Pulmonary vascular remodeling: a target for therapeutic intervention in pulmonary hypertension

Jeffery, Trina K.; Wanstall, Janet C.

doi:10.1016/s0163-7258(01)00157-7

Cited by 253 publications

(192 citation statements)

References 155 publications

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“…Pulmonary vascular remodeling is an important pathological part of pulmonary hypertension, leading to increased pulmonary vascular resistance and reduced vascular compliance. The increase in tenascin-C stimulates pulmonary vasculary remodeling 23) . Cowan et al showed in rats that pulmonary artery pressure and muscularization were reduced by myocyte apoptosis and loss of extracellular matrix, specifically elastin and tenascin-C 24) .…”

Section: Introductionmentioning

confidence: 99%

Tenascin-C May Be a Predictor of Acute Pulmonary Thromboembolism

Çelik

Koçyiğit

Çalapkorur

et al. 2011

JAT

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Aim:Numerous studies have shown an increase in NT-pro BNP, troponin and D-dimer levels with right ventricular dysfunction on echocardiography in patients with acute pulmonary thromboembolism (PTE). We found no data about the relation between tenascin-C and acute PTE in the literature. The aim of this study was to evaluate tenascin-C levels in acute PTE and correlate them with NT-pro BNP, troponin and D-dimer. Method: Thirty-four patients who have massive or submassive PTE on spiral thorax CT (PTE group) and twenty healthy volunteers (non-PTE group) were evaluated. In all patients, right ventricular functions were obtained on transthoracic echocardiography and plasma tenascin-C, NT-pro BNP, troponin , and D-dimer levels were measured. Results: The left ventricular systolic diameter, left ventricular diastolic diameter and left ventricular ejection fraction were similar in the two groups. The right heart chamber sizes and main pulmonary artery diameter were significantly larger in the PTE group and systolic pulmonary artery pressures were also significantly higher in this group. Tenascin-C, NT-pro BNP, and D-dimer levels were also significantly higher in the PTE group than in the non-PTE group ( p 0.001). The troponin I levels did not differ between the two groups ( p 0.4). Tenascin-C was found to be highly correlated with sPAP and NT-pro BNP and correlated with D-dimer; however, troponin I was not correlated with tenascin-C. Conclusion: This study demonstrates that tenascin-C may be an indicator of acute PTE. J Atheroscler Thromb, 2011; 18:487-493.

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Section: Introductionmentioning

confidence: 99%

Tenascin-C May Be a Predictor of Acute Pulmonary Thromboembolism

Çelik

Koçyiğit

Çalapkorur

et al. 2011

JAT

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“…Bovine pulmonary artery endothelial cells (BPAECs) are one model system for studying functionally important aspects of cytoskeleton. These cells are derived from the pulmonary vascular endothelium, where they function as a semi-permeable barrier [13]. In several instances, alterations of barrier permeability are mediated by cytoskeletal rearrangements, and hence cytoskeletal organization in these cells has been studied in some detail [14].…”

Section: Introductionmentioning

confidence: 99%

Modes of remodeling in the cortical cytoskeleton of vascular endothelial cells

Pesen

Hoh

2004

FEBS Letters

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The cortical cytoskeleton of vascular endothelial cells plays an important role in responding to mechanical stimuli and controlling the distribution of cell surface proteins. Here, we have used atomic force microscopy to visualize the dynamics of cortical cytoskeleton in living bovine pulmonary artery endothelial cells. We demonstrate that the cortical cytoskeleton, organized as a complex polygonal mesh, is highly dynamic and shows two modes of remodeling: intact-boundary-mode where mesh element boundaries remain intact but move at 0.08 lm/ min allowing the mesh element to change shape, and alteredboundary-mode where new mesh boundaries form and existing ones disappear.

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“…Pulmonary artery endothelial cells (PAECs) exposed to cyclic strain induce vascular endothelial cell growth factor and platelet-derived growth factor, which stimulate pulmonary artery smooth muscle cell (PASMC) growth (5,6). PAECs also produce factors that inhibit PASMC growth, such as nitric oxide (7), prostacyclin (8), heparin-like compounds (9)(10)(11), and xanthine oxidase (12).…”

mentioning

confidence: 99%

Cyclic Stretch Affects Pulmonary Endothelial Cell Control of Pulmonary Smooth Muscle Cell Growth

Ochoa¹,

Baker²,

Hasak³

et al. 2008

Am J Respir Cell Mol Biol

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Endothelial cells are subjected to mechanical forces in the form of cyclic stretch resulting from blood pulsatility. Pulmonary artery endothelial cells (PAECs) produce factors that stimulate and inhibit pulmonary artery smooth muscle cell (PASMC) growth. We hypothesized that PAECs exposed to cyclic stretch secrete proteins that inhibit PASMC growth. Media from PAECs exposed to cyclic stretch significantly inhibited PASMC growth in a time-dependent manner. Lyophilized material isolated from stretched PAEC-conditioned media significantly inhibited PASMC growth in a dose-dependent manner. This inhibition was reversed by trypsin inactivation, which is consistent with the relevant factor being a protein(s). To identify proteins that inhibited cell growth in conditioned media from stretched PAECs, we used proteomic techniques and found that thrombospondin (TSP)-1, a natural antiangiogenic factor, was up-regulated by stretch. In vitro, exogenous TSP-1 inhibited PASMC growth. TSP-1-blocking antibodies reversed conditioned media-induced inhibition of PASMC growth. Cyclic stretched PAECs secrete protein(s) that inhibit PASMC proliferation. TSP-1 may be, at least in part, responsible for this inhibition. The complete identification and understanding of the secreted proteome of stretched PAECs may lead to new insights into the pathophysiology of pulmonary vascular remodeling.

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Pulmonary vascular remodeling: a target for therapeutic intervention in pulmonary hypertension

Cited by 253 publications

References 155 publications

Tenascin-C May Be a Predictor of Acute Pulmonary Thromboembolism

Tenascin-C May Be a Predictor of Acute Pulmonary Thromboembolism

Modes of remodeling in the cortical cytoskeleton of vascular endothelial cells

Cyclic Stretch Affects Pulmonary Endothelial Cell Control of Pulmonary Smooth Muscle Cell Growth

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