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Left Ventricular Systolic Dysfunction in NBCe1-B/C-Knockout Mice.

Clayton T Brady1, Aniko Marshall1, Lisa A Eagler2

  • 1Department of Physiology and Biophysics, Jacobs School of Medicine and Biomedical Sciences, State University of New York: The University at Buffalo, Buffalo, NY 14203, USA.

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Summary

Congenital proximal renal tubular acidosis (pRTA) linked to NBCe1 gene mutations impairs heart function. Mice lacking NBCe1-B/C show reduced cardiac contractility and altered heart rhythms, despite no cardiac hypertrophy.

Keywords:
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Area of Science:

  • Molecular Biology
  • Cardiovascular Physiology
  • Genetics

Background:

  • Congenital proximal renal tubular acidosis (pRTA) is a rare genetic disorder caused by mutations in the SLC4A4 gene, affecting the NBCe1 sodium bicarbonate cotransporter.
  • NBCe1 has multiple variants (NBCe1-A, -B, -C) with distinct tissue expressions; NBCe1-B is crucial for cardiac function.
  • Previous studies in rats suggest NBCe1-B deficiency causes cardiac hypertrophy and prolonged QT intervals, but the effects of congenital, global NBCe1 loss on the heart remain unknown.

Purpose of the Study:

  • To investigate the cardiac function in juvenile mice with congenital, global absence of NBCe1-B and NBCe1-C variants (NBCe1-B/C-null mice).
  • To assess cardiac contractility, electrophysiology, and cardiomyocyte calcium handling in the absence of confounding acidemia.
  • To determine the impact of congenital NBCe1-B/C deficiency on cardiac phenotype independent of systemic acidosis.

Main Methods:

  • Characterization of cardiac function in NBCe1-B/C-null mice that survive up to 2 months of age.
  • Assessment of cardiac hypertrophy using heart-weight-to-body-weight ratios and cardiomyocyte cross-sectional area.
  • Echocardiography, intraventricular pressure-volume loop analysis, and measurement of Ca2+ transients in isolated cardiomyocytes using Fura-2 AM.

Main Results:

  • NBCe1-B/C-null mice did not exhibit cardiac hypertrophy compared to controls.
  • Echocardiography revealed reduced left ventricular ejection fraction, and pressure-volume measurements showed impaired load-independent cardiac contractility.
  • Increased QT length variation and reduced Ca2+ transient amplitude in cardiomyocytes were observed in NBCe1-B/C-null mice.

Conclusions:

  • Congenital, global absence of NBCe1-B/C variants leads to impaired cardiac contractility and increased QT length variation in juvenile mice.
  • The cardiac phenotype in these mice is characterized by functional deficits rather than structural changes like hypertrophy.
  • Further research is needed to elucidate the influence of neuronal and endocrine NBCe1-B/C absence on the observed cardiac phenotype.