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Low density lipoprotein receptor-related protein 1 regulates cardiac hypertrophy induced by pressure overload. | LitMetric

Low density lipoprotein receptor-related protein 1 regulates cardiac hypertrophy induced by pressure overload.

Int J Cardiol

Department of Medical of Sciences, Chosun University Graduate School, Gwangju 61452, Republic of Korea; Department of Biochemistry and Molecular Biology, Chosun University School of Medicine, Gwangju 61452, Republic of Korea. Electronic address:

Published: January 2020

AI Article Synopsis

  • * Researchers used adenoviral techniques to either increase or decrease LRP1 levels in both lab and animal experiments, finding that LRP1 was upregulated in hypertrophied heart tissue and increased cell size and hypertrophic markers when overexpressed.
  • * LRP1 appears to trigger cardiac hypertrophy through a signaling pathway involving PKCα and ERK, affecting calcium levels; thus, targeting LRP1 might offer new treatment options for managing cardiac hypertrophy.

Article Abstract

Background: Cardiac hypertrophy is associated with functional changes in cardiomyocytes, which often results in heart failure. The low-density lipoprotein receptor-related protein 1 (LRP1) is a large multifunctional endocytic receptor involved in many physiological and pathological processes. However, its function in the development of cardiac hypertrophy remains largely unclear.

Methods: Adenoviral constructs were used for either overexpression or silencing of LRP1 in both in vitro and in vivo experiments. Cardiac function was measured using the Millar catheter.

Results: LRP1 expression was upregulated in both transverse aortic constriction (TAC)-induced hypertrophic myocardium and catecholamine (phenylephrine (PE) and norepinephrine (NE))- and angiotensin II (AngII)-induced hypertrophic cardiomyocytes. In addition, cell surface area, protein/DNA ratio, and the mRNA levels of hypertrophic markers were significantly increased in LRP1-overexpressing cardiomyocytes without catecholamine stimulation. Conversely, LRP1 inhibition by LRP1-specific siRNA or a specific ligand-binding antagonist (RAP) significantly rescued hypertrophic effects in PE, NE, or AngII-induced cardiomyocytes. LRP1 overexpression induced PKCα, then activated ERK, resulting in cardiac hypertrophy with the downregulation of SERCA2a and calcium accumulation, which was successfully restored in both LRP1-silenced cardiomyocytes and TAC-induced hearts.

Conclusions: LRP1 regulates cardiac hypertrophy via the PKCα-ERK dependent signaling pathway resulting in the alteration of intracellular calcium levels, demonstrating that LRP1 might be a potential therapeutic target for cardiac hypertrophy.

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Source
http://dx.doi.org/10.1016/j.ijcard.2019.07.049DOI Listing

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