Oxidized high-density lipoprotein promotes CD36 palmitoylation and increases lipid uptake in macrophages

Oxidized high-density lipoprotein (oxHDL) reduces the ability of cells to mediate reverse cholesterol transport and also shows atherogenic properties. Palmitoylation of cluster of differentiation 36 (CD36), an important receptor mediating lipoprotein uptake, is required for fatty acid endocytosis. However, the relationship between oxHDL and CD36 has not been described in mechanistic detail. Here, we demonstrate using acyl-biotin exchange analysis that oxHDL activates CD36 by increasing CD36 palmitoylation, which promotes efficient uptake in macrophages. This modification increased CD36 incorporation into plasma lipid rafts and activated downstream signaling mediators, such as Lyn, Fyn, and c-Jun N-terminal kinase, which elicited enhanced oxHDL uptake and foam cell formation. Furthermore, blocking CD36 palmitoylation with the pharmacological inhibitor 2-bromopalmitate decreased cell surface translocation and lowered oxHDL uptake in oxHDL-treated macrophages. We verified these results by transfecting oxHDL-induced macrophages with vectors expressing wildtype or mutant CD36 (mCD36) in which the cytoplasmic palmitoylated cysteine residues were replaced. We show that cells containing mCD36 exhibited less palmitoylated CD36, disrupted plasma membrane trafficking, and reduced protein stability. Moreover, in ApoE^−/−CD36^−/− mice, lipid accumulation at the aortic root in mice receiving the mCD36 vector was decreased, suggesting that CD36 palmitoylation is responsible for lipid uptake in vivo. Finally, our data indicated that palmitoylation of CD36 was dependent on DHHC6 (Asp-His-His-Cys) acyltransferase and its cofactor selenoprotein K, which increased the CD36/caveolin-1 interaction and membrane targeting in cells exposed to oxHDL. Altogether, our study uncovers a causal link between oxHDL and CD36 palmitoylation and provides insight into foam cell formation and atherogenesis.     

珍稀濒危植物堇叶紫金牛对持续干旱的生理响应

采用盆栽控水法,研究了珍稀濒危植物堇叶紫金牛(Ardisia violacea)在持续干旱条件下的生理响应。随着持续干旱时间的延长,堇叶紫金牛应对持续干旱的阶段可分为适应期、轻度干旱期、中度干旱期和重度干旱期。在适应期和轻度干旱期,堇叶紫金牛叶片游离脯氨酸和可溶性糖含量稳定在一个较低水平,可溶性蛋白质含量先下降后快速上升,细胞膜系统和抗氧化酶系统能主动进行生理调节;中度干旱期,丙二醛(MDA)含量和质膜相对透性迅速升高,细胞膜系统受损加剧,游离脯氨酸、可溶性糖含量均急剧增加,对抵御干旱起到重要的渗透调节作用。在轻度干旱期和中度干旱期,光合色素中叶绿素a和叶绿素b含量显著提高,以抵抗干旱胁迫。重度干旱期,细胞膜系统、抗氧化酶SOD、游离脯氨酸和可溶性糖含量上升,但MDA略微下降,这时可能达到植物耐受干旱的极限,不再发生膜脂过氧化作用。综上表明,堇叶紫金牛具有较强的耐旱性,RWC为49.94%是细胞膜系统、抗氧化酶系统和渗透调节物质含量变化的拐点,渗透调节和抗氧化酶系统的主动适应是其耐旱的主要机制。     

洞庭湖洲滩速生杨树林变化信息提取方法

洞庭湖是我国第二大淡水湖,其湿地资源具有重要的生态功能和经济价值。近20年来,洞庭湖洲滩速生杨树林发展迅速,其中西洞庭湖杨树林的扩张最为明显,极大改变了湖区湿地植被分布格局,隐含极大的生态风险。以Landsat ETM+和HJ-1A/1B CCD影像为数据源,提出了洞庭湖速生杨树林变化信息提取的两种方法,并对这两种方法进行了比较研究。一种是分类的方法,即采用面向对象分层信息提取的方法先提取出树林滩地信息,再将距离大堤一定范围内的树林滩地归为防护林,速生杨树林变化的面积即为两个时相提取结果的差值。另一种是变化检测的方法,它是基于像元进行变化检测,先确定出总的变化区域,再从中筛选速生杨树林的变化信息。结果表明:(1)两种提取方法都是可行的,不同方法提取的速生林变化信息存在一定差异,但空间分布大体一致;(2)基于分类的方法总体精度和Kappa系数均略高于基于变化检测的方法:其中基于分类的方法总体精度达84.00%,Kappa系数为0.67,基于变化检测的方法总体精度达83.00%,Kappa系数为0.65;(3)基于分类的方法图斑较大、图斑数较少,基于变化检测的方法图斑较小且较破碎、图斑数多;(4)基于分类的方法漏分较少、错分较多,基于变化检测的方法漏分较多、错分较少。为洞庭湖洲滩杨树林的动态监测提供了研究方法,也为杨树林扩张原因及其生态效应分析提供研究基础。     

海南霸王岭天然次生林边缘效应下木质藤本与树木的关系

选择海南岛霸王岭天然恢复60 a的次生林样地中形成年限为17和13年的边缘,分别设置4条10 m100 m的样带,研究边缘效应下dbh ≥1 cm树木的攀藤率、被藤本攀附的频度和每木藤本数随距边缘距离的变化。结果表明：在0.8 hm2的样带中,树木的攀藤率分别为44.58%（17年边缘）和32.63%（13年边缘）。2种边缘中,dbh 1—5 cm、5—10 cm树木的攀藤率都随距离发生了变化,17年边缘中dbh ＞20 cm和13年边缘中dbh 10—20 cm树木的攀藤率都没有随距离的变化而变化。树木被藤本攀附的频度随距边缘距离的增加而降低,攀附3株以上藤本的树木最少,在17年边缘中变化趋势较明显;攀附1株藤本的树木最多,在13年边缘中变化明显。17年边缘中每木藤本数随距离增加而降低。在边缘形成初期,边缘形成年限对每木藤本数产生了影响,其在17年边缘中下降程度较大,但总体高于13年边缘中。     

近10年来蒙古高原植被覆盖变化对气候的响应

基于东亚干旱半干旱地区内蒙古和蒙古国67个气象站的观测资料和SPOTVEGETATION归一化植被指数(NDVI)数据,借助线性趋势、MK趋势性检验、最大化合成法和相关分析等常用数理统计方法,研究了内蒙古和蒙古国地区的植被覆盖变化和气候变化及其响应关系。结果表明:①近49年内蒙古和蒙古国地区年均气温显著上升,降水变化不明显。年均气温在空间上呈现出南高北低的空间分布格局,降水量表现出由西向东递增趋势。②空间分布上,内蒙的植被覆盖状况好于蒙古国。时间变化上,该地区植被覆盖变化分为2个阶段,1998—2001年NDVI呈整体退化趋势,2002—2012年波动上升,其中2009—2012年连续3a上升。空间变化上,内蒙古境内植被退化的区域主要集中在锡林郭勒盟周边地区,蒙古国境内退化的区域分布在中西部地区。③蒙古国境内荒漠和草原植被NDVI与降水呈正相关关系,与气温呈负相关。而对于内蒙古而言荒漠和草原植被的NDVI也与降水呈正相关关系,森林植被与气温呈正相关。就政策层面:内蒙古区域近年来受国家重大生态政策退耕还林、退牧还草的影响,大部分东部和西部植被恢复较快。在今后如果增强两国的文化和政策交流学习,将会对未来的游牧民族文化的保留和发展提供契机。     

SWAT模型对景观格局变化的敏感性分析——以丹江口库区老灌河流域为例

景观的空间配置与类型组成能够对流域的产流、产沙及非点源污染产生影响。在以往SWAT模型研究中,往往默认水文模型考虑了该影响。为分析SWAT模型对不同景观格局变化的敏感性,根据老灌河流域2000年土地利用在各子流域的组成,模拟研究区更为破碎、复杂的景观空间配置,通过设置多套试验参数,利用SWAT模型生成基于不同景观格局的模拟结果。结果表明,SWAT模型不能反映除坡度和面积变化之外的景观水平下各斑块之间因景观空间格局改变对流域产流、产沙以及非点源污染的影响;模型通过其他参数的调整,弥补了模型分析数据的不足,使实测数据与模型部分结果高度吻合。这表明,一个能够反映流域部分水文特征的SWAT模型,未必是对研究区真实情形的模拟,而是各个参数间平衡的结果。因此,在利用SWAT模型分析模拟景观变化时,不应默认模型能够模拟景观空间格局改变对流域水文过程的影响,同时研究者可以通过划分坡度带,提高模型对不同坡度土地利用的敏感性。     

缙云山川鄂连蕊茶在不同群落类型中的RAPD分析

采用随机扩增多态性DNA(RAPD)对常绿阔叶林灌木层广布种川鄂连蕊茶(Camellia rosthorniana)在缙云山3个群落类型(毛竹林、针阔混交林和常绿阔叶林)中的遗传结构和DNA多样性进行了研究。10个引物共扩增出138个产物,其中115个是多态性的,多态位点比率为83．33％。Shannon指数估算的3个种群的遗传多样性为常绿阔叶林0．3345,毛竹林0．3148,针阔混交林0．3085,遗传分化为8．12％;Nei指数计算的3个种群的基因多样性为常绿阔叶林0．2095,毛竹林0．1981,针阔混交林0．1934,遗传分化为7．51％。种群间遗传距离在0．0177～0．0393之间。川鄂连蕊茶在3个群落中的种群大小和生长状况不同,各种群遗传多样性的高低可能是对所处群落生境的适应。     

Exercise increases the release of NAMPT in extracellular vesicles and alters NAD + activity in recipient cells

Aging is associated with a loss of metabolic homeostasis, with cofactors such as nicotinamide adenine dinucleotide (NAD⁺) declining over time. The decrease in NAD⁺ production has been linked to the age‐related loss of circulating extracellular nicotinamide phosphoribosyltransferase (eNAMPT), the rate‐limiting enzyme in the NAD⁺ biosynthetic pathway. eNAMPT is found almost exclusively in extracellular vesicles (EVs), providing a mechanism for the distribution of the enzyme in different tissues. Currently, the physiological cause for the release of eNAMPT is unknown, and how it may be affected by age and physical exercise. Here, we show that release of small EVs into the bloodstream is stimulated following moderate intensity exercise in humans. Exercise also increased the eNAMPT content in EVs, most prominently in young individuals with higher aerobic fitness. Both mature fit and young unfit individuals exhibited a limited increase in EV‐eNAMPT release following exercise, indicating that this mechanism is related to both the age and physical fitness of a person. Notably, unfit mature individuals were unable to increase the release of eNAMPT in EVs after exercise, suggesting that lower fitness levels and aging attenuate this important signalling mechanism in the body. EVs isolated from exercising humans containing eNAMPT were able to alter the abundance of NAD⁺ and SIRT1 activity in recipient cells compared to pre‐exercise EVs, indicating a pathway for inter‐tissue signalling promoted through exercise. Our results suggest a mechanism to limit age‐related NAD⁺ decline, through the systemic delivery of eNAMPT via EVs released during exercise.