Cargando…
A reduction of Syndecan-4 in macrophages promotes atherosclerosis by aggravating the proinflammatory capacity of macrophages
BACKGROUND: Cardiovascular diseases (CVDs) are a significant cause of mortality worldwide and are characterized by severe atherosclerosis (AS) in patients. However, the molecular mechanism of AS formation remains elusive. In the present study, we investigated the role of syndecan-4 (SDC4), a member...
Autores principales: | , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2022
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9287986/ https://www.ncbi.nlm.nih.gov/pubmed/35842658 http://dx.doi.org/10.1186/s12967-022-03505-5 |
_version_ | 1784748366624718848 |
---|---|
author | Hu, Jiaxin Zhang, Ying Hu, Liaoping Chen, Haiting Wu, Han Chen, Jianzhou Xie, Jun Xu, Biao Wei, Zhonghai |
author_facet | Hu, Jiaxin Zhang, Ying Hu, Liaoping Chen, Haiting Wu, Han Chen, Jianzhou Xie, Jun Xu, Biao Wei, Zhonghai |
author_sort | Hu, Jiaxin |
collection | PubMed |
description | BACKGROUND: Cardiovascular diseases (CVDs) are a significant cause of mortality worldwide and are characterized by severe atherosclerosis (AS) in patients. However, the molecular mechanism of AS formation remains elusive. In the present study, we investigated the role of syndecan-4 (SDC4), a member of the syndecan family, in atherogenesis. METHODS AND RESULTS: The expression of SDC4 decreased in mouse severe AS models. Moreover, knockout of SDC4 accelerated high-cholesterol diets (HCD)-induced AS in ApoE(−/−) mice. Mechanistically, the decrease of SDC4 increased macrophage proinflammatory capacity may be through the PKCα-ABCA1/ABCG1 signaling pathway. CONCLUSION: These findings provide evidence that SDC4 reduction links macrophages and inflammation to AS and that SDC4 in macrophages provides a therapeutic target for preventing AS formation. |
format | Online Article Text |
id | pubmed-9287986 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-92879862022-07-17 A reduction of Syndecan-4 in macrophages promotes atherosclerosis by aggravating the proinflammatory capacity of macrophages Hu, Jiaxin Zhang, Ying Hu, Liaoping Chen, Haiting Wu, Han Chen, Jianzhou Xie, Jun Xu, Biao Wei, Zhonghai J Transl Med Research BACKGROUND: Cardiovascular diseases (CVDs) are a significant cause of mortality worldwide and are characterized by severe atherosclerosis (AS) in patients. However, the molecular mechanism of AS formation remains elusive. In the present study, we investigated the role of syndecan-4 (SDC4), a member of the syndecan family, in atherogenesis. METHODS AND RESULTS: The expression of SDC4 decreased in mouse severe AS models. Moreover, knockout of SDC4 accelerated high-cholesterol diets (HCD)-induced AS in ApoE(−/−) mice. Mechanistically, the decrease of SDC4 increased macrophage proinflammatory capacity may be through the PKCα-ABCA1/ABCG1 signaling pathway. CONCLUSION: These findings provide evidence that SDC4 reduction links macrophages and inflammation to AS and that SDC4 in macrophages provides a therapeutic target for preventing AS formation. BioMed Central 2022-07-16 /pmc/articles/PMC9287986/ /pubmed/35842658 http://dx.doi.org/10.1186/s12967-022-03505-5 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Hu, Jiaxin Zhang, Ying Hu, Liaoping Chen, Haiting Wu, Han Chen, Jianzhou Xie, Jun Xu, Biao Wei, Zhonghai A reduction of Syndecan-4 in macrophages promotes atherosclerosis by aggravating the proinflammatory capacity of macrophages |
title | A reduction of Syndecan-4 in macrophages promotes atherosclerosis by aggravating the proinflammatory capacity of macrophages |
title_full | A reduction of Syndecan-4 in macrophages promotes atherosclerosis by aggravating the proinflammatory capacity of macrophages |
title_fullStr | A reduction of Syndecan-4 in macrophages promotes atherosclerosis by aggravating the proinflammatory capacity of macrophages |
title_full_unstemmed | A reduction of Syndecan-4 in macrophages promotes atherosclerosis by aggravating the proinflammatory capacity of macrophages |
title_short | A reduction of Syndecan-4 in macrophages promotes atherosclerosis by aggravating the proinflammatory capacity of macrophages |
title_sort | reduction of syndecan-4 in macrophages promotes atherosclerosis by aggravating the proinflammatory capacity of macrophages |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9287986/ https://www.ncbi.nlm.nih.gov/pubmed/35842658 http://dx.doi.org/10.1186/s12967-022-03505-5 |
work_keys_str_mv | AT hujiaxin areductionofsyndecan4inmacrophagespromotesatherosclerosisbyaggravatingtheproinflammatorycapacityofmacrophages AT zhangying areductionofsyndecan4inmacrophagespromotesatherosclerosisbyaggravatingtheproinflammatorycapacityofmacrophages AT huliaoping areductionofsyndecan4inmacrophagespromotesatherosclerosisbyaggravatingtheproinflammatorycapacityofmacrophages AT chenhaiting areductionofsyndecan4inmacrophagespromotesatherosclerosisbyaggravatingtheproinflammatorycapacityofmacrophages AT wuhan areductionofsyndecan4inmacrophagespromotesatherosclerosisbyaggravatingtheproinflammatorycapacityofmacrophages AT chenjianzhou areductionofsyndecan4inmacrophagespromotesatherosclerosisbyaggravatingtheproinflammatorycapacityofmacrophages AT xiejun areductionofsyndecan4inmacrophagespromotesatherosclerosisbyaggravatingtheproinflammatorycapacityofmacrophages AT xubiao areductionofsyndecan4inmacrophagespromotesatherosclerosisbyaggravatingtheproinflammatorycapacityofmacrophages AT weizhonghai areductionofsyndecan4inmacrophagespromotesatherosclerosisbyaggravatingtheproinflammatorycapacityofmacrophages AT hujiaxin reductionofsyndecan4inmacrophagespromotesatherosclerosisbyaggravatingtheproinflammatorycapacityofmacrophages AT zhangying reductionofsyndecan4inmacrophagespromotesatherosclerosisbyaggravatingtheproinflammatorycapacityofmacrophages AT huliaoping reductionofsyndecan4inmacrophagespromotesatherosclerosisbyaggravatingtheproinflammatorycapacityofmacrophages AT chenhaiting reductionofsyndecan4inmacrophagespromotesatherosclerosisbyaggravatingtheproinflammatorycapacityofmacrophages AT wuhan reductionofsyndecan4inmacrophagespromotesatherosclerosisbyaggravatingtheproinflammatorycapacityofmacrophages AT chenjianzhou reductionofsyndecan4inmacrophagespromotesatherosclerosisbyaggravatingtheproinflammatorycapacityofmacrophages AT xiejun reductionofsyndecan4inmacrophagespromotesatherosclerosisbyaggravatingtheproinflammatorycapacityofmacrophages AT xubiao reductionofsyndecan4inmacrophagespromotesatherosclerosisbyaggravatingtheproinflammatorycapacityofmacrophages AT weizhonghai reductionofsyndecan4inmacrophagespromotesatherosclerosisbyaggravatingtheproinflammatorycapacityofmacrophages |