Overlapping and differential functions of ATF6α versus ATF6β in the mouse heart View Full Text


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Article Info

DATE

2019-12

AUTHORS

Robert N. Correll, Kelly M. Grimes, Vikram Prasad, Jeffrey M. Lynch, Hadi Khalil, Jeffery D. Molkentin

ABSTRACT

Hemodynamic stress on the mammalian heart results in compensatory hypertrophy and activation of the unfolded protein response through activating transcription factor 6α (ATF6α) in cardiac myocytes, but the roles of ATF6α or the related transcription factor ATF6β in regulating this hypertrophic response are not well-understood. Here we examined the effects of loss of ATF6α or ATF6β on the cardiac response to pressure overload. Mice gene-deleted for Atf6 or Atf6b were subjected to 2 weeks of transverse aortic constriction, and each showed a significant reduction in hypertrophy with reduced expression of endoplasmic reticulum (ER) stress-associated proteins compared with controls. However, with long-term pressure overload both Atf6 and Atf6b null mice showed enhanced decompensation typified by increased heart weight, pulmonary edema and reduced function compared to control mice. Our subsequent studies using cardiac-specific transgenic mice expressing the transcriptionally active N-terminus of ATF6α or ATF6β revealed that these factors control overlapping gene expression networks that include numerous ER protein chaperones and ER associated degradation components. This work reveals previously unappreciated roles for ATF6α and ATF6β in regulating the pressure overload induced cardiac hypertrophic response and in controlling the expression of genes that condition the ER during hemodynamic stress. More... »

PAGES

2059

References to SciGraph publications

  • 2006-08. Regulation of cardiac hypertrophy by intracellular signalling pathways in NATURE REVIEWS MOLECULAR CELL BIOLOGY
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41598-019-39515-5

    DOI

    http://dx.doi.org/10.1038/s41598-019-39515-5

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1112135071

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30765833


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