Abstract
Chronic hypertension can lead to kidney damage, known as hypertensive nephropathy or hypertensive nephrosclerosis. Further understanding of the molecular mechanisms via which hypertensive nephropathy develops is essential for effective diagnosis and treatment. The present study investigated the mechanisms by which endothelial progenitor cells (EPCs) repair primary rat kidney cells (PRKs). ELISA, Cell Counting Kit‑8 and flow cytometry assays were used to analyze the effects of EPCs or EPC‑MVs on the oxidative stress, inflammation, cell proliferation, apoptosis and cycle of PRKs induced by AngII. A PRK injury model was established using angiotensin II (Ang II). After Ang II induction, PRK proliferation was decreased, apoptosis was increased and the cell cycle was blocked at the G1 phase before entering the S phase. It was found that the levels of reactive oxygen species and malondialdehyde were increased, while the levels of glutathione peroxidase and superoxide dismutase were decreased. Moreover, the levels of the inflammatory cytokines IL‑1β, IL‑6 and TNF‑α were significantly increased. Thus, Ang II damaged PRKs by stimulating oxidative stress and promoting the inflammatory response. However, when PRKs were co‑cultured with EPCs, the damage induced by Ang II was significantly reduced. The current study collected the microvesicles (MVs) secreted by EPCs and co‑cultured them with Ang II‑induced PRKs, and identified that EPC‑MVs retained their protective effect on PRKs. In conclusion, EPCs protect PRKs from Ang II‑induced damage via secreted MVs.