Objectives: Hypertension is one of the factor which induce remodelation of extracellular matrix (ECM) and intercellular communication. Transforming growth factor &bgr; (TGF&bgr;), matrix metalloproteinases-2 (MMP2) and connexin 43 (Cx43) are… Click to show full abstract
Objectives: Hypertension is one of the factor which induce remodelation of extracellular matrix (ECM) and intercellular communication. Transforming growth factor &bgr; (TGF&bgr;), matrix metalloproteinases-2 (MMP2) and connexin 43 (Cx43) are proteins implicated in the origin of hypertrophy and arrhythmias due to hypertension. Methods: Our experiments were performed on male 10-month-old wistar euthyroid (EU) and hypertensive (SHR) rats with altered thyroid status, which were supplemented with PUFA (200 mg/kg/day) for six weeks. Hypothyroidism (HY) was induced by 0,05% methimazole and hyperthyroidism (TH) was induced by triiodothyronine (0,15 mg/kg) applied for two months. Left ventricle tissue was used for molecular analyzes of TGF&bgr;, MMP2 and Cx43. Histological analysis of ECM was performed by staining according to van Gieson. Results: We have found in HY rats decreased expression of TGF&bgr;, activity MMP2 and elevation of MMP2 activity as well as expression in SHR HY rats. On the other hand, in TH rats was decreased expression of TGF&bgr; and Cx43. Hypertension decreased TGF&bgr;, Cx43 and increased expression of MMP2 in SHR EU and SHR TH rats. The histological staining of collagen in the left ventricle showed a significant increase of collagen in the heart of SHR HY rats. PUFA diet slightly increased the expression and activity of MMP2 in HY rats and decreased activity of MMP2 due to TH. Conclusion: Our results indicate that we can assume that changes in MMP2, TGF-&bgr; and Cx43 associated with hypertension and altered thyroid status are implicated in the arrhythmogenic mechanism based from the Cx43 alternation after heart remodelation. This work was supported by grants: VEGA 2/0167/15, 2/0076/16, APVV-15-0119, SKS Egan Bec[Combining Caron]ová.
               
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