Distribution and Synthesis of Apolipoprotein J in the Atherosclerotic Aorta
Abstract
Abstract— The distribution of apolipoprotein (apo) J during the development of atherosclerosis in the human aorta was evaluated by immununohistochemical observation, together with the other apolipoprotein A-I, A-II, B, C-III, and E. Although apoJ was never observed in the normal aorta (ie, without any intimal lesions or intimal thickening), it was distributed not only in the intima but also in the media of aortas with diffuse, intimal thickening or atherosclerotic lesions. Double immunostaining with antibodies for apoJ and α-smooth muscle actin revealed apoJ deposition in smooth muscle cells (SMCs) or the aortic stroma in the vicinity of SMCs. The extent of apoJ distribution in the aortic wall increased with the degree of atherosclerosis development. In addition, the distribution pattern of apoJ was very similar to that of apoA-I and E. In situ hybridization with human apoJ cDNA demonstrated intense signals in cells scattered within the subendothelial space and medial SMCs of the aorta with advanced atherosclerosis but not in those of the normal aorta without intimal thickening. Furthermore, reverse transcriptase–polymerase chain reaction of the cultured human aortic SMCs revealed apoJ mRNA expression in these cells. The results indicate that apoJ in the aortic wall originates from not only apoJ circulated in the plasma but also apoJ produced by SMCs in the aortic wall. Considering the similarities of the distribution between apoJ and apo-A-I or E, we hypothesize that apoJ possibly has a protective role against human atherosclerosis by its involvement with cholesterol transport from the aortic wall to the liver.
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CLU was detected in the intima and media of human atherosclerotic aortas and shown to originate at least in part from smooth muscle cells in the arterial wall.
“It was detected in the intima and media of human atherosclerotic aortas and was shown to originate at least in part from smooth muscle cells in the arterial wall.48”
From Aortic valve-specific genes dysregulated in calcific aortic valve stenosis as potential biomarkers and therapeutic targets (2025) · cites this paper as [48]
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- Authors
- Ishikawa, Y., Akasaka, Y., Ishii, T., Komiyama, K., Masuda, S., Asuwa, N., Choi-Miura, N.-H., & Tomita, M.
- Affiliations
- Nihon University (JP)
- ORCID
- Akasaka, Yoshikiyo
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 1998-04
- Volume
- 18
- Issue
- 4
- Pages
- 665-672
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- OpenAlex
- W2047255042
- Cited by
- 86
- References
- 0
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 2 · 2023: 1 · 2022: 3 · 2021: 4 · 2020: 2 · 2019: 4 · 2018: 2 · 2016: 4 · 2015: 4 · 2014: 3 · 2013: 4 · 2012: 1
- FWCI
- 4.70
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Keywords
- clusterin, atherosclerosis, aorta, apolipoprotein A-I, apolipoprotein E, smooth muscle cells, intimal thickening, cholesterol transport, alpha-smooth muscle actin
- MeSH terms
- Adolescent, Adult, Aged, Aged, 80 and over, Aorta, Apolipoproteins E, Arteriosclerosis, Cells, Cultured, Child, Glycoproteins, Humans, Immunohistochemistry, Middle Aged, RNA-Directed DNA Polymerase, RNA, Messenger, Tissue Distribution, Polymerase Chain Reaction, Apolipoprotein A-I, In Situ Hybridization, Molecular Chaperones, Clusterin
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