PMID- 11463608
OWN - NLM
STAT- MEDLINE
DCOM- 20010927
LR  - 20071115
IS  - 1073-449X (Print)
IS  - 1073-449X (Linking)
VI  - 164
IP  - 2
DP  - 2001 Jul 15
TI  - Plasma monocyte chemoattractant protein-1 and pulmonary vascular resistance in 
      chronic thromboembolic pulmonary hypertension.
PG  - 319-24
AB  - 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.
FAU - Kimura, H
AU  - Kimura H
AD  - 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
FAU - Okada, O
AU  - Okada O
FAU - Tanabe, N
AU  - Tanabe N
FAU - Tanaka, Y
AU  - Tanaka Y
FAU - Terai, M
AU  - Terai M
FAU - Takiguchi, Y
AU  - Takiguchi Y
FAU - Masuda, M
AU  - Masuda M
FAU - Nakajima, N
AU  - Nakajima N
FAU - Hiroshima, K
AU  - Hiroshima K
FAU - Inadera, H
AU  - Inadera H
FAU - Matsushima, K
AU  - Matsushima K
FAU - Kuriyama, T
AU  - Kuriyama T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am J Respir Crit Care Med
JT  - American journal of respiratory and critical care medicine
JID - 9421642
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Chemokine CCL2/*blood
MH  - Chronic Disease
MH  - Cytokines/blood
MH  - Female
MH  - Hemodynamics
MH  - Humans
MH  - Hypertension, Pulmonary/*blood/pathology/*physiopathology
MH  - Male
MH  - Middle Aged
MH  - Pulmonary Artery/pathology/*physiopathology
MH  - Pulmonary Embolism/*blood/pathology/*physiopathology
MH  - Vascular Resistance/*physiology
EDAT- 2001/07/21 10:00
MHDA- 2001/09/28 10:01
CRDT- 2001/07/21 10:00
PHST- 2001/07/21 10:00 [pubmed]
PHST- 2001/09/28 10:01 [medline]
PHST- 2001/07/21 10:00 [entrez]
AID - 10.1164/ajrccm.164.2.2006154 [doi]
PST - ppublish
SO  - Am J Respir Crit Care Med. 2001 Jul 15;164(2):319-24. doi: 
      10.1164/ajrccm.164.2.2006154.