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CD44 expression in plexiform lesions of idiopathic pulmonary arterial hypertension

Authors

  • Keiko Ohta-Ogo,

    1. Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Kita-ku, Okayama
    2. Department of Pathology, National Cerebral and Cardiovascular Center, Suita, Osaka
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  • Hiroyuki Hao,

    Corresponding author
    1. Department of Pathology, National Cerebral and Cardiovascular Center, Suita, Osaka
    2. Department of Surgical Pathology, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan
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  • Hatsue Ishibashi-Ueda,

    1. Department of Pathology, National Cerebral and Cardiovascular Center, Suita, Osaka
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  • Seiichi Hirota,

    1. Department of Surgical Pathology, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan
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  • Kazufumi Nakamura,

    1. Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Kita-ku, Okayama
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  • Tohru Ohe,

    1. Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Kita-ku, Okayama
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  • Hiroshi Ito

    1. Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Kita-ku, Okayama
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Hiroyuki Hao, MD, PhD, Department of Surgical Pathology, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo 663-8501, Japan. Email: haohiro@hyo-med.ac.jp

Abstract

Plexiform lesions in pulmonary arteries are a characteristic histological feature for idiopathic pulmonary arterial hypertension (IPAH). The pathogenesis of the plexiform lesion is not fully understood, although it may be related to endothelial cell dysfunction and local inflammation. CD44 is a cell adhesion molecule and it is also involved in angiogenesis, endothelial cell proliferation and migration. The expression of CD44 was examined in lung plexiform lesions obtained from patients with IPAH (IPAH group, n= 7) and pulmonary arterial hypertension associated with atrial septal defect (ASD-PAH group, n= 4). Expression of CD44 was detected in 49 out of 52 plexiform lesions (93%) from all patients in the IPAH group, whereas 31 plexiform lesions obtained from the ASD-PAH group lacked CD44 positivity by immunohistochemistry. In the IPAH group, CD44 was localized in the endothelial cells of microvessels within plexiform lesions and activated T cells in and around the lesions. Furthermore, T cell infiltration and endothelial cell proliferation activity were prominent in the plexiform lesions of the IPAH group, compared to those of the ASD-PAH group. These findings suggest that CD44 and activated T cell infiltration play an important role in the development of plexiform lesions particularly in IPAH.

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