Intralesional pentraxin 3 increases with atherosclerotic disease progression, but may protect from thrombosis: Friend or foe?

Autor: Otani T; Department of Pathology, National Cerebral and Cardiovascular Center, 6-1 Kishibe-Shimmachi, Suita, Osaka 564-8565, Japan; Department of Pathology, Kindai University Faculty of Medicine, 377-2 Ono-higashi, Osaka-Sayama, Osaka 589-8511, Japan., Moriguchi-Goto S; Department of Pathology, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, Miyazaki 889-1692, Japan., Nishihira K; Department of Cardiology, Miyazaki Medical Association Hospital, 1173 Arita, Miyazaki 880-2102, Japan., Oguri N; Department of Pathology, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, Miyazaki 889-1692, Japan., Shibata Y; Department of Cardiology, Miyazaki Medical Association Hospital, 1173 Arita, Miyazaki 880-2102, Japan., Matsuura Y; Division of Cardiovascular Medicine and Nephrology, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, Miyazaki 889-1692, Japan., Kodama T; Department of Nuclear Receptor Medicine, Laboratories for Systems Biology and Medicine (LSBM) at the Research Center for Advanced Science and Technology (RCAST), The University of Tokyo, Tokyo 153-8904, Japan., Asada Y; Department of Pathology, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, Miyazaki 889-1692, Japan; Department of Pathology, Miyazaki Medical Association Hospital, 1173 Arita, Miyazaki 880-2102, Japan., Hatakeyama K; Department of Pathology, National Cerebral and Cardiovascular Center, 6-1 Kishibe-Shimmachi, Suita, Osaka 564-8565, Japan; Department of Diagnostic Pathology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan. Electronic address: kpathol@ncvc.go.jp., Yamashita A; Department of Pathology, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, Miyazaki 889-1692, Japan.
Jazyk: angličtina
Zdroj: Thrombosis research [Thromb Res] 2024 Feb; Vol. 234, pp. 134-141. Date of Electronic Publication: 2024 Jan 09.
DOI: 10.1016/j.thromres.2024.01.004
Abstrakt: Aim: To investigate the role of pentraxin 3 (PTX3) in atherosclerotic disease progression and plaque destabilization, as well as in coronary restenosis after directional coronary atherectomy (DCA).
Materials and Methods: PTX3 contents of early and advanced atherosclerotic lesions of the aorta obtained at autopsy were determined by ELISA and Western blot. Also, coronary plaques of patients with acute coronary syndrome (ACS) or stable angina pectoris (SAP) obtained by DCA were analyzed by immunohistochemistry for PTX3. The effects of PTX3 on smooth muscle cells (SMCs) and thrombogenesis were investigated with cultured human coronary artery SMCs and a flow chamber system, respectively.
Results: Advanced atherosclerotic lesions contained a significantly larger amount of PTX3 than early lesions (ELISA: 9.96 ± 2.77 ng/100 mg tissue, n = 8 vs 0.24 ± 0.18 ng/100 mg tissue, n = 6, P = 0.0097). Also, ACS plaques contained a significantly larger amount of PTX3 than SAP plaques (PTX3 immunohistochemistry-positive area percentage: 2.88 ± 0.53 %, n = 22 vs 0.67 ± 0.27 %, n = 23, P = 0.0009). Curiously, the patients who would remain free of post-DCA restenosis (n = 19) had plaques with a significantly higher PTX3 immunohistochemistry-positive area percentage than those who would develop restenosis (n = 12) (2.32 ± 0.49 % vs 0.49 ± 0.17 %, P = 0.002). In the mechanistic part of the study, PTX3 inhibited SMC proliferation and migration. PTX3 also inhibited platelet thrombus formation in the condition simulating arterial blood flow.
Conclusions: PTX3 is increased in advanced (vs early) atherosclerotic lesions and unstable (vs stable) coronary plaques. The inhibitory effects of PTX3 on SMCs and thrombogenesis suggest that intraplaque PTX3 might have atheroprotective effects.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)
Databáze: MEDLINE
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