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

Research output: Contribution to journalArticle

Abstract

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.
Original languageAmerican English
Pages (from-to)623-628
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume490
Issue number3
DOIs
StatePublished - 26 Aug 2017

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Betaine-Aldehyde Dehydrogenase
Betaine
Cardiomegaly
Pregnancy
Risk Reduction Behavior
Messenger RNA
Postpartum Period
Physiological Phenomena
Aminobutyrates
Physiological Adaptation
Osmoregulation
Aldehyde Dehydrogenase
Carnitine
Polyamines
Homocysteine
Biosynthesis
Enzyme activity
Heart Ventricles
Blood Vessels
NAD

Keywords

  • Betaine aldehyde dehydrogenase
  • Glycine betaine
  • Physiological cardiac hypertrophy
  • Protein expression and left ventricle
  • mRNA

Cite this

Rosas-Rodríguez, Jesús Alfredo ; Soñanez-Organis, José Guadalupe ; Godoy-Lugo, José Arquimides ; Espinoza-Salazar, Juan Alberto ; López-Jacobo, Cesar Jeravy ; Stephens-Camacho, Norma Aurora ; González-Ochoa, Guadalupe. / Betaine Aldehyde Dehydrogenase expression during physiological cardiac hypertrophy induced by pregnancy. In: Biochemical and Biophysical Research Communications. 2017 ; Vol. 490, No. 3. pp. 623-628.
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abstract = "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.",
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Betaine Aldehyde Dehydrogenase expression during physiological cardiac hypertrophy induced by pregnancy. / Rosas-Rodríguez, Jesús Alfredo; Soñanez-Organis, José Guadalupe; Godoy-Lugo, José Arquimides; Espinoza-Salazar, Juan Alberto; López-Jacobo, Cesar Jeravy; Stephens-Camacho, Norma Aurora; González-Ochoa, Guadalupe.

In: Biochemical and Biophysical Research Communications, Vol. 490, No. 3, 26.08.2017, p. 623-628.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Betaine Aldehyde Dehydrogenase expression during physiological cardiac hypertrophy induced by pregnancy

AU - Rosas-Rodríguez, Jesús Alfredo

AU - Soñanez-Organis, José Guadalupe

AU - Godoy-Lugo, José Arquimides

AU - Espinoza-Salazar, Juan Alberto

AU - López-Jacobo, Cesar Jeravy

AU - Stephens-Camacho, Norma Aurora

AU - González-Ochoa, Guadalupe

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Y1 - 2017/8/26

N2 - 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.

AB - 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.

KW - Betaine aldehyde dehydrogenase

KW - Glycine betaine

KW - Physiological cardiac hypertrophy

KW - Protein expression and left ventricle

KW - mRNA

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DO - 10.1016/j.bbrc.2017.06.087

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