Inhibitory effects of interleukin-6 on release of PGI2 by cultured human pulmonary artery smooth muscle cells

Wen, Fuqiang; Watanabe, Kentaro; Yoshida, Minoru

doi:10.1016/0090-6980(96)00055-x

Cited by 11 publications

(5 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We are currently undertaking an animal study to define the role of MIF in pulmonary hypertension. Another cytokine of note is IL‐6, which strongly inhibits 6‐keto‐PGF 1α production in human PASMC 28 . While apparently fundamental abnormalities in endothelial cells are being found in pulmonary hypertension, how they lead to dysfunction and proliferation of SMC remains poorly understood 29,30 .…”

Section: Discussionmentioning

confidence: 99%

“…Another cytokine of note is IL-6, which strongly inhibits 6-keto-PGF 1α production in human PASMC. 28 While apparently fundamental abnormalities in endothelial cells are being found in pulmonary hypertension, how they lead to dysfunction and proliferation of SMC remains poorly understood. 29,30 TNF-α, MIF, and IL-6 may represent targets for future treatments in pulmonary hypertension.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of IL‐1β, TNF‐α, and macrophage migration inhibitory factor on prostacyclin synthesis in rat pulmonary artery smooth muscle cells

et al. 2003

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effects of IL‐1β, TNF‐α, and macrophage migration inhibitory factor on prostacyclin synthesis in rat pulmonary artery smooth muscle cells

et al. 2003

View full text Add to dashboard Cite

show abstract

“…123,124 IL-6 causes an increase in C4b-binding protein, which also binds protein S and reduces the levels of free protein S. 125 IL-6 may suppress vascular production of PGI 2 . 126 Because fibrinogen degradation products can stimulate IL-6 production, there may be a positive feedback loop involving thrombosis and inflammation pathways. 127,128 NUTRITIONAL AND METABOLIC FUNCTION Plasma total homocysteine (tHcy) increases in older populations, and the association between adverse cardiovascular events and high tHcy levels persists in the elderly.…”

Section: Inflammation Aging and Thrombosismentioning

confidence: 99%

Aging and Thrombosis

Wilkerson¹,

Sane²

2002

Semin Thromb Hemost

189

122

View full text Add to dashboard Cite

Advanced age is associated with a dramatic increase in the rates of venous and arterial thrombotic events. Increases in fibrinogen, factors VIII and IX, and other coagulation proteins, without a proportional increase in anticoagulant factors, likely contribute to this risk. Recent studies have delineated a role for genomic elements in controlling age-related expression of some coagulation proteins. Enhanced platelet activity as well as molecular and anatomic changes in the vessel wall also contribute to the thrombotic propensity. Advanced age is associated with elevated interleukin-6 (IL-6) and C-reactive protein levels, indicating an inflammatory state that may be an important stimulus for thrombus formation in the elderly. Despite evidence of a prothrombotic state, many elderly people do not experience clinical thrombotic events. It is possible that the increase in coagulation proteins and activation markers conveys a survival advantage, such as inhibiting tumor angiogenesis. The recent epidemic in obesity may heighten thrombotic risks in the elderly because adipose tissue is an important source of inflammatory cytokines and plasminogen activator inhibitor-1 (PAI-1). As the population ages, further studies will be warranted to define the mechanisms for thrombosis in the elderly.

show abstract

“…Use of iEPO has shown a significant decrease in PVR and PAP, and an increase in PaO 2 and PaO 2 /FiO 2 without affecting SVR or MAP [Zwissler et al 1996;Walmrath et al 1996;van Heerden et al 2000;Dunkley et al 2013;Domenighetti et al 2001;Dahlem et al 2004;Torbic et al 2013]. Compared with iNO, iEPO may also provide some pleotropic effects outside of improved oxygenation and thus outcomes with iNO likely cannot be extrapolated to iEPO [Adhikari et al 2014;Rose et al 1999;Eisenhut et al 1993;Wen et al 1996]. While iEPO also impacts arterial oxygenation by decreasing V/Q mismatching and pulmonary shunt flow, this effect is not different from iNO.…”

Section: Iloprostmentioning

confidence: 99%

“…Eisenhut and colleagues first reported the impact of prostacyclins on inflammatory cytokines when they identified a prostacyclin-mediated suppression of tumor necrosis factor (TNF) α synthesis in activated monocytes [Eisenhut et al 1993]. Release of these inflammatory cytokines produces a profound suppression of prostacyclin release in pulmonary vasculature, potentially shifting the balance towards proinflammatory [Wen et al 1996]. Given the proinflammatory state of ARDS and the significant expression of interleukin (IL) 6, IL-1, IL-10 and TNF-α, supplementation of prostacyclins may be beneficial.…”

Section: Introductionmentioning

confidence: 99%

The role of inhaled prostacyclin in treating acute respiratory distress syndrome

Searcy

Morales

Ferreira

et al. 2015

Ther Adv Respir Dis

View full text Add to dashboard Cite

Acute respiratory distress syndrome (ARDS) is a syndrome of acute lung injury that is characterized by noncardiogenic pulmonary edema and severe hypoxemia second to a pathogenic impairment of gas exchange. Despite significant advances in the area, mortality remains high among ARDS patients. High mortality and a limited spectrum of therapeutic options have left clinicians searching for alternatives, spiking interest in selective pulmonary vasodilators (SPVs). Despite the lack of robust evidence, SPVs are commonly employed for their therapeutic role in improving oxygenation in patients who have developed refractory hypoxemia in ARDS. While inhaled epoprostenol (iEPO) also impacts arterial oxygenation by decreasing ventilation-perfusion (V/Q) mismatching and pulmonary shunt flow, this effect is not different from inhaled nitric oxide (iNO). The most effective and safest dose for yielding a clinically significant increase in PaO 2 and reduction in pulmonary artery pressure (PAP) appears to be 20-30 ng/kg/min in adults and 30 ng/kg/min in pediatric patients. iEPO appears to have a ceiling effect above these doses in which no additional benefit may be derived. iNO and iEPO have shown similar efficacy profiles; however, they differ with respect to cost and ease of therapeutic administration. The most beneficial effects of iEPO have been seen in adult patients with secondary ARDS as compared with primary ARDS, most likely due to the difference in etiology of the two disease states, and in patients suffering from baseline right ventricular heart failure. Although iEPO has demonstrated improvements in hemodynamic parameters and oxygenation in ARDS patients, due to the limited number of randomized clinical trials and the lack of studies investigating mortality, the use of iEPO cannot be recommended as standard of care in ARDS. iEPO should be reserved for those refractory to traditional therapies.

show abstract

Inhibitory effects of interleukin-6 on release of PGI2 by cultured human pulmonary artery smooth muscle cells

Cited by 11 publications

References 26 publications

Effects of IL‐1β, TNF‐α, and macrophage migration inhibitory factor on prostacyclin synthesis in rat pulmonary artery smooth muscle cells

Effects of IL‐1β, TNF‐α, and macrophage migration inhibitory factor on prostacyclin synthesis in rat pulmonary artery smooth muscle cells

Aging and Thrombosis

The role of inhaled prostacyclin in treating acute respiratory distress syndrome

Contact Info

Product

Resources

About