Matches in SemOpenAlex for { <https://semopenalex.org/work/W4376134908> ?p ?o ?g. }
Showing items 1 to 74 of
74
with 100 items per page.
- W4376134908 endingPage "185" @default.
- W4376134908 startingPage "185" @default.
- W4376134908 abstract "PDE9 is a phosphodiesterase which has recently emerged as a regulator of cGMP in cardiac and vascular myocytes. Its contribution in vasculature is, however, unclear. We sought to investigate PDE9 expression and function in mouse pulmonary artery by comparing wild type (WT) and PDE9-deficient, Pde9a(-/-), mice. We also addressed the hypothesis that PDE9 could represent a new therapeutic target to treat pulmonary arterial hypertension, a severe, deadly disease. PDE9 expression was examined in mouse tissues and human pulmonary artery from subjects with or without pulmonary arterial hypertension using RT-PCR and immunoblots. Relaxant responses were studied in mouse pulmonary arteries mounted on a myograph and contracted with phenylephrine. A challenge with 21-day, 10% O2-hypoxia was used as a model of pulmonary hypertension in mice and was compared to normoxia. Right ventricle and pulmonary artery morphology and function were determined by echocardiography, right ventricle catheterization and gravimetric analysis. PDE9 protein and Pde9a transcript were detected in human and mouse pulmonary arteries, respectively. Pulmonary arteries from Pde9a(-/-) mice displayed more potent relaxant responses to acetylcholine, to the NO donor diethylamine NONOate and to atrial natriuretic peptide than vessels from WT animals. Following hypoxia, Pde9a expression was increased in lung and right ventricle from WT mice. PDE9 deficiency failed to ameliorate pulmonary hypertension hemodynamic criteria, namely higher right ventricular systolic pressure and lower echocardiographic pulmonary arterial acceleration time. Right ventricle hypertrophy, reflected by increased Fulton index, right ventricle thickness and fetal genes expression, were also similar in Pde9a(-/-) and WT groups. PDE9 is expressed in pulmonary artery and takes part in the relaxant responses mediated by the cGMP pathway. The ablation of Pde9a in mouse, however, does not prevent the development of pulmonary hypertension in a 21-day hypoxia model, nor does it attenuate right ventricle deleterious remodeling." @default.
- W4376134908 created "2023-05-12" @default.
- W4376134908 creator A5000586185 @default.
- W4376134908 creator A5011104124 @default.
- W4376134908 creator A5026302630 @default.
- W4376134908 creator A5029745665 @default.
- W4376134908 creator A5030898168 @default.
- W4376134908 creator A5062743460 @default.
- W4376134908 creator A5066599847 @default.
- W4376134908 creator A5079705755 @default.
- W4376134908 creator A5079763125 @default.
- W4376134908 date "2023-05-01" @default.
- W4376134908 modified "2023-10-18" @default.
- W4376134908 title "Phosphodiesterase type 9 opposes relaxation of mouse pulmonary artery but does not influence chronic hypoxia-induced pulmonary hypertension in mouse" @default.
- W4376134908 doi "https://doi.org/10.1016/j.acvdsp.2023.03.016" @default.
- W4376134908 hasPublicationYear "2023" @default.
- W4376134908 type Work @default.
- W4376134908 citedByCount "0" @default.
- W4376134908 crossrefType "journal-article" @default.
- W4376134908 hasAuthorship W4376134908A5000586185 @default.
- W4376134908 hasAuthorship W4376134908A5011104124 @default.
- W4376134908 hasAuthorship W4376134908A5026302630 @default.
- W4376134908 hasAuthorship W4376134908A5029745665 @default.
- W4376134908 hasAuthorship W4376134908A5030898168 @default.
- W4376134908 hasAuthorship W4376134908A5062743460 @default.
- W4376134908 hasAuthorship W4376134908A5066599847 @default.
- W4376134908 hasAuthorship W4376134908A5079705755 @default.
- W4376134908 hasAuthorship W4376134908A5079763125 @default.
- W4376134908 hasConcept C126322002 @default.
- W4376134908 hasConcept C164705383 @default.
- W4376134908 hasConcept C178790620 @default.
- W4376134908 hasConcept C185592680 @default.
- W4376134908 hasConcept C2777952589 @default.
- W4376134908 hasConcept C2778921608 @default.
- W4376134908 hasConcept C2779376020 @default.
- W4376134908 hasConcept C2780930700 @default.
- W4376134908 hasConcept C2780940725 @default.
- W4376134908 hasConcept C540031477 @default.
- W4376134908 hasConcept C71924100 @default.
- W4376134908 hasConcept C7836513 @default.
- W4376134908 hasConcept C84393581 @default.
- W4376134908 hasConceptScore W4376134908C126322002 @default.
- W4376134908 hasConceptScore W4376134908C164705383 @default.
- W4376134908 hasConceptScore W4376134908C178790620 @default.
- W4376134908 hasConceptScore W4376134908C185592680 @default.
- W4376134908 hasConceptScore W4376134908C2777952589 @default.
- W4376134908 hasConceptScore W4376134908C2778921608 @default.
- W4376134908 hasConceptScore W4376134908C2779376020 @default.
- W4376134908 hasConceptScore W4376134908C2780930700 @default.
- W4376134908 hasConceptScore W4376134908C2780940725 @default.
- W4376134908 hasConceptScore W4376134908C540031477 @default.
- W4376134908 hasConceptScore W4376134908C71924100 @default.
- W4376134908 hasConceptScore W4376134908C7836513 @default.
- W4376134908 hasConceptScore W4376134908C84393581 @default.
- W4376134908 hasIssue "2" @default.
- W4376134908 hasLocation W43761349081 @default.
- W4376134908 hasOpenAccess W4376134908 @default.
- W4376134908 hasPrimaryLocation W43761349081 @default.
- W4376134908 hasRelatedWork W145595520 @default.
- W4376134908 hasRelatedWork W2061933791 @default.
- W4376134908 hasRelatedWork W2086335790 @default.
- W4376134908 hasRelatedWork W2343896499 @default.
- W4376134908 hasRelatedWork W2355100107 @default.
- W4376134908 hasRelatedWork W2382696197 @default.
- W4376134908 hasRelatedWork W2383562306 @default.
- W4376134908 hasRelatedWork W2473200681 @default.
- W4376134908 hasRelatedWork W3142999030 @default.
- W4376134908 hasRelatedWork W4244201864 @default.
- W4376134908 hasVolume "15" @default.
- W4376134908 isParatext "false" @default.
- W4376134908 isRetracted "false" @default.
- W4376134908 workType "article" @default.