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Fibulin-3 has been suggested to function in the remodeling of the extracellular matrix, however its role remains unclear in hypertensive vascular remodeling. In the current study, 10 Wistar-Kyoto (WKY) rats (control group) and 30 spontaneously hypertensive rats (SHRs) were used. SHRs were randomized into three groups: The placebo group, intravenous (I.V.) physiological saline; the FBLN‑1 group, low‑dose fibulin‑3 protein (I.V.; 120 ng/kg); and the FBLN-2 group, high-dose fibulin-3 protein (I.V.; 240 ng/kg). Histological analysis was used to analyze vascular remodeling. The expression of fibulin‑3, matrix metalloproteinase (MMP)‑2, MMP‑9 and tissue inhibitor of metalloproteinase (TIMP)‑3 were detected by immunohistochemistry, western blotting and reverse transcription‑quantitative polymerase chain reaction. Oxidative stress was detected by dihydroethidium staining. The systolic blood pressure (SBP) of SHRs was observed to be significantly greater than that of WKY rats (P0.05). Reactive oxygen species (ROS) were increased in the placebo group vs. the control group. Fibulin‑3 was able to alleviate the levels of ROS in the FBLN groups. It is suggested that fibulin‑3 may act as a growth factor in the arteries. In addition, the results indicated that fibulin‑3 may reduce the levels of MMP‑2 and ‑9 and oxidative stress in hypertensive vascular remodeling. Upregulating fibulin-3 may be beneficial for improving vascular health and offsetting certain cardiovascular risk factors of hypertension.
Lin et al. (Mon,) studied this question.