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Zequn Zhang,Qijuan Dong,Zhibin Chen,Junsheng Wu,Jiuyang Xia,Kang Huang,Pengcheng Zuo,Wei Xue,Bowei Zhang 대한금속·재료학회 2024 METALS AND MATERIALS International Vol.30 No.2
The influence of Co content on the microstructure and corrosion behavior of Al0.3CoxCrFeNi (x = 0.25, 0.5 and 1.0) highentropy alloys were investigated. The results indicated that the increased content of Co improve the corrosion resistanceof alloy, which can be attributed to the distinction of phase composition in alloys caused by different Co content. TheAl0.3CoxCrFeNi alloy shows a double-phase (FCC + BCC) structure for x = 0.25 and 0.5, and BCC phase consists of (Al,Ni)-rich B2 phase and (Cr, Fe, Co)-rich A2 phase. The increase of Co content induces the transformations of crystalstructuresfrom BCC to FCC, resulting in the decrease of BCC phase proportion. The Al0.3CoCrFeNi alloy exhibits thesingle FCC structure, and all elements tend to be homogeneously distributed. The difference in the potential of FCC andBCC phases indicates the BCC phase acts as anode resulting to localized corrosion, while B2 phase preferentially dissolvescompared to the A2 phase due to the lower potential. Therefore, the existence of selective corrosion is found in thealloys with double-phase, by contrast, the alloy with single FCC phase shows random pitting corrosion.
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Defang Pang,Lu Wang,Jing Dong,Xiaoyin Lai,Qijuan Huang,Richard Milner,Longxuan Li 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
We have previously demonstrated that in response to cerebral ischemia (CI), the growth factor angiopoietin-1 (Ang1) and α5β1 integrin are both induced in cerebral vessels, which likely provide positive signals driving the endogenous angiogenic response and vascular protection after CI. However, the precise relationship between endothelial Ang1 and α5β1 integrin after CI remains poorly understood. Here, we investigated the effects of the interaction between the Ang1/Tie2 system and α5β1 integrin on brain endothelial cells (BECs) under cerebral ischemic conditions in vivo and in vitro. Immunofluorescence analysis demonstrated that integrin α5β1 co-localized with Tie2/phosphorylated Tie2 on cerebral vessels in the penumbra. The in vitro study showed that oxygen–glucose deprivation/restoration (OGD/R) induced the expression of the Ang1 receptor Tie2 on BECs in a manner similar to that for integrin α5 and Ang1 in response to OGD/R, accompanied by increased activation of Tie2 and its downstream effectors focal adhesion kinase (FAK) and Akt. Knockdown of α5 integrin markedly suppressed OGD/R-induced Tie2 receptor activation in BECs, while in contrast, priming BECs with Ang1 promoted the expression of α5 integrin as well as the Tie2 downstream transcription factor Ets-1 in OGD-treated BECs. In line with this, Ets-1 knockdown significantly attenuated Ang1- mediated upregulation of α5 integrin. Functionally, Ang1 induced cell migration and tube formation of BECs after OGD, but this effect was inhibited by diminishment of the levels of α5 integrin in BECs. Taken together, our data indicate that the Ang1/Tie2 system cross-talks with integrin α5β1 in BECs after CI, which may contribute to the endogenous angiogenic vascular protective response following CI.
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