Orai1 Inhibitors as Potential Treatments for Pulmonary Arterial Hypertension

Autor: Bastien Masson, Hélène Le Ribeuz, Jessica Sabourin, Loann Laubry, Emily Woodhouse, Richard Foster, Yann Ruchon, Mary Dutheil, Angèle Boët, Maria-Rosa Ghigna, Vincent Thomas De Montpreville, Olaf Mercier, David J. Beech, Jean-Pierre Benitah, Marc A. Bailey, Marc Humbert, David Montani, Véronique Capuano, Fabrice Antigny

Publikováno v: Circulation research. 131(9)

Background: Pulmonary arterial hypertension (PAH) is characterized by progressive distal pulmonary artery (PA) obstruction, leading to right ventricular hypertrophy and failure. Exacerbated intracellular calcium (Ca 2+ ) signaling contributes to abno

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8692343c7e0d9d531cc40f4d38e6d047
https://pubmed.ncbi.nlm.nih.gov/36164973

T-type Ca 2+ channels elicit pro-proliferative and anti-apoptotic responses through impaired PP2A/Akt1 signaling in PASMCs from patients with pulmonary arterial hypertension

Autor: Peter Dorfmüller, Sevasti Manousakidi, Saadia Eddahibi, Safietou Sankhe, Jennifer Arthur Ataam, Elie Fadel, Véronique Capuano, Laura C. Price, Marc Humbert, Fabrice Antigny, Florence Lecerf, Yann Ruchon, Sana Bentebbal, Frédéric Perros, Jessica Sabourin

Publikováno v: Biochimica et Biophysica Acta-Molecular Cell Research
Biochimica et Biophysica Acta-Molecular Cell Research, Elsevier, 2017, 1864 (10), pp.1631-1641. ⟨10.1016/j.bbamcr.2017.06.018⟩
Biochimica et Biophysica Acta-Molecular Cell Research, 2017, 1864 (10), pp.1631-1641. ⟨10.1016/j.bbamcr.2017.06.018⟩

International audience; Idiopathic pulmonary arterial hypertension (iPAH) is characterized by obstructive hyperproliferation and apoptosis resistance of distal pulmonary artery smooth muscle cells (PASMCs). T-type Ca2+ channel blockers have been show

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f5aa6ce725e9140d5574b46acdaf3f50
https://hal.umontpellier.fr/hal-01836102

T-type Ca2+ signalling downregulates MEK1/2 phosphorylation and cross-talk with the RAAS transcriptional response in cardiac myocytes

Autor: Jean-François Renaud, Yann Ruchon, Safietou Sankhe, Véronique Capuano, Laurent Ferron

Publikováno v: Journal of Molecular and Cellular Cardiology. 53:291-298

Cardiac dysfunction is often associated with an increase in the activity of the renin–angiotensin II–aldosterone system (RAAS). Here, we highlight the cross-talk between the Ca 2 + signalling generated by cardiac T-type current (I CaT ) and RAAS

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::55f18c1262ddc45401cd711eb2ee7efb
https://doi.org/10.1016/j.yjmcc.2012.05.006

Identification of functional corticosteroid response elements involved in regulation of Cacna1g expression in cardiac myocytes

Autor: Yann Ruchon, Jean-François Renaud, Fatima BenMohamed, Véronique Capuano

Publikováno v: Molecular and Cellular Biochemistry. 335:47-51

We recently reported that corticosteroids increase the expression of the T-type channel Ca(v)3.1 through a transcriptional up-regulation of the Ca(v)3.1 encoding gene cacna1g. The nucleotide sequence analysis of cacna1g promoter revealed putative glu

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f5ffd428ec112e74a5b867b674eb6960
https://doi.org/10.1007/s11010-009-0239-6

T-type Ca²⁺ signalling downregulates MEK1/2 phosphorylation and cross-talk with the RAAS transcriptional response in cardiac myocytes

Autor: Yann, Ruchon, Laurent, Ferron, Safietou, Sankhe, Jean-François, Renaud, Véronique, Capuano

Publikováno v: Journal of molecular and cellular cardiology. 53(2)

Cardiac dysfunction is often associated with an increase in the activity of the renin-angiotensin II-aldosterone system (RAAS). Here, we highlight the cross-talk between the Ca(2+) signalling generated by cardiac T-type current (I(CaT)) and RAAS sign

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=pmid________::06ef32471fe229c014a9172c589b2c13
https://pubmed.ncbi.nlm.nih.gov/22634504