Betaine Aldehyde Dehydrogenase expression during physiological cardiac hypertrophy induced by pregnancy

Jesús Alfredo Rosas-Rodríguez, José Guadalupe Soñanez-Organis, José Arquimides Godoy-Lugo, Juan Alberto Espinoza-Salazar, Cesar Jeravy López-Jacobo, Norma Aurora Stephens-Camacho, Guadalupe González-Ochoa

Producción científica: Contribución a una revistaArtículorevisión exhaustiva

4 Citas (Scopus)

Resumen

© 2017 Elsevier Inc. Betaine Aldehyde Dehydrogenase (betaine aldehyde: NAD(P)+oxidoreductase, (E.C. 1.2.1.8; BADH) catalyze the irreversible oxidation of betaine aldehyde (BA) to glycine betaine (GB) and is essential for polyamine catabolism, γ-aminobutyric acid synthesis, and carnitine biosynthesis. GB is an important osmolyte that regulates the homocysteine levels, contributing to a vascular risk factor reduction. In this sense, distinct investigations describe the physiological roles of GB, but there is a lack of information about the GB novo synthesis process and regulation during cardiac hypertrophy induced by pregnancy. In this work, the BADH mRNA expression, protein level, and activity were quantified in the left ventricle before, during, and after pregnancy. The mRNA expression, protein content and enzyme activity along with GB content of BADH increased 2.41, 1.95 and 1.65-fold respectively during late pregnancy compared to not pregnancy, and returned to basal levels at postpartum. Besides, the GB levels increased 1.53-fold during pregnancy and remain at postpartum. Our results demonstrate that physiological cardiac hypertrophy induced BADH mRNA expression and activity along with GB production, suggesting that BADH participates in the adaptation process of physiological cardiac hypertrophy during pregnancy, according to the described GB role in cellular osmoregulation, osmoprotection and reduction of vascular risk.
Idioma originalInglés estadounidense
Páginas (desde-hasta)623-628
Número de páginas6
PublicaciónBiochemical and Biophysical Research Communications
Volumen490
N.º3
DOI
EstadoPublicada - 26 ago. 2017

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© 2017 Elsevier Inc.

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