碱性成纤维细胞生长因子对激光烧伤大兔皮肤愈合的影响分析

摘要 目的：探讨碱性成纤维细胞生长因子对激光烧伤大兔皮肤愈合的影响分析。方法：通过热辐射仪激光灼烧对大兔耳朵进行烧伤处理,根据实验需求,将其随机分为三组：对照组,bFGF组,bFGF + DAPT组。通过ImageJ软件测量伤口面积和疤痕组织的厚度,并定期计算残余伤口面积率和疤痕指数。通过组织学分析大兔伤口愈合的新血管生成量。通过蛋白印迹分析Notch1、Jagged1和Hes1的蛋白表达。通过免疫荧光分析愈合后的皮肤中α-SMA,Col I和Col III的相对蛋白水平。结果：bFGF组较对照组的疤痕指数降低（P<0.05）,bFGF+DAPT组较bFGF组疤痕指数升高（P<0.05）。bFGF组较对照组的愈合面积增加（P<0.05）,bFGF + DAPT组较bFGF组愈合面积降低（P<0.05）。与对照组相比,bFGF组的愈合时间明显缩短,较低的残余伤口面积和较低的疤痕指数（P<0.05）,而bFGF + DAPT组表现出明显的愈合延迟和较高的疤痕指数（P<0.05）。bFGF组较对照组的新血管生成量增加（P<0.05）,bFGF + DAPT组较bFGF组心血管生成量减少（P<0.05）。bFGF组较对照组的肉芽组织平均厚度增加,表皮间隙的闭合百分比升高（P<0.05）,bFGF + DAPT组较bFGF组肉芽组织平均厚度增加、表皮间隙的闭合百分比减少（P<0.05）。H＆E染色进行组织学分析发现,与对照组和bFGF + DAPT组相比,bFGF组出现明显的再上皮化和新血管形成,愈合效率较高（P<0.05）。bFGF组较对照组Notch1、Jagged1和Hes1的蛋白表达升高（P<0.05）,bFGF + DAPT组较bFGF组Notch1、Jagged1和Hes1的蛋白表达降低（P<0.05）。bFGF组较对照组?琢-SMA,Col I和Col III的蛋白表达降低（P<0.05）,bFGF + DAPT组较bFGF组表达升高（P<0.05）。结论：bFGF可以通过促进ESC的增殖并通过激活Notch1 / Jagged1途径抑制其向肌成纤维细胞（Myofibroblasts,MFB）的分化加快伤口愈合,减少疤痕形成。     

Potassium and phosphorus transport and signaling in plants

Nitrogen(N), potassium(K), and phosphorus(P) are essential macronutrients for plant growth and development, and their availability affects crop yield. Compared with N, the relatively low availability of K and P in soils limits crop production and thus threatens food security and agricultural sustainability. Improvement of plant nutrient utilization efficiency provides a potential route to overcome the effects of K and P deficiencies. Investigation of the molecular mechanisms underlying how plants sense, absorb, transport, and use K and P is an important prerequisite to improve crop nutrient utilization efficiency. In this review, we summarize current understanding of K and P transport and signaling in plants, mainly taking Arabidopsis thaliana and rice(Oryza sativa) as examples. We also discuss the mechanisms coordinating transport of N and K, as well as P and N.     

鳞翅目昆虫抗病毒免疫反应的研究进展

鳞翅目昆虫种类繁多,对农业生产和人类生活产生重大影响,宿主昆虫与病毒相互关系的研究对于利用病毒杀虫剂进行害虫治理和益虫病毒性疾病的预防具有重要意义.因此,鳞翅目昆虫与病毒的互作研究显得尤为重要,宿主昆虫的免疫系统在抗病毒感染过程中发挥着关键作用,对病毒产生不同程度的免疫反应.本文综述了昆虫围食膜和中肠对病毒入侵的防御作用,病毒进入体腔后昆虫所产生的细胞免疫和体液免疫反应,以及RNAi、细胞的自噬与凋亡、Toll、Imd、JAK-STAT和STING信号通路等相关的抗病毒免疫途径,并对昆虫抗病毒免疫研究的制约因素和未来鳞翅目昆虫抗病毒免疫的研究重点进行了讨论,以期为害虫的生物防治和益虫疾病的防控提供理论依据.     

Targeting P2 receptors in purinergic signaling: a new strategy of active ingredients in traditional Chinese herbals for diseases treatment

Adenosine triphosphate (ATP) and its metabolites adenosine diphosphate, adenosine monophosphate, and adenosine in purinergic signaling pathway play important roles in many diseases. Activation of P2 receptors (P2R) channels and subsequent membrane depolarization can induce accumulation of extracellular ATP, and furtherly cause kinds of diseases, such as pain- and immune-related diseases, cardiac dysfunction, and tumorigenesis. Active ingredients of traditional Chinese herbals which exhibit superior pharmacological activities on diversified P2R channels have been considered as an alternative strategy of disease treatment. Experimental evidence of potential ingredients in Chinese herbs targeting P2R and their pharmacological activities were outlined in the study.

     

Epithelial cell adhesion molecule promotes breast cancer resistance protein-mediated multidrug resistance in breast cancer by inducing partial epithelial–mesenchymal transition

Overexpression of breast cancer resistance protein (BCRP) plays a crucial role in the acquired multidrug resistance (MDR) in breast cancer. The elucidation of molecular events that confer BCRP-mediated MDR is of major therapeutic importance in breast cancer. Epithelial cell adhesion molecule (EpCAM) has been implicated in tumor progression and drug resistance in various types of cancers, including breast cancer. However, the role of EpCAM in BCRP-mediated MDR in breast cancer remains unknown. In the present study, we revealed that EpCAM expression was upregulated in BCRP-overexpressing breast cancer MCF-7/MX cells, and EpCAM knockdown using siRNA reduced BCRP expression and increased the sensitivity of MCF-7/MX cells to mitoxantrone (MX). The epithelial–mesenchymal transition (EMT) promoted BCRP-mediated MDR in breast cancer cells, and EpCAM knockdown partially suppressed EMT progression in MCF-7/MX cells. In addition, Wnt/β-catenin signaling was activated in MCF-7/MX cells, and the inhibition of this signaling attenuated EpCAM and BCRP expression and partially reversed EMT. Together, this study illustrates that EpCAM upregulation by Wnt/β-catenin signaling induces partial EMT to promote BCRP-mediated MDR resistance in breast cancer cells. EpCAM may be a potential therapeutic target for overcoming BCRP-mediated resistance in human breast cancer.     

Genistein-3′-sodium sulfonate Attenuates Neuroinflammation in Stroke Rats by Down-Regulating Microglial M1 Polarization through α7nAChR-NF-κB Signaling Pathway

Microglial M1 depolarization mediated prolonged inflammation contributing to brain injury in ischemic stroke. Our previous study revealed that Genistein-3′-sodium sulfonate (GSS) exerted neuroprotective effects in ischemic stroke. This study aimed to explore whether GSS protected against brain injury in ischemic stroke by regulating microglial M1 depolarization and its underlying mechanisms. We established transient middle cerebral artery occlusion and reperfusion (tMCAO) model in rats and used lipopolysaccharide (LPS)-stimulated BV2 microglial cells as in vitro model. Our results showed that GSS treatment significantly reduced the brain infarcted volume and improved the neurological function in tMCAO rats. Meanwhile, GSS treatment also dramatically reduced microglia M1 depolarization and IL-1β level, reversed α7nAChR expression, and inhibited the activation of NF-κB signaling in the ischemic penumbra brain regions. These effects of GSS were further verified in LPS-induced M1 depolarization of BV2 cells. Furthermore, pretreatment of α7nAChR inhibitor (α-BTX) significantly restrained the neuroprotective effect of GSS treatment in tMCAO rats. α-BTX also blunted the regulating effects of GSS on neuroinflammation, M1 depolarization and NF-κB signaling activation. This study demonstrates that GSS protects against brain injury in ischemic stroke by reducing microglia M1 depolarization to suppress neuroinflammation in peri-infarcted brain regions through upregulating α7nAChR and thereby inhibition of NF-κB signaling. Our findings uncover a potential molecular mechanism for GSS treatment in ischemic stroke.     

Amplification of RAD54B promotes progression of hepatocellular carcinoma via activating the Wnt/β-catenin signaling

Liver cancer was reported to be the sixth most frequently diagnosed cancer, and hepatocellular carcinoma (HCC) accounts for 75%-85% of primary liver cancer. Nevertheless, the concrete molecular mechanisms of HCC progression remain obscure, which is essential to elucidate. The expression profile of RAD54B in HCC was measured using qPCR and western blotting. Moreover, the levels of RAD54B in paraffin-embedded samples were evaluated using immunohistochemistry (IHC). The effect of RAD54B on HCC progression was testified by in vitro experiments, and in vivo orthotopic xenograft tumor experiments. The mechanisms of RAD54B promoting HCC progression were investigated through molecular and function experiments. Herein, RAD54B are dramatically upregulated in HCC tissues and cell lines both on mRNA and protein levels, and RAD54B can servers as an independent prognostic parameter of 5-year overall survival and 5-year disease-free survival for patients with HCC. Moreover, up-regulation of RAD54B dramatically increases the capacity for in vitro cell viability and motility, and in vivo intrahepatic metastasis of HCC cells. Mechanistically, RAD54B promotes the HCC progression through modulating the wnt/β-catenin signaling. Notably, blocking the wnt/β-catenin signaling axis can counteract the activating effects of RAD54B on motility of HCC cells. Besides, further analysis illustrates that DNA amplification is one of the mechanisms leading to mRNA overexpression of RAD54B in HCC. Our findings indicate that RAD54B might be a promising potential prognostic marker and a candidate therapeutic target to therapy HCC.     

禾谷镰刀菌蛋白激酶研究进展

由禾谷镰刀菌引起的小麦赤霉病是小麦生产最重要的真菌病害之一,除了造成严重的产量损失外,其病原菌还会产生多种真菌毒素危害人畜健康。蛋白激酶在禾谷镰刀菌生长发育、植物侵染和胁迫应答等方面具有重要作用。综述了禾谷镰刀菌主要蛋白激酶在生物学功能和分子作用机制等方面的研究进展,并对未来禾谷镰刀菌蛋白激酶的研究趋势进行了展望,以期为今后禾谷镰刀菌蛋白激酶的研究与小麦赤霉病的防治提供理论参考。     

RGMb/DRAGON与BMP信号转导

RGMb/DRAGON为RGM家族成员之一,在许多组织和器官中存在并表达.最初它作为粘附分子在神经系统中调节轴突排斥被发现.近来研究发现,它还是BMP的辅助受体,与BMP配体和受体结合,通过调控BMP信号通路在繁殖、肾脏机能的维持以及免疫疾病等生理和病理条件下发挥重要作用.本文评述了RGMb的基因及蛋白结构特征、表达定位及其在神经系统中的作用,并重点介绍了其在BMP信号通路中的作用机制和生物学研究进展.