Nitric-oxide synthase 2 interacts with CD74 and inhibits its cleavage by caspase during dendritic cell development

Dendritic cells (DC) are professional antigen-presenting cells that possess specific and efficient mechanisms to initiate immune responses. Upon encounter with pathogens, immature DC will go through a maturation process that converts them to highly immunogenic mature DC. Despite the fact that nitric oxide (NO) was produced in large amounts in maturing DC, it is still unclear whether NO is the key molecule that initiates and enhances DC maturation and T cell proliferation, respectively. Here, we report that NO donor and overexpression of either nitric-oxide synthase 2 (NOS2) or nitric-oxide synthase 3 (NOS3) alone can induce surface expression of major histocompatibility complex class II (MHC II) and both the essential co-stimulatory molecules CD80 and CD86 in immature DC. Consistently, NO donor-treated immature DC were capable of enhancing T cell proliferation in vitro in the absence of lipolysaccharide. Interestingly, NOS2 interacts with CD74 (the MHC II-associated invariant chain), and the degradation of CD74 by caspases in immature DC was inhibited upon treatment with NO donor. Because the trafficking of MHC II is CD74-dependent, the increase in cell surface localization of MHC II in maturing DC is in part due to the increase in CD74 protein expression in the presence of NOS2 and NO.     

Icariin Protects Against Glucocorticoid-Induced Osteoporosis In Vitro and Prevents Glucocorticoid-Induced Osteocyte Apoptosis In Vivo

Icariin is the major active ingredient in Herba epimedii which is a commonly used Chinese herbal medicine for the treatment of osteoporosis. The present study aims to evaluate the osteoprotective effect of Icariin in glucocorticoid-induced osteoporosis in vivo and investigate the effect of Icariin on glucocorticoid-induced osteocyte apoptosis in vitro. A total of 48 female Sprague–Dawley rats were used. Glucocorticoid-induced osteoporosis was induced by daily injections of dexamethasone (0.1 mg/kg, daily, s.c.) for 60 days, whereas sham animals were injected daily with vehicle. At the end of the osteoporosis development period, osteoporotic rats were randomized to receive: vehicle (n = 8), Icariin (5,125 mg/kg, i.g.; n = 8), or alendronate (0.03 mg/kg, s.c.; n = 8) for 12 weeks. Sham animals were treated with vehicle for 12 weeks. At the beginning and at the end of treatments, animals were examined for bone mineral density. Serum bone-alkaline phosphatase and carboxy-terminal collagen cross links were measured. Primary osteocytes were isolated, and apoptosis was determined by trypan-blue assay. Interaction between Icariin and estrogen receptor and prosurvival signaling pathways activated by Icariin were also investigated. Icariin showed a comparable efficacy with alendronate in increasing bone mass. Icariin significantly increased bone-alkaline phosphatase (bone formation marker) and reduced carboxy-terminal collagen cross links (bone resorption marker). In vitro studies demonstrated that Icariin significantly prevented GC-induced apoptosis in osteocytes by activating ERK signaling via estrogen receptor. Our results suggest that Icariin might exert osteoprotective effect by maintaining osteocyte viability, thereby, regulating bone remodeling. Furthermore, our study provides preclinical evidence for the efficacy of Icariin for management of Glucocorticoid-induced osteoporosis.     

Brief Report: Estimating the size and number of autophagic bodies by electron microscopy

Much recent and ongoing research is focused on understanding the mechanisms and regulation of autophagy, a cellular self-degradation pathway with many links to human health. Although many assays exist to measure the total magnitude of autophagy, electron microscopy remains the tool of choice for the determination of the size and the number of autophagosomes formed in a given mutant or under given induction conditions. Here we present a detailed protocol for measuring autophagic bodies in the yeast Saccharomyces cerevisiae by electron microscopy. Furthermore, we present an improved mathematical method for estimating body size and a new method for estimating body number. Finally, we include a discussion of the merits and limitations of these methods and an example of their application to autophagic bodies formed in the ume6∆ strain.     

海洋生态资本理论框架下海洋生物资源的存量评估

海洋生态资本是能够直接或间接作用于人类社会经济生产、提供有用的产品流或服务流的海洋生态资源。海洋生态资源包括海洋生物资源及其生境资源。海洋生态资源的存量价值由海洋生物资源存量价值和海洋生境资源存量价值构成。针对我国海洋生物资源的特征,在海洋生态资本理论框架下,提出了鱼类、贝类、甲壳类、头足类、大型海藻等主要海洋生物资源的存量价值评估技术方法,包括物质量评估和价值量评估。探讨了海洋生物资源单位价格确定、评估价值修正、评估方法的适用性、成本扣除等问题。     

外生菌根菌对油松幼苗抗氧化酶活性及根系构型的影响

研究盆栽条件下,接种褐环乳牛肝菌(Suillus luteus)和红汁乳菇(Lactarius hatsudake)对油松(Pinus tabulaeformis)苗木生长,抗氧化酶活性和根系构型的影响。结果表明:(1)褐环乳牛肝菌和红汁乳菇均可与油松合成外生菌根,并显著提高苗木的苗高、地径、鲜重和干重。(2)接种褐环乳牛肝菌苗木针叶抗氧化酶(SOD、CAT、POD)活性分别比接种红汁乳菇苗木高14.77%、20.77%、34.68%;接种褐环乳牛肝菌苗木根系抗氧化酶(SOD、CAT、POD)活性分别比接种红汁乳菇苗木高8.54%,4.34%,33.31%;接种处理苗木抗氧化酶活性均显著高于不接种处理。接种处理苗木根长、表面积、体积、平均直径、根尖数、分叉数显著高于不接种处理;接种处理间苗木只有根尖数存在显著差异;接种褐环乳牛肝菌的油松根系分支成80°—90°的一级侧根数占23.81%,显著多于接种红汁乳菇和对照苗木。研究表明,接种褐环乳牛肝菌和红汁乳菇均能促进油松苗木生长,提高油松体内抗氧化酶活性,扩大苗木根系的吸收范围,其中褐环乳牛肝菌各方面的促进效果要优于红汁乳菇。     

耕地和林地土壤动物群落组成和多样性的差异——中国区域的整合分析

采用Meta分析对中国区域耕地和林地的土壤动物数量、组成和多样性差异进行定量研究。整合分析结果表明,在中国区域耕地比林地有显著低的土壤动物个体密度(-55.74%)、类群数(-27.56%)和Shannon-Wiener多样性指数(-24.51%),其中个体密度的响应与类群数和Shannon-Wiener多样性的响应存在显著差异。年均温高于20℃地区耕地和林地间土壤动物数量、类群数和多样性的响应绝对值显著低于年均温小于20℃地区,且耕地与林地间无差异;年降水量400—800mm地区耕地和林地间土壤动物多样性的响应绝对值最大,其次在年降水量大于800mm地区,最小值在年降水量小于400mm地区(耕地与林地无差异)。耕地中水田土壤动物Shannon-Wiener多样性与林地无差异;经济林土壤动物Shannon-Wiener多样性与耕地间无差异。在不同土壤动物尺寸的亚组中,大型土壤动物数量、类群数和多样性的响应绝对值大于小型土壤动物的响应绝对值,且类群数差异显著。耕地中蜱螨类(Acarina)数量显著低于林地(-64.11%),而耕地的弹尾目(Collembola)数量与林地无差异;膜翅目(...     

The Enhancement Effect of Calcium Ions on Ectomycorrhizal Fungi-Mediated Drought Resistance in Pinus sylvestris var. mongolica

Journal of Plant Growth Regulation - This study evaluated the overall influence of ectomycorrhizal fungi (ECMF) and exogenous Ca2+ supplementation on the growth, physiological, and metabolic traits...     

Postconditioning inhibits myocardial apoptosis during prolonged reperfusion via a JAK2-STAT3-Bcl-2 pathway

Background  

Postconditioning (PostC) inhibits myocardial apoptosis after ischemia-reperfusion (I/R) injury. The JAK2-STAT3 pathway has anti-apoptotic effects and plays an essential role in the late protection of preconditioning. Our aim was to investigate the anti-apoptotic effect of PostC after prolonged reperfusion and the role of the JAK2-STAT3 pathway in the anti-apoptotic effect of PostC.