Endothelial dysfunction in patients with chronic thromboembolic pulmonary hypertension (CTEPH)

Tura-Ceide, Olga; Aventín, Núria; Piccari, Lucilla; Morén, Constanza; Guitart‐Mampel, Mariona; Garrabou, Glòria; García-Lucio, Jéssica; Chamorro, Núria; Blanco, Isabel; Peinado, Víctor I.; Castellà, Manuel; Barberà, Joan Albert

doi:10.1183/13993003.congress-2016.pa3606

Cited by 2 publications

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“…ECs isolated from endarterectomy specimens, referred to as CTEPH-ECs, were cultured as previously described [ 28 ]. In short, ECs were plated onto 0.1% gelatin-coated wells and grown in an endothelium cell medium (ScienceCell Research Laboratories) supplemented with endothelial cell growth supplement, 5% fetal bovine serum (FBS), and Penicillin/Streptomycin solution (ScienceCell Research Laboratories).…”

Section: Methodsmentioning

confidence: 99%

“…In short, ECs were plated onto 0.1% gelatin-coated wells and grown in an endothelium cell medium (ScienceCell Research Laboratories) supplemented with endothelial cell growth supplement, 5% fetal bovine serum (FBS), and Penicillin/Streptomycin solution (ScienceCell Research Laboratories). The cell phenotype was characterized by staining the cells with antibodies against a panel of endothelial and smooth muscle cell-specific markers, including endothelial nitric oxide synthase (eNOS) and alpha smooth muscle Actin (αSMA) [ 28 ]. The patient characteristics are presented in Table 1 .…”

Section: Methodsmentioning

confidence: 99%

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The Inflammatory Profile of CTEPH-Derived Endothelial Cells Is a Possible Driver of Disease Progression

Smolders

Lodder

Rodrı́guez

et al. 2021

Cells

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Chronic thromboembolic pulmonary hypertension (CTEPH) is a form of pulmonary hypertension characterized by the presence of fibrotic intraluminal thrombi and causing obliteration of the pulmonary arteries. Although both endothelial cell (EC) dysfunction and inflammation are linked to CTEPH pathogenesis, regulation of the basal inflammatory response of ECs in CTEPH is not fully understood. Therefore, in the present study, we investigated the role of the nuclear factor (NF)-κB pro-inflammatory signaling pathway in ECs in CTEPH under basal conditions. Basal mRNA levels of interleukin (IL)-8, IL-1β, monocyte chemoattractant protein-1 (MCP-1), C-C motif chemokine ligand 5 (CCL5), and vascular cell adhesion molecule-1 (VCAM-1) were upregulated in CTEPH-ECs compared to the control cells. To assess the involvement of NF-κB signaling in basal inflammatory activation, CTEPH-ECs were incubated with the NF-κB inhibitor Bay 11-7085. The increase in pro-inflammatory cytokines was abolished when cells were incubated with the NF-κB inhibitor. To determine if NF-κB was indeed activated, we stained pulmonary endarterectomy (PEA) specimens from CTEPH patients and ECs isolated from PEA specimens for phospho-NF-κB-P65 and found that especially the vessels within the thrombus and CTEPH-ECs are positive for phospho-NF-κB-P65. In summary, we show that CTEPH-ECs have a pro-inflammatory status under basal conditions, and blocking NF-κB signaling reduces the production of inflammatory factors in CTEPH-ECs. Therefore, our results show that the increased basal pro-inflammatory status of CTEPH-ECs is, at least partially, regulated through activation of NF-κB signaling and potentially contributes to the pathophysiology and progression of CTEPH.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

The Inflammatory Profile of CTEPH-Derived Endothelial Cells Is a Possible Driver of Disease Progression

Smolders

Lodder

Rodrı́guez

et al. 2021

Cells

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“…The existence of endothelial dysfunction in CTEPH pathogenesis is further supported by the fact that conditioned medium from CTEPH-derived PAECs, containing high levels of growth factors and inflammatory cytokines, increased PASMC proliferation and monocyte migration [ 157 ]. In addition, PAECs from CTEPH patients show an increased proliferation, altered angiogenic potential and metabolism, and apoptosis resistance [ 158 , 159 , 160 , 161 , 162 ]. Increased levels of soluble intracellular adhesion molecule-1 (ICAM1) in PAECs from CTEPH patients and in endarterectomy may contribute to EC proliferation and apoptosis resistance through its effect on cell survival pathways [ 161 ].…”

Section: Ec Dysfunction In Other Ph Groupsmentioning

confidence: 99%

Endothelial Dysfunction in Pulmonary Hypertension: Cause or Consequence?

et al. 2021

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Pulmonary arterial hypertension (PAH) is a rare, complex, and progressive disease that is characterized by the abnormal remodeling of the pulmonary arteries that leads to right ventricular failure and death. Although our understanding of the causes for abnormal vascular remodeling in PAH is limited, accumulating evidence indicates that endothelial cell (EC) dysfunction is one of the first triggers initiating this process. EC dysfunction leads to the activation of several cellular signalling pathways in the endothelium, resulting in the uncontrolled proliferation of ECs, pulmonary artery smooth muscle cells, and fibroblasts, and eventually leads to vascular remodelling and the occlusion of the pulmonary blood vessels. Other factors that are related to EC dysfunction in PAH are an increase in endothelial to mesenchymal transition, inflammation, apoptosis, and thrombus formation. In this review, we outline the latest advances on the role of EC dysfunction in PAH and other forms of pulmonary hypertension. We also elaborate on the molecular signals that orchestrate EC dysfunction in PAH. Understanding the role and mechanisms of EC dysfunction will unravel the therapeutic potential of targeting this process in PAH.

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Endothelial dysfunction in patients with chronic thromboembolic pulmonary hypertension (CTEPH)

Cited by 2 publications

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The Inflammatory Profile of CTEPH-Derived Endothelial Cells Is a Possible Driver of Disease Progression

The Inflammatory Profile of CTEPH-Derived Endothelial Cells Is a Possible Driver of Disease Progression

Endothelial Dysfunction in Pulmonary Hypertension: Cause or Consequence?

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