Swiprosin-1 deficiency in macrophages alleviated atherogenesis

Abstract Macrophages play a vital role in the development of atherosclerosis. Previously, we have found that swiprosin-1 was abundantly expressed in macrophages. Here, we investigated the role of swiprosin-1 expressed in macrophages in atherogenesis. Bone marrow transplantation was performed from sw...

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Autores principales: Ling-Chang Tong, Zhi-Bin Wang, Jia-Qi Zhang, Yue Wang, Wei-Ye Liu, Hao Yin, Jia-Cheng Li, Ding-Feng Su, Yong-Bing Cao, Li-Chao Zhang, Ling Li
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Publicado: Nature Publishing Group 2021
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Acceso en línea:https://doaj.org/article/7eca3c2e0311419ba0bfd78fb4d626e1
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spelling oai:doaj.org-article:7eca3c2e0311419ba0bfd78fb4d626e12021-11-14T12:12:38ZSwiprosin-1 deficiency in macrophages alleviated atherogenesis10.1038/s41420-021-00739-y2058-7716https://doaj.org/article/7eca3c2e0311419ba0bfd78fb4d626e12021-11-01T00:00:00Zhttps://doi.org/10.1038/s41420-021-00739-yhttps://doaj.org/toc/2058-7716Abstract Macrophages play a vital role in the development of atherosclerosis. Previously, we have found that swiprosin-1 was abundantly expressed in macrophages. Here, we investigated the role of swiprosin-1 expressed in macrophages in atherogenesis. Bone marrow transplantation was performed from swiprosin-1-knockout (Swp −/− ) mice and age-matched ApoE −/− mice. Atherosclerotic lesion, serum lipid, and interleukin-β (IL-β) levels were detected. In vitro, the peritoneal macrophages isolated from Swp −/− and wild-type mice were stimulated with oxidized low-density lipoprotein (ox-LDL) and the macrophage of foam degree, cellular lipid content, apoptosis, inflammatory factor, migration, and autophagy were determined. Our results showed that swiprosin-1 was mainly expressed in macrophages of atherosclerotic plaques in aorta from ApoE −/− mice fed with high-cholesterol diet (HCD). The expression of swiprosin-1 in the foaming of RAW264.7 macrophages gradually increased with the increase of the concentration and time stimulated with ox-LDL. Atherosclerotic plaques, accumulation of macrophages, collagen content, serum total cholesterol, LDL, and IL-β levels were decreased in Swp − /− → ApoE −/− mice compared with Swp +/+  → ApoE −/− mice fed with HCD for 16 weeks. The macrophage foam cell formation and cellular cholesterol accumulation were reduced, while the lipid uptake and efflux increased in macrophages isolated from Swp −/− compared to wild-type mice treated with ox-LDL. Swiprosin-1 deficiency in macrophages could inhibit apoptosis, inflammation, migration, and promote autophagy. Taken together, our results demonstrated that swiprosin-1 deficiency in macrophages could alleviate the development and progression of AS. The role of swiprosin-1 may provide a promising new target for ameliorating AS.Ling-Chang TongZhi-Bin WangJia-Qi ZhangYue WangWei-Ye LiuHao YinJia-Cheng LiDing-Feng SuYong-Bing CaoLi-Chao ZhangLing LiNature Publishing GrouparticleNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282CytologyQH573-671ENCell Death Discovery, Vol 7, Iss 1, Pp 1-11 (2021)
institution DOAJ
collection DOAJ
language EN
topic Neoplasms. Tumors. Oncology. Including cancer and carcinogens
RC254-282
Cytology
QH573-671
spellingShingle Neoplasms. Tumors. Oncology. Including cancer and carcinogens
RC254-282
Cytology
QH573-671
Ling-Chang Tong
Zhi-Bin Wang
Jia-Qi Zhang
Yue Wang
Wei-Ye Liu
Hao Yin
Jia-Cheng Li
Ding-Feng Su
Yong-Bing Cao
Li-Chao Zhang
Ling Li
Swiprosin-1 deficiency in macrophages alleviated atherogenesis
description Abstract Macrophages play a vital role in the development of atherosclerosis. Previously, we have found that swiprosin-1 was abundantly expressed in macrophages. Here, we investigated the role of swiprosin-1 expressed in macrophages in atherogenesis. Bone marrow transplantation was performed from swiprosin-1-knockout (Swp −/− ) mice and age-matched ApoE −/− mice. Atherosclerotic lesion, serum lipid, and interleukin-β (IL-β) levels were detected. In vitro, the peritoneal macrophages isolated from Swp −/− and wild-type mice were stimulated with oxidized low-density lipoprotein (ox-LDL) and the macrophage of foam degree, cellular lipid content, apoptosis, inflammatory factor, migration, and autophagy were determined. Our results showed that swiprosin-1 was mainly expressed in macrophages of atherosclerotic plaques in aorta from ApoE −/− mice fed with high-cholesterol diet (HCD). The expression of swiprosin-1 in the foaming of RAW264.7 macrophages gradually increased with the increase of the concentration and time stimulated with ox-LDL. Atherosclerotic plaques, accumulation of macrophages, collagen content, serum total cholesterol, LDL, and IL-β levels were decreased in Swp − /− → ApoE −/− mice compared with Swp +/+  → ApoE −/− mice fed with HCD for 16 weeks. The macrophage foam cell formation and cellular cholesterol accumulation were reduced, while the lipid uptake and efflux increased in macrophages isolated from Swp −/− compared to wild-type mice treated with ox-LDL. Swiprosin-1 deficiency in macrophages could inhibit apoptosis, inflammation, migration, and promote autophagy. Taken together, our results demonstrated that swiprosin-1 deficiency in macrophages could alleviate the development and progression of AS. The role of swiprosin-1 may provide a promising new target for ameliorating AS.
format article
author Ling-Chang Tong
Zhi-Bin Wang
Jia-Qi Zhang
Yue Wang
Wei-Ye Liu
Hao Yin
Jia-Cheng Li
Ding-Feng Su
Yong-Bing Cao
Li-Chao Zhang
Ling Li
author_facet Ling-Chang Tong
Zhi-Bin Wang
Jia-Qi Zhang
Yue Wang
Wei-Ye Liu
Hao Yin
Jia-Cheng Li
Ding-Feng Su
Yong-Bing Cao
Li-Chao Zhang
Ling Li
author_sort Ling-Chang Tong
title Swiprosin-1 deficiency in macrophages alleviated atherogenesis
title_short Swiprosin-1 deficiency in macrophages alleviated atherogenesis
title_full Swiprosin-1 deficiency in macrophages alleviated atherogenesis
title_fullStr Swiprosin-1 deficiency in macrophages alleviated atherogenesis
title_full_unstemmed Swiprosin-1 deficiency in macrophages alleviated atherogenesis
title_sort swiprosin-1 deficiency in macrophages alleviated atherogenesis
publisher Nature Publishing Group
publishDate 2021
url https://doaj.org/article/7eca3c2e0311419ba0bfd78fb4d626e1
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