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Preventing the Increase in Lysophosphatidic Acids: A New Therapeutic Target in Pulmonary Hypertension?

Λεπτομέρειες βιβλιογραφικής εγγραφής
Τίτλος: Preventing the Increase in Lysophosphatidic Acids: A New Therapeutic Target in Pulmonary Hypertension?
Συγγραφείς: Duflot, Thomas, Tu, Ly, Leuillier, Matthieu, Messaoudi, Hind, Groussard, Déborah, Feugray, Guillaume, Azhar, Saïda, Thuillet, Raphaël, Bauer, Fabrice, Humbert, Marc, Richard, Vincent, Guignabert, Christophe, Bellien, Jérémy
Συνεισφορές: Endothélium, valvulopathies et insuffisance cardiaque (EnVI), Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Rouen, Normandie Université (NU), UNIROUEN - UFR Santé (UNIROUEN UFR Santé), Normandie Université (NU)-Normandie Université (NU), Université Paris-Saclay, Hôpital Marie-Lannelongue, Hypertension pulmonaire : physiopathologie et innovation thérapeutique (HPPIT), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, TargEDys Rouen, Hôpital Bicêtre AP-HP, Le Kremlin-Bicêtre, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), ANR-16-CE17-0012,SAPHIR,Impact de la modulation des activités enzymatiques de l'époxyde hydrolase soluble sur l'hypertension pulmonaire et la dysfonction ventriculaire droite lors de l'insuffisance cardiaque expérimentale et humaine(2016)
Πηγή: ISSN: 2218-1989 ; Metabolites ; https://hal.science/hal-04532610 ; Metabolites, 2021, 11 (11), pp.784. ⟨10.3390/metabo11110784⟩.
Στοιχεία εκδότη: CCSD
MDPI
Έτος έκδοσης: 2021
Θεματικοί όροι: [SDV]Life Sciences [q-bio]
Περιγραφή: International audience ; Cardiovascular diseases (CVD) are the leading cause of premature death and disability in humans that are closely related to lipid metabolism and signaling. This study aimed to assess whether circulating lysophospholipids (LPL), lysophosphatidic acids (LPA) and monoacylglycerols (MAG) may be considered as potential therapeutic targets in CVD. For this objective, plasma levels of 22 compounds (13 LPL, 6 LPA and 3 MAG) were monitored by liquid chromatography coupled with tandem mass spectrometry (HPLC/MS2) in different rat models of CVD, i.e., angiotensin-II-induced hypertension (HTN), ischemic chronic heart failure (CHF) and sugen/hypoxia(SuHx)-induced pulmonary hypertension (PH). On one hand, there were modest changes on the monitored compounds in HTN (LPA 16:0, 18:1 and 20:4, LPC 16:1) and CHF (LPA 16:0, LPC 18:1 and LPE 16:0 and 18:0) models compared to control rats but these changes were no longer significant after multiple testing corrections. On the other hand, PH was associated with important changes in plasma LPA with a significant increase in LPA 16:0, 18:1, 18:2, 20:4 and 22:6 species. A deleterious impact of LPA was confirmed on cultured human pulmonary smooth muscle cells (PA-SMCs) with an increase in their proliferation. Finally, plasma level of LPA(16:0) was positively associated with the increase in pulmonary artery systolic pressure in patients with cardiac dysfunction. This study demonstrates that circulating LPA may contribute to the pathophysiology of PH. Additional experiments are needed to assess whether the modulation of LPA signaling in PH may be of interest.
Τύπος εγγράφου: article in journal/newspaper
Γλώσσα: English
DOI: 10.3390/metabo11110784
Διαθεσιμότητα: https://hal.science/hal-04532610
https://hal.science/hal-04532610v1/document
https://hal.science/hal-04532610v1/file/metabolites-11-00784.pdf
https://doi.org/10.3390/metabo11110784
Rights: http://creativecommons.org/licenses/by/ ; info:eu-repo/semantics/OpenAccess
Αριθμός Καταχώρησης: edsbas.DB256C74
Βάση Δεδομένων: BASE
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  Data: Preventing the Increase in Lysophosphatidic Acids: A New Therapeutic Target in Pulmonary Hypertension?
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  Data: <searchLink fieldCode="AR" term="%22Duflot%2C+Thomas%22">Duflot, Thomas</searchLink><br /><searchLink fieldCode="AR" term="%22Tu%2C+Ly%22">Tu, Ly</searchLink><br /><searchLink fieldCode="AR" term="%22Leuillier%2C+Matthieu%22">Leuillier, Matthieu</searchLink><br /><searchLink fieldCode="AR" term="%22Messaoudi%2C+Hind%22">Messaoudi, Hind</searchLink><br /><searchLink fieldCode="AR" term="%22Groussard%2C+Déborah%22">Groussard, Déborah</searchLink><br /><searchLink fieldCode="AR" term="%22Feugray%2C+Guillaume%22">Feugray, Guillaume</searchLink><br /><searchLink fieldCode="AR" term="%22Azhar%2C+Saïda%22">Azhar, Saïda</searchLink><br /><searchLink fieldCode="AR" term="%22Thuillet%2C+Raphaël%22">Thuillet, Raphaël</searchLink><br /><searchLink fieldCode="AR" term="%22Bauer%2C+Fabrice%22">Bauer, Fabrice</searchLink><br /><searchLink fieldCode="AR" term="%22Humbert%2C+Marc%22">Humbert, Marc</searchLink><br /><searchLink fieldCode="AR" term="%22Richard%2C+Vincent%22">Richard, Vincent</searchLink><br /><searchLink fieldCode="AR" term="%22Guignabert%2C+Christophe%22">Guignabert, Christophe</searchLink><br /><searchLink fieldCode="AR" term="%22Bellien%2C+Jérémy%22">Bellien, Jérémy</searchLink>
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  Data: Endothélium, valvulopathies et insuffisance cardiaque (EnVI)<br />Université de Rouen Normandie (UNIROUEN)<br />Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM)<br />CHU Rouen<br />Normandie Université (NU)<br />UNIROUEN - UFR Santé (UNIROUEN UFR Santé)<br />Normandie Université (NU)-Normandie Université (NU)<br />Université Paris-Saclay<br />Hôpital Marie-Lannelongue<br />Hypertension pulmonaire : physiopathologie et innovation thérapeutique (HPPIT)<br />Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay<br />TargEDys Rouen<br />Hôpital Bicêtre AP-HP, Le Kremlin-Bicêtre<br />Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)<br />ANR-16-CE17-0012,SAPHIR,Impact de la modulation des activités enzymatiques de l'époxyde hydrolase soluble sur l'hypertension pulmonaire et la dysfonction ventriculaire droite lors de l'insuffisance cardiaque expérimentale et humaine(2016)
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  Data: <i>ISSN: 2218-1989 ; Metabolites ; https://hal.science/hal-04532610 ; Metabolites, 2021, 11 (11), pp.784. ⟨10.3390/metabo11110784⟩</i>.
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  Data: International audience ; Cardiovascular diseases (CVD) are the leading cause of premature death and disability in humans that are closely related to lipid metabolism and signaling. This study aimed to assess whether circulating lysophospholipids (LPL), lysophosphatidic acids (LPA) and monoacylglycerols (MAG) may be considered as potential therapeutic targets in CVD. For this objective, plasma levels of 22 compounds (13 LPL, 6 LPA and 3 MAG) were monitored by liquid chromatography coupled with tandem mass spectrometry (HPLC/MS2) in different rat models of CVD, i.e., angiotensin-II-induced hypertension (HTN), ischemic chronic heart failure (CHF) and sugen/hypoxia(SuHx)-induced pulmonary hypertension (PH). On one hand, there were modest changes on the monitored compounds in HTN (LPA 16:0, 18:1 and 20:4, LPC 16:1) and CHF (LPA 16:0, LPC 18:1 and LPE 16:0 and 18:0) models compared to control rats but these changes were no longer significant after multiple testing corrections. On the other hand, PH was associated with important changes in plasma LPA with a significant increase in LPA 16:0, 18:1, 18:2, 20:4 and 22:6 species. A deleterious impact of LPA was confirmed on cultured human pulmonary smooth muscle cells (PA-SMCs) with an increase in their proliferation. Finally, plasma level of LPA(16:0) was positively associated with the increase in pulmonary artery systolic pressure in patients with cardiac dysfunction. This study demonstrates that circulating LPA may contribute to the pathophysiology of PH. Additional experiments are needed to assess whether the modulation of LPA signaling in PH may be of interest.
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