AIM: To investigate the effect of vasoactive intestinal peptide (VIP) on pulmonary surfactants (PS) phospholipid synthesis in cultured lung explants. METHODS: Lung explants were cultured with serum-free medium, [methyl-3H]choline incorporation, total phospholipid, phosphatidylcholine, activity of choline-phosphate cytidylyltransferase (CCT) and CCTalpha mRNA level in lung explants were determined. RESULTS: (1) VIP (10(-10)-10(-7) mol/L) for 16 h promoted [methyl-3H]choline incorporation in dose dependence and VIP (10(-8) mol/L) for 2 h-16 h promoted [methyl-3H]choline incorporation in time dependence. (2) VIP (10(-8) mol/L) enhanced the contents of total phospholipids and phosphatidylcholine in lung explants. (3) VIP (10(-10)-10(-7) mol/L) elevated microsomal CCT activity of lung explants in dose dependence. (4) VIP (10(-8) mol/L) increased expression of CCTalpha mRNA in lung explants and alveolar type II cells (ATII). (5) [D-P-Cl-Phe(6)-Leu(17)]-VIP (10(-6) mol/L), a VIP receptors antagonist, abolished the increase of [3H]choline incorporation, microsomal CCT activity and CCTalpha mRNA level induced by VIP (10(-8) mol/L) in lung explants. CONCLUSION: VIP could enhance synthesis of phosphatidylcholine, the major component of pulmonary surfactants by enhancing microsomal CCT activity and CCTalpha mRNA level via VIP receptor-mediated pathway.
AIM: To investigate the effect of vasoactive intestinal peptide (VIP) on pulmonary surfactants (PS) phospholipid synthesis in cultured lung explants. METHODS: Lung explants were cultured with serum-free medium, [methyl-3H]choline incorporation, total phospholipid, phosphatidylcholine, activity of choline-phosphate cytidylyltransferase (CCT) and CCTalpha mRNA level in lung explants were determined. RESULTS: (1) VIP (10(-10)-10(-7) mol/L) for 16 h promoted [methyl-3H]choline incorporation in dose dependence and VIP (10(-8) mol/L) for 2 h-16 h promoted [methyl-3H]choline incorporation in time dependence. (2) VIP (10(-8) mol/L) enhanced the contents of total phospholipids and phosphatidylcholine in lung explants. (3) VIP (10(-10)-10(-7) mol/L) elevated microsomal CCT activity of lung explants in dose dependence. (4) VIP (10(-8) mol/L) increased expression of CCTalpha mRNA in lung explants and alveolar type II cells (ATII). (5) [D-P-Cl-Phe(6)-Leu(17)]-VIP (10(-6) mol/L), a VIP receptors antagonist, abolished the increase of [3H]choline incorporation, microsomal CCT activity and CCTalpha mRNA level induced by VIP (10(-8) mol/L) in lung explants. CONCLUSION:VIP could enhance synthesis of phosphatidylcholine, the major component of pulmonary surfactants by enhancing microsomal CCT activity and CCTalpha mRNA level via VIP receptor-mediated pathway.
Authors: Jihad Georges Youssef; Philip Lavin; David A Schoenfeld; Richard A Lee; Rainer Lenhardt; David J Park; Javier Perez Fernandez; Melvin L Morganroth; Jonathan C Javitt; Dushyantha Jayaweera Journal: Crit Care Med Date: 2022-08-29 Impact factor: 9.296
Authors: Jihad Georges Youssef; Mohammad Z Bitar; Faisal Zahiruddin; Mukhtar Al-Saadi; Mahmoud Elshawwaf; Simon Yau; Ahmad Goodarzi; Jonathan C Javitt Journal: Crit Care Explor Date: 2022-01-05
Authors: Maria Boesing; Kristin Abig; Michael Brändle; Martin Brutsche; Emanuel Burri; Björn C Frye; Stéphanie Giezendanner; Jan C Grutters; Philippe Haas; Justian Heisler; Fabienne Jaun; Anne B Leuppi-Taegtmeyer; Giorgia Lüthi-Corridori; Joachim Müller-Quernheim; Reto Nüesch; Wolfgang Pohl; Frank Rassouli; Jörg D Leuppi Journal: Trials Date: 2022-09-20 Impact factor: 2.728