A proteomic analysis of aorta from spontaneously hypertensive rat: RhoGDI alpha upregulation by angiotensin II via AT(1) receptor

Arteries undergo remodeling as a consequence of increased wall stress during hypertension. However, the molecular mechanisms of the vascular remodeling are largely unknown. Proteomics is a powerful tool to screen for differentially expressed proteins, but little effort was made on vascular disease research, especially on hypertension. In the present study, the differentially expressed proteins in aortas from 18-week-old spontaneously hypertensive rats (SHR) and their normotensive counterpart, Wistar Kyoto rats (WKY), were examined by two-dimensional electrophoresis (2-DE). We found 50 proteins to be differentially expressed, among which 27 were highly or only expressed in SHR and 23 in WKY. Using matrix-assisted laser desorption/ionisation-time of flight mass spectrometry (MALDI-TOF-MS) and online data search, nine proteins, including Rho GDP dissociation inhibitor alpha (RhoGDIalpha), were identified with high confidence. Further, the upregulation of RhoGDIalpha was verified at both mRNA and protein level in SHR. In addition, when cultured vascular smooth muscle cells (VSMCs) from aortas of SHR and WKY were treated with angiotensin II (Ang II) and antagonist of angiotensin II type I (AT(1)) receptor, L158809, respectively, RhoGDIalpha was upregulated by Ang II and downregulated by L158809 in VSMCs of SHR. These results demonstrate that vascular remodeling results in significant alterations in the protein expression profile of the aorta during hypertension and suggest that the upregulation of RhoGDIalpha in hypertension is induced by Ang II via AT(1) receptor.     

Poloxamer-188 Attenuates TBI-Induced Blood–Brain Barrier Damage Leading to Decreased Brain Edema and Reduced Cellular Death

Neurochemical Research - Plasmalemma permeability plays an important role in the secondary neuronal death induced by traumatic brain injury (TBI). Previous works showed that Poloxamer 188 (P188)...     

轮梗霉原生质体的制备*

本文比较了酶浓度、菌龄、渗透压稳定剂以及酶解温度和时间等因素对轮梗霉原生质体得率的影响。结果基本获得了制备原生质体的适宜条件:用0.6mol/L甘露醇稳渗剂配制成的4%纤维素酶和0.5%蜗牛酶混合酶,35℃酶解培养了30h的菌丝1.0h,即可得到较高产量的原生质体。对该原生质体进行了再生实验,其再生率约为23.8%。     

细根对竹林-阔叶林界面两侧土壤养分异质性形成的贡献

土壤养分异质性是竹林-阔叶林界面(bamboo and broad-leaved forest interface, 以下简称竹阔界面)的重要特征, 细根生长、周转和分解影响土壤养分供应能力, 但其在竹阔界面养分异质性形成中的贡献尚不清楚。该文选取竹阔界面两侧的毛竹(Phyllostachys pubescens)林和常绿阔叶林为研究对象, 开展土壤养分(C、N、P)含量、细根生物量及周转、细根分解及养分回归等指标的对比研究。结果表明: (1)竹阔界面两侧毛竹林和常绿阔叶林土壤养分差异明显, 毛竹林0-60 cm土壤有机碳(SOC)和土壤总氮(STN)含量分别为20.51和0.53 g·kg^-1, 常绿阔叶林0-60 cm土壤有机碳(SOC)和土壤总氮(STN)含量分别为13.42和0.26 g·kg^-1, 前者比后者分别高出34.53%和50.35%, 但毛竹林土壤全磷(STP)含量低于常绿阔叶林25.54%; (2)竹阔界面两侧细根生物量、养分密度及养分回归量差异明显, 毛竹林细根生物量高达1201.60 g·m^-2, 是常绿阔叶林的5.86倍; 养分密度分别为591.42 g C·m^-2、5.44 g N·m^-2、0.25 g P·m^-2, 分别是常绿阔叶林的6.12倍、3.77倍和3.11倍; 年均养分回归量分别为278.54 g C·m^-2·a^-1、2.36 g N·m^-2·a^-1、0.11 g P·m^-2·a^-1, 是常绿阔叶林的6.93倍、4.29倍和3.67倍; (3)细根对界面两侧土壤SOC、STN异质性形成的年均潜在贡献分别为76.79%和28.33%, 但对STP异质性形成起减缓作用, 贡献率为6.17%。这些结果说明毛竹扩张可以改变常绿阔叶林土壤的养分状况, 且细根对不同养分的异质性形成贡献不一致, 是土壤SOC、STN异质性形成的重要原因。     

毛竹种群向常绿阔叶林扩张的细根策略

为了探讨毛竹(Phyllostachys pubescens)种群向常绿阔叶林扩张的根系策略, 该文采用根钻法和内生长法, 在江西大岗山选取毛竹林与阔叶林的交错区——竹阔界面(bamboo-broad-leaved forest interface), 并垂直于界面连续设置毛竹林、毛竹与阔叶树的混交林(以下简称为竹阔混交林)、常绿阔叶林3种样地, 比较分析其细根的空间分布格局、比根长、根长密度、生长速率和周转率等指标。结果表明: 毛竹林细根生物量(1201.60 g·m^-2) >竹阔混交林(601.18 g·m ^-2) >常绿阔叶林(204.88 g·m ^-2); 在毛竹与阔叶树竞争的混交林中, 毛竹细根分布趋向于上层土壤(与毛竹林细根相比), 且其比根长也显著增加, 平均增幅高达123.42%, 总根长密度比阔叶树大2.1倍; 同时, 毛竹细根生长速率和周转率均高于阔叶树。这些结果说明毛竹可通过广布、精准、灵活、快速等细根竞争策略, 提高资源获取能力, 实现种群扩张。     

Necrostatin-1 Suppresses Autophagy and Apoptosis in Mice Traumatic Brain Injury Model

Traumatic brain injury (TBI) results in neuronal apoptosis, autophagic cell death and necroptosis. Necroptosis is a newly discovered caspases-independent programmed necrosis pathway which can be triggered by activation of death receptor. Previous works identified that necrostatin-1 (NEC-1), a specific necroptosis inhibitor, could reduce tissue damage and functional impairment through inhibiting of necroptosis process following TBI. However, the role of NEC-1 on apoptosis and autophagy after TBI is still not very clear. In this study, the amount of TBI-induced neural cell deaths were counted by PI labeling method as previously described. The expression of autophagic pathway associated proteins (Beclin-1, LC3-II, and P62) and apoptotic pathway associated proteins (Bcl-2 and caspase-3) were also respectively assessed by immunoblotting. The data showed that mice pretreated with NEC-1 reduced the amount of PI-positive cells from 12 to 48?h after TBI. Immunoblotting results showed that NEC-1 suppressed TBI-induced Beclin-1 and LC3-II activation which maintained p62 at high level. NEC-1 pretreatment also reversed TBI-induced Bcl-2 expression and caspase-3 activation, as well as the ratio of Beclin-1/Bcl-2. Both 3-MA and NEC-1 suppressed TBI-induced caspase-3 activation and LC3-II formation, Z-VAD only inhibited caspase-3 activation but increased LC3-II expression at 24?h post-TBI. All these results revealed that multiple cell death pathways participated in the development of TBI, and NEC-1 inhibited apoptosis and autophagy simultaneously. These coactions may further explain how can NEC-1 reduce TBI-induced tissue damage and functional deficits and reflect the interrelationship among necrosis, apoptosis and autophagy.