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Chronic kidney disease induces left ventricular overexpression of the pro-hypertrophic microRNA-212.

Abstract：

:Chronic kidney disease (CKD) is a public health problem that increases the risk of cardiovascular morbidity and mortality. Heart failure with preserved ejection fraction (HFpEF) characterized by left ventricular hypertrophy (LVH) and diastolic dysfunction is a common cardiovascular complication of CKD. MicroRNA-212 (miR-212) has been demonstrated previously to be a crucial regulator of pathologic LVH in pressure-overload-induced heart failure via regulating the forkhead box O3 (FOXO3)/calcineurin/nuclear factor of activated T-cells (NFAT) pathway. Here we aimed to investigate whether miR-212 and its hypertrophy-associated targets including FOXO3, extracellular signal-regulated kinase 2 (ERK2), and AMP-activated protein kinase (AMPK) play a role in the development of HFpEF in CKD. CKD was induced by 5/6 nephrectomy in male Wistar rats. Echocardiography and histology revealed LVH, fibrosis, preserved systolic function, and diastolic dysfunction in the CKD group as compared to sham-operated animals eight and/or nine weeks later. Left ventricular miR-212 was significantly overexpressed in CKD. However, expressions of FOXO3, AMPK, and ERK2 failed to change significantly at the mRNA or protein level. The protein kinase B (AKT)/FOXO3 and AKT/mammalian target of rapamycin (mTOR) pathways are also proposed regulators of LVH induced by pressure-overload. Interestingly, phospho-AKT/total-AKT ratio was increased in CKD without significantly affecting phosphorylation of FOXO3 or mTOR. In summary, cardiac overexpression of miR-212 in CKD failed to affect its previously implicated hypertrophy-associated downstream targets. Thus, the molecular mechanism of the development of LVH in CKD seems to be independent of the FOXO3, ERK1/2, AMPK, and AKT/mTOR-mediated pathways indicating unique features in this form of LVH.

journal_name

Sci Rep

journal_title

Scientific reports

authors

Sárközy M,Gáspár R,Zvara Á,Siska A,Kővári B,Szűcs G,Márványkövi F,Kovács MG,Diószegi P,Bodai L,Zsindely N,Pipicz M,Gömöri K,Kiss K,Bencsik P,Cserni G,Puskás LG,Földesi I,Thum T,Bátkai S,Csont T

doi

10.1038/s41598-018-37690-5

subject

Has Abstract

pub_date

2019-02-04 00:00:00

pages

1302

issue

1

issn

2045-2322

pii

10.1038/s41598-018-37690-5

journal_volume

9

pub_type

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