregulating AP-1 |
title_full | Degraded products generated by iron stent inhibit the vascular smooth muscle cell proliferation by downregulating AP-1 |
title_fullStr | Degraded products generated by iron stent inhibit the vascular smooth muscle cell proliferation by downregulating AP-1 |
title_full_unstemmed | Degraded products generated by iron stent inhibit the vascular smooth muscle cell proliferation by downregulating AP-1 |
title_short | Degraded products generated by iron stent inhibit the vascular smooth muscle cell proliferation by downregulating AP-1 |
title_sort | degraded products generated by iron stent inhibit the vascular smooth muscle cell proliferation by downregulating ap 1 |
url | https://doi.org/10.1007/s10856-024-06854-3 |
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