Browsing by Author "Li, Xiaoyan"

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    Contrasting water use characteristics of riparian trees under different water tables along a losing river
    (Elsevier, 2022-08) Li, Yue; Ma, Ying; Song, Xianfang; Wang, Lixin; Yang, Lihu; Li, Xiaoyan; Li, Binghua; Earth and Environmental Sciences, School of Science
    Rivers losing flow into surrounding aquifers (‘losing’ rivers) are common under changing climates and groundwater overexploitation. The riparian plant-water relations under various water table dynamics along a losing river remain unclear. In this study, the water isotopes (δ2H and δ18O), leaf δ13C, and MixSIAR model were used combinedly for determining the root water uptake patterns and leaf water use efficiency (WUE) of Salix babylonica (L.) at three sites (A, B, and C) with different water table depths (WTDs) in the riparian zone of Jian and Chaobai River in Beijing, China. The correlations of water source contributions with WTD and WUE were quantified. The riparian S. babylonica primarily took up upper (0–80 cm) soil water (71.5%) with the lowest leaf δ13C (−28.8 ± 1.1 ‰) at site A under deep WTD (20.5 ± 0.5 m). In contrast, deep water below 80 cm depth including groundwater contributed 55.1% to S. babylonica at site B with fluctuated shallow WTD (1.9 ± 0.4 m), where leaf δ13C was highest (−27.9 ± 1.0 ‰). The S. babylonica mainly used soil water in 30–170 cm layer (56.9%) with mean leaf δ13C of − 28.2 ‰ ± 0.7 ‰ at site C with stable shallow WTD (1.5 ± 0.1 m). It was found that both the contributions of upper soil water in 0–80 cm and deep water below 80 cm had significantly quadratic correlations with WTD under shallow water table conditions (p < 0.05). Leaf δ13C was negatively correlated with contributions of upper soil water above 80 cm depth, but it was positively related to the contributions of deep water below 80 cm in linear functions (p < 0.001). The results indicated that 2.1 m was the optimum WTD for riparian trees, because they maximized the use of deep water sources to get the highest WUE. This study provides insights into managing groundwater, surface water resources and riparian afforestation in losing rivers.
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    Rnd3/RhoE Modulates HIF1α/VEGF Signaling by Stabilizing HIF1α and Regulates Responsive Cardiac Angiogenesis
    (American Heart Association, 2016-03) Yue, Xiaojing; Yang, Tingli; Lin, Xi; Yang, Xiangsheng; Yi, Xin; Jiang, Xuejun; Li, Xiaoyan; Li, Tianfa; Guo, Junli; Dai, Yuan; Shi, Jianjian; Wei, Lei; Youker, Keith A.; Torre-Amione, Guillermo; Yu, Yanhong; Andrade, Kelsey C.; Chang, Jiang; Department of Pediatrics, IU School of Medicine
    The insufficiency of compensatory angiogenesis in the heart of patients with hypertension contributes to heart failure transition. The hypoxia-inducible factor 1α-vascular endothelial growth factor (HIF1α-VEGF) signaling cascade controls responsive angiogenesis. One of the challenges in reprograming the insufficient angiogenesis is to achieve a sustainable tissue exposure to the proangiogenic factors, such as HIF1α stabilization. In this study, we identified Rnd3, a small Rho GTPase, as a proangiogenic factor participating in the regulation of the HIF1α-VEGF signaling cascade. Rnd3 physically interacted with and stabilized HIF1α, and consequently promoted VEGFA expression and endothelial cell tube formation. To demonstrate this proangiogenic role of Rnd3 in vivo, we generated Rnd3 knockout mice. Rnd3 haploinsufficient (Rnd3(+/-)) mice were viable, yet developed dilated cardiomyopathy with heart failure after transverse aortic constriction stress. The poststress Rnd3(+/-) hearts showed significantly impaired angiogenesis and decreased HIF1α and VEGFA expression. The angiogenesis defect and heart failure phenotype were partially rescued by cobalt chloride treatment, a HIF1α stabilizer, confirming a critical role of Rnd3 in stress-responsive angiogenesis. Furthermore, we generated Rnd3 transgenic mice and demonstrated that Rnd3 overexpression in heart had a cardioprotective effect through reserved cardiac function and preserved responsive angiogenesis after pressure overload. Finally, we assessed the expression levels of Rnd3 in the human heart and detected significant downregulation of Rnd3 in patients with end-stage heart failure. We concluded that Rnd3 acted as a novel proangiogenic factor involved in cardiac responsive angiogenesis through HIF1α-VEGFA signaling promotion. Rnd3 downregulation observed in patients with heart failure may explain the insufficient compensatory angiogenesis involved in the transition to heart failure.