Role of KCNK3 Dysfunction in Dasatinib-associated Pulmonary Arterial Hypertension and Endothelial Cell Dysfunction

Ribeuz, Hélène Le; Willer, Anaïs Saint-Martin; Chevalier, Benoit; Sancho, Maria; Masson, Bastien; Eyries, Mélanie; Jung, Vincent; Guerrera, Ida Chiara; Dutheil, Mary; Jekmek, Kristelle El; Laubry, Loann; Carpentier, Gilles; Perez-Vizcaino, Francisco; Tu, Ly; Guignabert, Christophe; Chaumais, Marie-Camille; Péchoux, Christine; Humbert, Marc; Hinzpeter, Alexandre; Mercier, Olaf; Capuano, Véronique; Montani, David; Antigny, Fabrice

doi:10.1165/rcmb.2023-0185oc

Am J Respir Cell Mol Biol

2024

DOI: 10.1165/rcmb.2023-0185oc

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Role of KCNK3 Dysfunction in Dasatinib-associated Pulmonary Arterial Hypertension and Endothelial Cell Dysfunction

Hélène Le Ribeuz,

Anaïs Saint-Martin Willer,

Benoit Chevalier

et al.

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Transcriptome analyses reveal common immune system dysregulation in PAH patients and Kcnk3‐deficient rats

Ruffenach,

Le Ribeuz,

Dutheil

et al. 2024

Pulm. circ.

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Pulmonary arterial hypertension (PAH) is a severe disease caused by progressive distal pulmonary artery obstruction. One cause of PAH are loss‐of‐function mutations in the potassium channel subfamily K member 3 (KCNK3). KCNK3 encodes a two‐pore domain potassium channel, which is crucial for pulmonary circulation homeostasis. However, our understanding of the pathophysiological mechanisms underlying KCNK3 dysfunction in PAH is still incomplete. Taking advantage of unique Kcnk3‐deficient rats, we analyzed the transcriptomic changes in the lungs from homozygous Kcnk3‐deficient rats and wild‐type (WT) littermates and compared them to PAH patient transcriptomic data. Transcriptome analysis of lung tissue obtained from WT and Kcnk3‐deficient rats identified 1915 down‐ or upregulated genes. In addition, despite limited similarities at the gene level, we found a strong common signature at the pathway level in PAH patients and Kcnk3‐deficient rat lungs, especially for immune response. Using the dysregulated genes involved in the immune response, we identified Spleen Associated Tyrosine Kinase (SYK), a significantly downregulated gene in human PAH patients and Kcnk3‐deficient rats, as a hub gene. Our data suggests that the altered immune system response observed in PAH patients may be partly explained by KCNK3 dysfunction through the alteration of SYK expression.

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Transcriptome analyses reveal common immune system dysregulation in PAH patients and Kcnk3‐deficient rats

Ruffenach,

Le Ribeuz,

Dutheil

et al. 2024

Pulm. circ.

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show abstract

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Role of KCNK3 Dysfunction in Dasatinib-associated Pulmonary Arterial Hypertension and Endothelial Cell Dysfunction

Cited by 1 publication

References 48 publications

Transcriptome analyses reveal common immune system dysregulation in PAH patients and Kcnk3‐deficient rats

Transcriptome analyses reveal common immune system dysregulation in PAH patients and Kcnk3‐deficient rats

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