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Cardiovascular Research 2006 70(1):158-164; doi:10.1016/j.cardiores.2006.02.003
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Copyright © 2006, European Society of Cardiology

Adrenomedullin in mast cells of abdominal aortic aneurysm

Toshihiro Tsurudaa,b,*, Johji Katoa, Kinta Hatakeyamac, Atsushi Yamashitac, Kunihide Nakamurad, Takuroh Imamuraa, Kazuo Kitamuraa, Toshio Onitsukad, Yujiro Asadac and Tanenao Etoa

aFirst Department of Internal Medicine, Miyazaki Medical College, University of Miyazaki, Japan
bDepartment of Nutrition Management, Faculty of Health and Nutrition, Minami-Kyushu University, Japan
cDepartment of Pathology, Miyazaki Medical College, University of Miyazaki, Japan
dSecond Department of Surgery, Miyazaki Medical College, University of Miyazaki, Japan

* Corresponding author. First Department of Internal Medicine, Miyazaki Medical College, University of Miyazaki, 5200 Kihara Kiyotake, Miyazaki 889-1692, Japan. Tel.: +81 985 85 0872; fax: +81 985 85 6596. Email address: ttsuruda{at}med.miyazaki-u.ac.jp

Objectives Produced by vascular walls, adrenomedullin (AM) exerts antifibrotic actions in the process of cardiovascular remodeling. The purpose of this study was to examine the pathophysiological role of AM in the development of human abdominal aortic aneurysm (AAA).

Methods and results Immunohistochemical analyses revealed that vascular smooth muscle cells in the media were positive for AM in the early stage of atherosclerotic aorta. Intense immunoreactivity was observed in mast cells of the outer media and adventitia of AAA, and the number of mast cells was greater (p<0.01) in AAA than in atherosclerotic aorta without any aneurysmal change. To determine the role of AM in mast cells, we examined cultured human mast cell leukemia line-1 (HMC-1) and fibroblasts isolated from AAA patients. Cultured HMC-1 cells were found to express preproAM gene and release AM peptide into the cultured media. When assessed by collagenase-sensitive [3H]proline incorporation and procollagen type I C-peptide secretion, collagen synthesis in co-culture of HMC-1 and the fibroblasts was reduced by 10– 6 mol/L synthetic AM, while conversely, it increased following blockade of the action of endogenous AM with 10µg/mL anti-AM monoclonal antibody.

Conclusion The present study suggests an anti-fibrotic role for AM released from mast cells, providing new insight into the biological actions of mast cell-derived AM in the development of AAA.

KEYWORDS Adrenomedullin; Abdominal aortic aneurysm; Mast cell; Fibrosis

Time for primary review 22 days


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