Pulmonary venous hypertension and mechanical strain stimulate monocyte chemoattractant protein-1 release and structural remodelling of the lung in human and rodent chronic heart failure models

Park, John E. S.; Lyon, Alexander R.; Shao, Dongmin; Hector, Lauren R.; Xu, Hua; O’Gara, Peter; Pinhu, Liao; Chambers, Rachel C.; Wort, Stephen J.; Griffiths, Mark

doi:10.1136/thoraxjnl-2013-204190

Cited by 12 publications

(9 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Tissue remodeling is common in many other cell types following mechanical stress and the resulting inflammatory response (vascular smooth muscle, 58-60 endothelium, 61-63 colonic smooth muscle, 64 endometrial stromal cells, 65 lung epithelium 66 ). Extensive remodeling of myometrial smooth muscle and the extracellular matrix is required for the onset of labor.…”

Section: Commentmentioning

confidence: 99%

Uterine overdistention induces preterm labor mediated by inflammation: observations in pregnant women and nonhuman primates

Waldorf

Singh

Mohan

et al. 2015

American Journal of Obstetrics and Gynecology

127

118

View full text Add to dashboard Cite

OBJECTIVE Uterine overdistention is thought to induce preterm labor in women with twin and multiple pregnancies, but the pathophysiology remains unclear. We investigated for the first time the pathogenesis of preterm birth associated with rapid uterine distention in a pregnant nonhuman primate model. STUDY DESIGN A nonhuman primate model of uterine overdistention was created using preterm chronically catheterized pregnant pigtail macaques (Macaca nemestrina) by inflation of intraamniotic balloons (N = 6), which were compared to saline controls (N = 5). Cesarean delivery was performed due to preterm labor or at experimental end. Microarray, quantitative reverse transcriptase polymerase chain reaction, Luminex (Austin, TX), and enzyme-linked immunosorbent assay were used to measure messenger RNA (mRNA) and/or protein levels from monkey (amniotic fluid, myometrium, maternal plasma) and human (amniocytes, amnion, myometrium) tissues. Statistical analysis employed analysis of covariance and Wilcoxon rank sum. Biomechanical forces were calculated using the law of Laplace. RESULTS Preterm labor occurred in 3 of 6 animals after balloon inflation and correlated with greater balloon volume and uterine wall stress. Significant elevations of inflammatory cytokines and prostaglandins occurred following uterine overdistention in an “inflammatory pulse” that correlated with preterm labor (interleukin [IL]-1β, tumor necrosis factor [TNF]-α, IL-6, IL-8, CCL2, prostaglandin E2, prostaglandin F2α, all P < .05). A similar inflammatory response was observed in amniocytes in vitro following mechanical stretch (IL1β, IL6, and IL8 mRNA multiple time points, P < .05), in amnion of women with polyhydramnios (IL6 and TNF mRNA, P < .05) and in amnion (TNF-α) and myometrium of women with twins in early labor (IL6, IL8, CCL2, all P < .05). Genes differentially expressed in the nonhuman primate after balloon inflation and in women with polyhydramnios and twins are involved in tissue remodeling and muscle growth. CONCLUSION Uterine overdistention by inflation of an intraamniotic balloon is associated with an inflammatory pulse that precedes and correlates with preterm labor. Our results indicate that inflammation is an early event after a mechanical stress on the uterus and leads to preterm labor when the stress is sufficiently great. Further, we find evidence of uterine tissue remodeling and muscle growth as a common, perhaps compensatory, response to uterine distension.

show abstract

Section: Commentmentioning

confidence: 99%

Uterine overdistention induces preterm labor mediated by inflammation: observations in pregnant women and nonhuman primates

Waldorf

Singh

Mohan

et al. 2015

American Journal of Obstetrics and Gynecology

127

118

View full text Add to dashboard Cite

show abstract

“…Recently, Park et al 7 found that lung microvascular endothelial cells exposed to cyclic mechanical strain in vitro released proinflammatory and profibrotic mediators identifying a specific putative role for the monocyte chemoattractant protein 1 (MCP-1).…”

Section: Accepted Manuscriptmentioning

confidence: 99%

“…There is strong preclinical evidence that lung microcirculation impairment warrants attention as a determinant of unfavorable clinical outcome 7 . When lung capillaries are exposed to an excessive hydrostatic pressure a stress failure phenomenon occurs, initially described by West and co-workers in a series of experimental preparations in different animal models 8 .…”

Section: Accepted M Manuscriptmentioning

confidence: 99%

Endothelial Dysfunction and Lung Capillary Injury in Cardiovascular Diseases

Guazzi¹,

Phillips²,

Arena³

et al. 2015

Progress in Cardiovascular Diseases

View full text Add to dashboard Cite

Cardiac dysfunction of both systolic and diastolic origin leads to increased left atrial pressure, lung capillary injury and increased resistance to gas transfer. Acutely, pressure-induced trauma disrupts the endothelial and alveolar anatomical configuration and definitively causes an impairment of cellular pathways involved in fluid-flux regulation and gas exchange efficiency, a process well identified as stress failure of the alveolarcapillary membrane. In chronic heart failure (HF), additional stimuli other than pressure may trigger the true remodeling process of capillaries and small arteries characterized by endothelial dysfunction, proliferation of myofibroblasts, fibrosis and extracellular matrix deposition. In parallel there is a loss of alveolar gas diffusion properties due to the increased path from air to blood (thickening of extracellular matrix) and loss of fine molecular mechanism involved in fluid reabsorption and clearance. Deleterious changes in gas transfer not only reflect the underlying lung tissue damage but also portend independent prognostic information and may play a role in the pathogenesis of exercise limitations and ventilatory abnormalities observed in these patients. Few currently approved treatments for chronic HF have the potential to positively affect structural remodeling of the lung capillary network; angiotensin-converting enzyme inhibitors are one of the few currently established options. Recently, more attention has been paid to novel therapies specifically targeting the nitric oxide pathway as a suitable target to improve endothelial function and permeability as well as alveolar gas exchange properties.

show abstract

“… 125 At the same time, a series of inflammation-related mediators are generated to cause pulmonary vascular EC damage and mPAP increase. 126 RES significantly decreases the mRNA and protein levels of MCP-1. It suggests that RES can reduce the recruitment of monocytes and alleviate the injury of PAECs caused by inflammatory cells and inflammatory mediators.…”

Section: Stilbenesmentioning

confidence: 88%

Natural plant products in treatment of pulmonary arterial hypertension

Xiang

Deng

et al. 2018

Pulm. circ.

View full text Add to dashboard Cite

Pulmonary arterial hypertension (PAH) is a severe disease characterized by progressive remodeling of distal pulmonary arteries and persistent elevation of pulmonary vascular resistance (PVR), which leads to right ventricular dysfunction, heart failure, and eventually death. Although treatment responsiveness for this disease is improving, it continues to be a life-threatening condition. With the clinical efficacy of natural plant products being fully confirmed by years of practice, more and more recognition and attention have been obtained from the international pharmaceutical industry. Moreover, studies over the past decades have demonstrated that drugs derived from natural plants show unique advantages and broad application prospects in PAH treatment, not to mention the historical application of Chinese traditional medicine in cardiopulmonary diseases. In this review, we focus on summarizing natural plant compounds with therapeutic properties in PAH, according to the extracts, fractions, and pure compounds from plants into categories, hoping it to be helpful for basic research and clinical application.

show abstract

Pulmonary venous hypertension and mechanical strain stimulate monocyte chemoattractant protein-1 release and structural remodelling of the lung in human and rodent chronic heart failure models

Cited by 12 publications

References 46 publications

Uterine overdistention induces preterm labor mediated by inflammation: observations in pregnant women and nonhuman primates

Uterine overdistention induces preterm labor mediated by inflammation: observations in pregnant women and nonhuman primates

Endothelial Dysfunction and Lung Capillary Injury in Cardiovascular Diseases

Natural plant products in treatment of pulmonary arterial hypertension

Contact Info

Product

Resources

About