Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Evaluation of the Canonical Wnt Signaling Pathway in the Hearts of Hypertensive Rats of Various Etiology

Version 1 : Received: 20 May 2024 / Approved: 21 May 2024 / Online: 21 May 2024 (08:46:50 CEST)

How to cite: Młynarczyk, M.; Domian, N.; Kasacka, I. Evaluation of the Canonical Wnt Signaling Pathway in the Hearts of Hypertensive Rats of Various Etiology. Preprints 2024, 2024051358. https://doi.org/10.20944/preprints202405.1358.v1 Młynarczyk, M.; Domian, N.; Kasacka, I. Evaluation of the Canonical Wnt Signaling Pathway in the Hearts of Hypertensive Rats of Various Etiology. Preprints 2024, 2024051358. https://doi.org/10.20944/preprints202405.1358.v1

Abstract

The Wnt/β-catenin signaling deregulation is associated with the pathogenesis of many human diseases, including hypertension and heart disease. The aim of the study was to immunohisto-chemically evaluate and compare the expression of Fzd8, WNT1, GSK-3ß and β-catenin genes in the hearts of rats with spontaneous hypertension (SHR) and DOCA-salt- induced hypertension. The myocardial expression Fzd8, WNT1, GSK-3ß and β-catenin was detected by immunohisto-chemistry and the gene expression was assessed with real-time PCR method. In SHR immunore-activity of Fzd8, WNT1, GSK-3β and β-catenin was attenuated in comparison to normotensive animals. In DOCA-salt immunoreactivity of Fzd8, WNT1, GSK-3β and β-catenin was enhanced. In SHR, decrease in the expression of genes encoding Fzd8, WNT1, GSK-3ß and β-catenin was observed compared to the control group. Increased expression of genes encoding Fzd8, WNT1, GSK-3ß and β-catenin was demonstrated in the hearts of rats DOCA-salt. Wnt signaling may play an essential role in the pathogenesis of arterial hypertension and the accompanying heart damage. Obtained results may constitute the basis for further research aimed at better under-standing the role of the Wnt/β-catenin pathway in the functioning of the heart.

Keywords

Wnt/β-catenin; Arterial Hypertension; Essential hypertension; Secondary hypertension; Myocardium

Subject

Biology and Life Sciences, Cell and Developmental Biology

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