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11 August 2018 : Animal Research  

Doxycycline Attenuates Atrial Remodeling by Interfering with MicroRNA-21 and Downstream Phosphatase and Tensin Homolog (PTEN)/Phosphoinositide 3-Kinase (PI3K) Signaling Pathway

Kai Zhang1BCDEF, Linru Zhao1BCDEF, Zuowang Ma1BC, Weiding Wang1BC, Xiongfeng Li1BC, Yue Zhang1B, Meng Yuan1B, Xue Liang1DF, Guangping Li1AG*

DOI: 10.12659/MSM.909800

Med Sci Monit 2018; 24: ANS5580-5587

Abstract

BACKGROUND: Atrial remodeling especially in the form of fibrosis is the most important substrate of atrial fibrillation (AF). The aim of this study was to investigate the effects of doxycycline on chronic intermittent hypoxia (CIH)-induced atrial remodeling and the pathophysiological mechanisms underlying such changes.

MATERIAL AND METHODS: A total of 30 Sprague-Dawley rats were randomized into 3 groups: Control group, CIH group, and CIH with doxycycline treatment group. CIH rats were subjected to CIH 6 h/d for 30 days and treatment rats were administrated doxycycline while they received CIH. After the echocardiography examination, rats were sacrificed at 31 days. The tissues of atria were collected for histological and molecular biological experiments, Masson staining was used to evaluate the extent of atrial fibrosis, microRNA-21, and its downstream target phosphatase and tensin homolog (PTEN), phosphoinositide 3-kinase (PI3K) were assessed.

RESULTS: Compared to the control group, the CIH rats showed higher atrial interstitial collagen fraction, increased microRNA-21, PI3K levels, and decreased PTEN levels. Doxycycline treatment attenuated CIH-induced atrial fibrosis, reduced microRNA-21 and PI3K, and increased PTEN.

CONCLUSIONS: CIH induced significant atrial remodeling, which was attenuated by doxycycline in our rat model. These changes may be explained due to alterations in the microRNA-21-related signaling pathways by doxycycline.

Keywords: Atrial Remodeling, doxycycline, PTEN Phosphohydrolase

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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750