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  • Title: [The change of fractalkine in serum and pulmonary arterioles of hypoxic rat].
    Author: Chen XJ, Cheng DY, Yang L, Xia XQ.
    Journal: Sichuan Da Xue Xue Bao Yi Xue Ban; 2007 Sep; 38(5):756-60. PubMed ID: 17953351.
    Abstract:
    OBJECTIVE: In order to evaluate the role of fractalkine in the pathogenesis of hypoxic pulmonary hypertension, we observed the change of serum soluble fractalkine and the expression of fractalkine in pulmonary arterioles of rat at different phase of hypoxia-induced pulmonary hypertension development. METHODS: The rat model of hypoxic pulmonary hypertension was duplicated by intermittent hypoxia. Mean pulmonary arterial pressure (mPAP) was measured by a right cardiac catheterization. The thickness of pulmonary arterioles was measured with a computerized image analyzer. Serum soluble fractalkine concentrations were measured by enzyme-linked immunosorbent assay. The expressions of fractalkine mRNA and protein in pulmonary arterioles were detected by in situ hybridization and immunohistochemical analysis, respectively. RESULTS: Compared to control, the mPAP of rats was markedly elevated after hypoxia for 14 days (P < 0.01), but the index of wall thickness of pulmonary arterioles (WT% and WA%) and the index of right ventricular hypertrophy CRV/(LV+S)] increased significantly at 21 days of hypoxia (P < 0.01). In rats exposed to hypoxia for 21 days, the fractalkine mRNA and protein levels in pulmonary arterioles were up-regulated significantly (P < 0.01), and the serum soluble fractalkine concentrations were also elevated (P < 0.01), as compared with control. Linear correlation analysis showed that the fractalkine mRNA level in pulmonary arterioles was associated with WA% (r = 0.749, P < 0.01) and WT% (r = 0.732, P < 0.01), the fractalkine protein level in pulmonary arterioles was also correlated with WA% (r = 0.727, P < 0.01) and WT% (r = 0.683, P < 0.01). CONCLUSION: The chronic hypoxia stimulates the synthesis and release of fractalkine. Fractalkine plays an important role in regulating the pulmonary vascular remodeling.
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