HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (14) Citing Articles via Google Scholar Google Scholar Articles by Mitani, Y. Articles by Sakurai, M. Search for Related Content PubMed PubMed Citation Articles by Mitani, Y. Articles by Sakurai, M.

Vascular smooth muscle cell phenotypes in primary pulmonary hypertension

¹ Dept of Pediatrics and ² Dept of Anesthesiology, Mie University School of Medicine, Tsu, Mie, Japan. ³ Dept of Pathology, Osaka City University Medical School, Osaka, Japan. ⁴ Second Dept of Medicine, Gunma University School of Medicine, Gunma, Japan. ⁵ Dept of Pediatrics, Tenri Hospital, Nara, Japan

CORRESPONDENCE: M. Ueda, Dept of Pathology, Osaka City University Medical School, 1-4-3 Asahi-machi, Osaka, Japan. Fax: 81 666453742

Keywords: cytoskeletal proteins, fibronectin, intimal hyperplasia, macrophage, plexiform lesion

Received: January 13, 1999
Accepted July 18, 2000

Abstract

Primary pulmonary hypertension (PPH) is associated with specific structural alterations, including cellular intimal thickening, intimal fibrosis, and plexiform lesions.

To determine the phenotypes of smooth muscle cells (SMCs) in such lesions, the authors conducted an immunohistochemical analysis of lung tissues from two patients with PPH, using two antimuscle actin antibodies, HHF35 and CGA7, and two anti-SMC myosin heavy chain markers, anti-SM1 and anti-SM2 antibodies and related antibodies. Cells that stained positive (+) with HHF35, CGA7, anti-SM1, and anti-SM2 were considered to be SMCs of a mature state. Conversely, those that stained positive with HHF35 and anti-SM1, but weakly positive (+/–) or negative (–) with CGA7 and anti-SM2, were considered to be SMCs exhibiting an immature state.

Cellular intimal thickening was composed of SMCs of an immature phenotype (HHF35+, CGA7+/–, SM1+, SM2+/–), accompanied by the expression of fibronectin and the presence of macrophages; intimal fibrosis contained mature SMCs (HHF35+, CGA7+, SM1+, SM2+); and plexiform lesion consisted of proliferative endothelial cells (von Willebrand factor-positive cells, proliferating cell nuclear antigen-positive cells) and underlying immature SMCs (HHF35+, CGA7–, SM1+, SM2–) associated with fibronectin expression and macrophage infiltration.

These findings suggest that smooth muscle cells with specific phenotypes may contribute to the development of specific vascular lesions in primary pulmonary hypertension.