Increased plasma monocyte chemoattractant protein‐1 level in idiopathic pulmonary arterial hypertension

Itoh, Takefumi; Nagaya, Noritoshi; Ishibashi‐Ueda, Hatsue; Kyotani, Shingo; Oya, Hideo; Sakamaki, Fumio; Kimura, Hiroshi; Nakanishi, Norifumi

doi:10.1111/j.1440-1843.2006.00821.x

Cited by 121 publications

(108 citation statements)

References 25 publications

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“…Consistent with these observations, we also found significantly increased perivascular cell infiltrates around remodeled vessels in addition to a trend toward up-regulation of proinflammatory mediators such as MCP-1 and IL-8 in the VM group. Both MCP-1 and IL-8 have been shown to be elevated in the plasma of patients with various forms of PAH (50,51).…”

Section: Discussionmentioning

confidence: 99%

Enhanced Pulmonary Arteriopathy in Simian Immunodeficiency Virus–infected Macaques Exposed to Morphine

Spikes

Dalvi

Tawfik

et al. 2012

Am J Respir Crit Care Med

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Section: Discussionmentioning

confidence: 99%

Enhanced Pulmonary Arteriopathy in Simian Immunodeficiency Virus–infected Macaques Exposed to Morphine

Spikes

Dalvi

Tawfik

et al. 2012

Am J Respir Crit Care Med

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“…Macrophage inhibitory factor concentration was also found to be elevated in bronchoalveolar lavage of animals and patients with PH induced by hypoxia (43). Compared to healthy controls, patients with idiopathic or associated PH exhibit higher circulating levels and pulmonary expression of various inflammatory cytokines and chemokines including interleukin (IL)-1β, IL-6 and monocyte chemoattractant protein-1 (MCP-1) (44)(45)(46). Lung expression of adhesion molecules such as intracellular adhesion molecule-1 and vascular cell adhesion molecule-1, and of the cytokine MCP-1, were markedly higher with hypoxia than normoxia in WT mice (47,48).…”

Section: E C -S O D a N D T R E A T M E N T O F P U L M O N A R Y H Ymentioning

confidence: 99%

Extracellular Superoxide Dismutase Overexpression Can Reverse the Course of Hypoxia-Induced Pulmonary Hypertension

Ahmed

Zhang

Codipilly

et al. 2011

Mol Med

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Hypoxia leads to free radical production, which has a pivotal role in the pathophysiology of pulmonary hypertension (PH). We hypothesized that treatment with extracellular superoxide dismutase (EC-SOD) could ameliorate the development of PH induced by hypoxia. In vitro studies using pulmonary microvascular endothelial cells showed that cells transfected with EC-SOD had significantly less accumulation of xanthine oxidase and reactive oxygen species than nontransfected cells after hypoxia exposure for 24 h. To study the prophylactic role of EC-SOD, adult male wild-type (WT) and transgenic (TG) mice, with lung-specific overexpression of human EC-SOD (hEC-SOD), were exposed to fraction of inspired oxygen (FiO 2 ) 10% for 10 d. After exposure, right ventricular systolic pressure (RVSP), right ventricular mass (RV/S + LV), pulmonary vascular wall thickness (PVWT) and pulmonary artery contraction/relaxation were assessed. TG mice were protected against PH compared with WT mice with significantly lower RVSP (23.9 ± 1.24 versus 47.2 ± 3.4), RV/S + LV (0.287 ± 0.015 versus 0.335 ± 0.022) and vascular remodeling, indicated by PVWT (14.324 ± 1.107 versus 18.885 ± 1.529). Functional studies using pulmonary arteries isolated from mice indicated that EC-SOD prevents hypoxia-mediated attenuation of nitric oxide-induced relaxation. Therapeutic potential was assessed by exposing WT mice to FiO 2 10% for 10 d. Half of the group was transfected with plasmid containing cDNA encoding human EC-SOD. The remaining animals were transfected with empty vector. Both groups were exposed to FiO 2 10% for a further 10 d. Transfected mice had significantly reduced RVSP (18.97 ± 1.12 versus 41.3 ± 1.5), RV/S + LV (0.293 ± 0.012 versus 0.372 ± 0.014) and PVWT (12.51 ± 0.72 versus 18.98 ± 1.24). On the basis of these findings, we concluded that overexpression of EC-SOD prevents the development of PH and ameliorates established PH.

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“…130 The pathogenesis of PH includes an inflammatory response, resulting in a higher circulating levels of monocyte chemoattractant protein 1 (MCP-1), interleukin (IL) 6, IL-8, and tumor necrosis factor α (TNF-α) in patients with IPAH and chronic thromboembolic PH than in healthy controls. [131][132][133][134] Oxidized lipids are known to promote inflammatory processes in many diseases such as atherosclerosis. 135 For example, oxidized LDL has been demonstrated to promote MCP-1 expression (Fig.…”

Section: Role Of Oxidized Lipids In Pah Inflammationmentioning

confidence: 99%

Role of Oxidized Lipids in Pulmonary Arterial Hypertension

et al. 2016

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Pulmonary arterial hypertension (PAH) is a multifactorial disease characterized by interplay of many cellular, molecular, and genetic events that lead to excessive proliferation of pulmonary cells, including smooth muscle and endothelial cells; inflammation; and extracellular matrix remodeling. Abnormal vascular changes and structural remodeling associated with PAH culminate in vasoconstriction and obstruction of pulmonary arteries, contributing to increased pulmonary vascular resistance, pulmonary hypertension, and right ventricular failure. The complex molecular mechanisms involved in the pathobiology of PAH are the limiting factors in the development of potential therapeutic interventions for PAH. Over the years, our group and others have demonstrated the critical implication of lipids in the pathogenesis of PAH. This review specifically focuses on the current understanding of the role of oxidized lipids, lipid metabolism, peroxidation, and oxidative stress in the progression of PAH. This review also discusses the relevance of apolipoprotein A-I mimetic peptides and microRNA-193, which are known to regulate the levels of oxidized lipids, as potential therapeutics in PAH.

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Increased plasma monocyte chemoattractant protein‐1 level in idiopathic pulmonary arterial hypertension

Abstract: Plasma MCP-1 levels were elevated in patients with IPAH, and this elevation was particularly marked in the early stage of disease. Taking into account the chemoattractant activity of MCP-1, these results imply a contribution of MCP-1 to the development of pulmonary hypertension.

Cited by 121 publications

References 25 publications

Enhanced Pulmonary Arteriopathy in Simian Immunodeficiency Virus–infected Macaques Exposed to Morphine

Enhanced Pulmonary Arteriopathy in Simian Immunodeficiency Virus–infected Macaques Exposed to Morphine

Extracellular Superoxide Dismutase Overexpression Can Reverse the Course of Hypoxia-Induced Pulmonary Hypertension

Role of Oxidized Lipids in Pulmonary Arterial Hypertension

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