title: Plasma monocyte chemoattractant protein-1 and pulmonary vascular resistance in chronic thromboembolic pulmonary hypertension.
abstract: The pathogenesis of severe pulmonary hypertension seems to be related to inflammatory response in diseased sites. Monocyte chemoattractant protein-1 (MCP-1) has been reported to play a role in the development of congestive heart failure. In this immunological response, activation and migration of leukocytes including macrophages to the inflammatory region are important factors. We hypothesized that the severity of pulmonary hypertension may be related to MCP-1, which is thought to be upregulated by blood pressure or shear stress in pulmonary vasculature as well as by immunological and inflammatory reactions in chronic thromboembolic pulmonary hypertension (CTEPH). Circulating levels of MCP-1, interleukin-1beta (IL-1beta), and tumor necrosis factor-alpha (TNF-alpha) were measured by sandwich ELISA in 14 patients with CTEPH. The plasma level of MCP-1 was significantly correlated with pulmonary vascular resistance. In IL-1beta and TNF-alpha, on the other hand, there was no correlation between cytokines and pulmonary hemodynamics. Pathological specimens obtained from the patients with CTEPH undergoing thromboendarterectomy demonstrated immunoreactivity of MCP-1 in endothelium, smooth muscle cells, and macrophages within neointima in the hypertensive large elastic pulmonary artery. We conclude that MCP-1 is upregulated in the remodeling of pulmonary arteries in close association with increased pulmonary vascular resistance in CTEPH.
authors.affiliation: Department of Chest Medicine, Institute of Pulmonary Cancer Research, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8679, Japan. kimura@nmu-gw.naramed-u.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Kimura
authors.forename: O
authors.initials: O
authors.lastname: Okada
authors.forename: N
authors.initials: N
authors.lastname: Tanabe
authors.forename: Y
authors.initials: Y
authors.lastname: Tanaka
authors.forename: M
authors.initials: M
authors.lastname: Terai
authors.forename: Y
authors.initials: Y
authors.lastname: Takiguchi
authors.forename: M
authors.initials: M
authors.lastname: Masuda
authors.forename: N
authors.initials: N
authors.lastname: Nakajima
authors.forename: K
authors.initials: K
authors.lastname: Hiroshima
authors.forename: H
authors.initials: H
authors.lastname: Inadera
authors.forename: K
authors.initials: K
authors.lastname: Matsushima
authors.forename: T
authors.initials: T
authors.lastname: Kuriyama
mesh_terms: D000328:Adult; D000368:Aged; D018932:Chemokine CCL2 / Q000097:blood*; D002908:Chronic Disease; D016207:Cytokines / Q000097:blood; D005260:Female; D006439:Hemodynamics; D006801:Humans; D006976:Hypertension, Pulmonary / Q000097:blood* / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D011651:Pulmonary Artery / Q000473:pathology / Q000503:physiopathology*; D011655:Pulmonary Embolism / Q000097:blood* / Q000473:pathology / Q000503:physiopathology*; D014655:Vascular Resistance / Q000502:physiology*
chemical_list: D018932:Chemokine CCL2; D016207:Cytokines