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Pulmonary Hypertension - Cellular and Molecular Changes in the Lung...
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Pulmonary Hypertension - Cellular and Molecular Changes in the Lung and in the Right Ventricle

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (1 July 2024) | Viewed by 11192

Special Issue Editor

Prof. Dr. Véronique C. Freund-Michel

E-Mail Website
Guest Editor
Centre de Recherche Cardio-Thoracique de Bordeaux-INSERM U1045, Université de Bordeaux, Bordeaux, France
Interests: nerve growth factor (NGF); TrkA and p75NTR receptors; pulmonary hypertension; cardiac dysfunction and remodelling; cardiovascular and pulmonary pathophysiology and pharmacology; chronic hypoxia; animal models; cell cultures; smooth muscle cells; endothelial cells; fibroblasts; inflammation; pro-inflammatory cytokines; neurotrophins; macrophages; mast cells; pulmonary arterial remodelling; pulmonary arterial reactivity; calcium signalling; calcium sensitization mechanisms; TRP channels; Piezo channels; proliferation; migration; connexins; GAP junctions

Special Issue Information

Dear Colleagues, 

Pulmonary hypertension (PH) is a severe disease characterized by sustained elevated pulmonary arterial pressures leading to right ventricular hypertrophy, right heart failure, and patient death. Since the currently available PH treatments improve patients’ quality of life and prolong their survival but fail to reverse the disease, new and efficient treatments are urgently needed. The key pathophysiological mechanisms of PH involve pulmonary arterial remodeling, inflammation, and altered reactivity, but all the cellular and molecular changes in the lung contributing to these alterations remain unknown. Gaining a better understanding of these changes may help us to highlight new potential therapeutic targets, undoubtedly leading to new perspectives in the treatment of PH. Another current challenge in PH is developing a strategy that would also be able to decrease/delay the development of right heart failure, which is often responsible for the death of PH patients. Gaining a better understanding of the right ventricular cellular and molecular changes associated with PH would also allow us to highlight new potential therapeutic targets. The aim of this Special Issue, entitled “Pulmonary hypertension – cellular and molecular changes in the lung and in the right ventricle”, is therefore to welcome both original papers and comprehensive review papers exploring the cellular and molecular changes in the lung and/or right ventricle during pulmonary hypertension, which may lead to opening new and exciting therapeutic perspectives on this devastating disease.  

We look forward to receiving your contributions. 

Prof. Dr. Véronique C. Freund-Michel
Guest Editor

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Keywords

  • pulmonary hypertension
  • pulmonary arterial smooth muscle cells
  • endothelial cells
  • fibroblasts
  • inflammatory cells
  • vascular remodelling
  • reactivity
  • inflammation
  • endothelial dysfunction
  • right ventricular dysfunction
  • remodelling

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Published Papers (5 papers)

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Research

Jump to: Review, Other

20 pages, 7552 KiB  
Article
Analysis of MicroRNA Cargo in Circulating Extracellular Vesicles from HIV-Infected Individuals with Pulmonary Hypertension
by Aatish Mahajan, Sumedha Gunewardena, Alison Morris, Matthias Clauss and Navneet K. Dhillon
Cells 2024, 13(11), 886; https://doi.org/10.3390/cells13110886 - 21 May 2024
Viewed by 1199
Abstract
The risk of developing pulmonary hypertension (PH) in people living with HIV is at least 300-fold higher than in the general population, and illicit drug use further potentiates the development of HIV-associated PH. The relevance of extracellular vesicles (EVs) containing both coding as [...] Read more.
The risk of developing pulmonary hypertension (PH) in people living with HIV is at least 300-fold higher than in the general population, and illicit drug use further potentiates the development of HIV-associated PH. The relevance of extracellular vesicles (EVs) containing both coding as well as non-coding RNAs in PH secondary to HIV infection and drug abuse is yet to be explored. We here compared the miRNA cargo of plasma-derived EVs from HIV-infected stimulant users with (HIV + Stimulants + PH) and without PH (HIV + Stimulants) using small RNA sequencing. The data were compared with 12 PH datasets available in the GEO database to identify potential candidate gene targets for differentially altered miRNAs using the following functional analysis tools: ingenuity pathway analysis (IPA), over-representation analysis (ORA), and gene set enrichment analysis (GSEA). MiRNAs involved in promoting cell proliferation and inhibition of intrinsic apoptotic signaling pathways were among the top upregulated miRNAs identified in EVs from the HIV + Stimulants + PH group compared to the HIV + Stimulants group. Alternatively, the downregulated miRNAs in the HIV + Stimulants + PH group suggested an association with the negative regulation of smooth muscle cell proliferation, IL-2 mediated signaling, and transmembrane receptor protein tyrosine kinase signaling pathways. The validation of significantly differentially expressed miRNAs in an independent set of HIV-infected (cocaine users and nondrug users) with and without PH confirmed the upregulation of miR-32-5p, 92-b-3p, and 301a-3p positively regulating cellular proliferation and downregulation of miR-5571, -4670 negatively regulating smooth muscle proliferation in EVs from HIV-PH patients. This increase in miR-301a-3p and decrease in miR-4670 were negatively correlated with the CD4 count and FEV1/FVC ratio, and positively correlated with viral load. Collectively, this data suggest the association of alterations in the miRNA cargo of circulating EVs with HIV-PH. Full article
(This article belongs to the Special Issue Pulmonary Hypertension - Cellular and Molecular Changes in the Lung and in the Right Ventricle)
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11 pages, 2440 KiB  
Article
Inhibition of Soluble Epoxide Hydrolase Does Not Promote or Aggravate Pulmonary Hypertension in Rats
by Matthieu Leuillier, Valentin Platel, Ly Tu, Guillaume Feugray, Raphaël Thuillet, Déborah Groussard, Hind Messaoudi, Mina Ottaviani, Mustapha Chelgham, Lionel Nicol, Paul Mulder, Marc Humbert, Vincent Richard, Christophe Morisseau, Valéry Brunel, Thomas Duflot, Christophe Guignabert and Jérémy Bellien
Cells 2023, 12(4), 665; https://doi.org/10.3390/cells12040665 - 20 Feb 2023
Viewed by 2201
Abstract
Inhibitors of soluble epoxide hydrolase (sEH), which catalyzes the hydrolysis of various natural epoxides to their corresponding diols, present an opportunity for developing oral drugs for a range of human cardiovascular and inflammatory diseases, including, among others, diabetes and neuropathic pain. However, some [...] Read more.
Inhibitors of soluble epoxide hydrolase (sEH), which catalyzes the hydrolysis of various natural epoxides to their corresponding diols, present an opportunity for developing oral drugs for a range of human cardiovascular and inflammatory diseases, including, among others, diabetes and neuropathic pain. However, some evidence suggests that their administration may precipitate the development of pulmonary hypertension (PH). We thus evaluated the impact of chronic oral administration of the sEH inhibitor TPPU (N-[1-(1-Oxopropyl)-4-piperidinyl]-N′-[4-(trifluoromethoxy)phenyl]-urea) on hemodynamics, pulmonary vascular reactivity, and remodeling, as well as on right ventricular (RV) dimension and function at baseline and in the Sugen (SU5416) + hypoxia (SuHx) rat model of severe PH. Treatment with TPPU started 5 weeks after SU5416 injection for 3 weeks. No differences regarding the increase in pulmonary vascular resistance, remodeling, and inflammation, nor the abolishment of phenylephrine-induced pulmonary artery constriction, were noted in SuHx rats. In addition, TPPU did not modify the development of RV dysfunction, hypertrophy, and fibrosis in SuHx rats. Similarly, none of these parameters were affected by TPPU in normoxic rats. Complementary in vitro data demonstrated that TPPU reduced the proliferation of cultured human pulmonary artery-smooth muscle cells (PA-SMCs). This study demonstrates that inhibition of sEH does not induce nor aggravate the development of PH and RV dysfunction in SuHx rats. In contrast, a potential beneficial effect against pulmonary artery remodeling in humans is suggested. Full article
(This article belongs to the Special Issue Pulmonary Hypertension - Cellular and Molecular Changes in the Lung and in the Right Ventricle)
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18 pages, 3751 KiB  
Article
Piezo1 Channel Activation Reverses Pulmonary Artery Vasoconstriction in an Early Rat Model of Pulmonary Hypertension: The Role of Ca2+ Influx and Akt-eNOS Pathway
by Thais Porto Ribeiro, Solène Barbeau, Isabelle Baudrimont, Pierre Vacher, Véronique Freund-Michel, Guillaume Cardouat, Patrick Berger, Christelle Guibert, Thomas Ducret and Jean-François Quignard
Cells 2022, 11(15), 2349; https://doi.org/10.3390/cells11152349 - 30 Jul 2022
Cited by 15 | Viewed by 3491
Abstract
In intrapulmonary arteries (IPAs), mechanical forces due to blood flow control vessel tone, and these forces change during pulmonary hypertension (PH). Piezo1, a stretch-activated calcium channel, is a sensor of mechanical stress present in both endothelial cells (ECs) and smooth muscle cells (SMCs). [...] Read more.
In intrapulmonary arteries (IPAs), mechanical forces due to blood flow control vessel tone, and these forces change during pulmonary hypertension (PH). Piezo1, a stretch-activated calcium channel, is a sensor of mechanical stress present in both endothelial cells (ECs) and smooth muscle cells (SMCs). The present study investigated the role of Piezo1 on IPA in the chronic hypoxia model of PH. Rats were raised in chronically hypoxic conditions for 1 (1W-CH, early stage) or 3 weeks (3W-CH, late-stage) of PH or in normoxic conditions (Nx). Immunofluorescence labeling and patch-clamping revealed the presence of Piezo1 in both ECs and SMCs. The Piezo1 agonist, Yoda1, induced an IPA contraction in Nx and 3W-CH. Conversely, Yoda1 induced an endothelial nitric oxide (eNOS) dependent relaxation in 1W-CH. In ECs, the Yoda1-mediated intracellular calcium concentration ([Ca2+]i) increase was greater in 1W-CH as compared to Nx. Yoda1 induced an EC hyperpolarization in 1W-CH. The eNOS levels were increased in 1W-CH IPA compared to Nx or 3W-CH PH and Yoda1 activated phosphorylation of Akt (Ser473) and eNOS (Ser1177). Thus, we demonstrated that endothelial Piezo1 contributes to intrapulmonary vascular relaxation by controlling endothelial [Ca2+]i, endothelial-dependent hyperpolarization, and Akt-eNOS pathway activation in the early stage of PH. Full article
(This article belongs to the Special Issue Pulmonary Hypertension - Cellular and Molecular Changes in the Lung and in the Right Ventricle)
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Review

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13 pages, 1367 KiB  
Review
Emerging Epigenetic Targets and Their Molecular Impact on Vascular Remodeling in Pulmonary Hypertension
by A. Dushani C. U. Ranasinghe, T. M. Parinda B. Tennakoon and Margaret A. Schwarz
Cells 2024, 13(3), 244; https://doi.org/10.3390/cells13030244 - 28 Jan 2024
Cited by 1 | Viewed by 1727
Abstract
Pulmonary Hypertension (PH) is a terminal disease characterized by severe pulmonary vascular remodeling. Unfortunately, targeted therapy to prevent disease progression is limited. Here, the vascular cell populations that contribute to the molecular and morphological changes of PH in conjunction with current animal models [...] Read more.
Pulmonary Hypertension (PH) is a terminal disease characterized by severe pulmonary vascular remodeling. Unfortunately, targeted therapy to prevent disease progression is limited. Here, the vascular cell populations that contribute to the molecular and morphological changes of PH in conjunction with current animal models for studying vascular remodeling in PH will be examined. The status quo of epigenetic targeting for treating vascular remodeling in different PH subtypes will be dissected, while parallel epigenetic threads between pulmonary hypertension and pathogenic cancer provide insight into future therapeutic PH opportunities. Full article
(This article belongs to the Special Issue Pulmonary Hypertension - Cellular and Molecular Changes in the Lung and in the Right Ventricle)
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Other

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43 pages, 501 KiB  
Systematic Review
Right Ventricle and Epigenetics: A Systematic Review
by Victoria Toro, Naomie Jutras-Beaudoin, Olivier Boucherat, Sebastien Bonnet, Steeve Provencher and François Potus
Cells 2023, 12(23), 2693; https://doi.org/10.3390/cells12232693 - 23 Nov 2023
Cited by 1 | Viewed by 1601
Abstract
There is an increasing recognition of the crucial role of the right ventricle (RV) in determining the functional status and prognosis in multiple conditions. In the past decade, the epigenetic regulation (DNA methylation, histone modification, and non-coding RNAs) of gene expression has been [...] Read more.
There is an increasing recognition of the crucial role of the right ventricle (RV) in determining the functional status and prognosis in multiple conditions. In the past decade, the epigenetic regulation (DNA methylation, histone modification, and non-coding RNAs) of gene expression has been raised as a critical determinant of RV development, RV physiological function, and RV pathological dysfunction. We thus aimed to perform an up-to-date review of the literature, gathering knowledge on the epigenetic modifications associated with RV function/dysfunction. Therefore, we conducted a systematic review of studies assessing the contribution of epigenetic modifications to RV development and/or the progression of RV dysfunction regardless of the causal pathology. English literature published on PubMed, between the inception of the study and 1 January 2023, was evaluated. Two authors independently evaluated whether studies met eligibility criteria before study results were extracted. Amongst the 817 studies screened, 109 studies were included in this review, including 69 that used human samples (e.g., RV myocardium, blood). While 37 proposed an epigenetic-based therapeutic intervention to improve RV function, none involved a clinical trial and 70 are descriptive. Surprisingly, we observed a substantial discrepancy between studies investigating the expression (up or down) and/or the contribution of the same epigenetic modifications on RV function or development. This exhaustive review of the literature summarizes the relevant epigenetic studies focusing on RV in human or preclinical setting. Full article
(This article belongs to the Special Issue Pulmonary Hypertension - Cellular and Molecular Changes in the Lung and in the Right Ventricle)
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