Literature DB >> 21345877

Comparison of ADAMTS-1, -4 and -5 expression in culprit plaques between acute myocardial infarction and stable angina.

Cheol Whan Lee1, Ilseon Hwang, Chan-Sik Park, Hyangsin Lee, Duk-Woo Park, Su-Jin Kang, Seung-Hwan Lee, Young-Hak Kim, Seong-Wook Park, Seung-Jung Park.   

Abstract

BACKGROUND: ADAMTS (a disintegrin and metalloproteinase with thrombospondin type 1 motifs) proteases might contribute to plaque destabilisation by weakening the fibrous cap. However, little is known about the expression of ADAMTS proteases in coronary atherosclerotic plaques.
OBJECTIVE: To examine the expression of ADAMTS proteases in coronary atherectomy samples obtained from patients with acute myocardial infarction (AMI) or stable angina.
METHODS: Atherectomy specimens were obtained from 34 patients with AMI (n=23) or stable angina (n=11) who underwent directional coronary atherectomy. The specimens were stained with H&E and analysed immunohistochemically using antibodies specific to ADAMTS-1, -4 and -5; versican cleavage products; and markers for endothelial cells, macrophages and smooth muscle cells.
RESULTS: Baseline characteristics were similar between the two groups. The proportion of CD31 and CD68 immunopositive areas did not differ between the two groups, but the area immunopositive for smooth muscle α-actin was smaller in the AMI group. The relative area immunopositive for ADAMTS-1 in AMI (1.04% (IQR 0.59-2.09%)) was significantly greater than that in stable angina (0.24% (0.15-0.39%); p<0.001). In contrast, the proportion of areas immunopositive for ADAMTS-4 or -5 was similar in the two groups. Areas that stained for ADAMTS-1 largely overlapped with those positive for CD68 and versican cleavage products. The areas immunopositive for ADAMTS-1 were significantly correlated with CD68 immunostained areas (r=0.50, p=0.003).
CONCLUSIONS: ADAMTS-1, -4 and -5 were present in human coronary atherosclerotic plaques, and ADATS-1 was more strongly expressed in AMI plaques than in stable plaques. ADAMTS-1 may play a role in plaque instability.

Entities:  

Mesh:

Substances:

Year:  2011        PMID: 21345877     DOI: 10.1136/jcp.2010.088484

Source DB:  PubMed          Journal:  J Clin Pathol        ISSN: 0021-9746            Impact factor:   3.411


  8 in total

1.  Pro-atherogenic proteoglycanase ADAMTS-1 is down-regulated by lauric acid through PI3K and JNK signaling pathways in THP-1 derived macrophages.

Authors:  Melissa-Hui-Ling Ong; Hong-Kin Wong; Tengku-Sifzizul Tengku-Muhammad; Quok-Cheong Choo; Choy-Hoong Chew
Journal:  Mol Biol Rep       Date:  2019-04-15       Impact factor: 2.316

2.  ADAM and ADAMTS disintegrin and metalloproteinases as major factors and molecular targets in vascular malfunction and disease.

Authors:  HaiFeng Yang; Raouf A Khalil
Journal:  Adv Pharmacol       Date:  2022-01-24

3.  The Role of ADAMTS1 and Versican in Human Myocardial Infarction: A Postmortem Study.

Authors:  Sultan Pehlivan; Murat Serdar Gurses; Mustafa Numan Ural; Sumeyya Akyol; Filiz Eren; Nursel Turkmen Inanir; Mehmet Akif Gulec; Bulent Eren; Recep Fedakar; Kadir Demircan; Omer Akyol
Journal:  Lab Med       Date:  2016-06-26

Review 4.  Pathophysiology of native coronary, vein graft, and in-stent atherosclerosis.

Authors:  Kazuyuki Yahagi; Frank D Kolodgie; Fumiyuki Otsuka; Aloke V Finn; Harry R Davis; Michael Joner; Renu Virmani
Journal:  Nat Rev Cardiol       Date:  2015-10-27       Impact factor: 32.419

5.  Regulation of ADAMTS-1, -4 and -5 expression in human macrophages: differential regulation by key cytokines implicated in atherosclerosis and novel synergism between TL1A and IL-17.

Authors:  Tim G Ashlin; Alvin P L Kwan; Dipak P Ramji
Journal:  Cytokine       Date:  2013-07-13       Impact factor: 3.861

6.  Association between plasma ADAMTS-7 levels and ventricular remodeling in patients with acute myocardial infarction.

Authors:  Wenjing Wu; Yifeng Zhou; Yiyang Li; Jiahui Li; Yuannan Ke; Yong Wang; Jingang Zheng
Journal:  Eur J Med Res       Date:  2015-03-21       Impact factor: 2.175

7.  The anti-atherogenic cytokine interleukin-33 inhibits the expression of a disintegrin and metalloproteinase with thrombospondin motifs-1, -4 and -5 in human macrophages: Requirement of extracellular signal-regulated kinase, c-Jun N-terminal kinase and phosphoinositide 3-kinase signaling pathways.

Authors:  Tim G Ashlin; Melanie L Buckley; Rebecca C Salter; Jason L Johnson; Alvin P L Kwan; Dipak P Ramji
Journal:  Int J Biochem Cell Biol       Date:  2013-11-22       Impact factor: 5.085

8.  Adventitial delivery of lentivirus-shRNA-ADAMTS-1 reduces venous stenosis formation in arteriovenous fistula.

Authors:  Evelyn C Nieves Torres; Binxia Yang; Bhaskar Roy; Rajiv Janardhanan; Akshaar Brahmbhatt; Ed Leof; Debabrata Mukhopadhyay; Sanjay Misra
Journal:  PLoS One       Date:  2014-04-14       Impact factor: 3.240

  8 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.