一氧化氮的细胞内信号转导

从多个方面对一氧化氮(NO)的细胞内信号转导途径进行了阐述。     

哺乳动物细胞中一氧化氮与MAPK信号转导途径的调节关系

一氧化氮(NO)广泛存在于各种细胞中,在哺乳动物的心血管系统、神经系统、免疫系统和生殖系统等正常的生理活动和病理变化中发挥着十分重要作用.一氧化氮合酶(NOS)催化底物后生成NO,NO与可溶性鸟苷酸环化酶结合,促使GTP转化成cGMP,再激活cGMP依赖性的蛋白激酶(PKG),使蛋白质磷酸化而发挥生物学效应.即NOS/NO/cGMP/PKG作用通路.丝裂原活化蛋白激酶(MAPK)是哺乳动物细胞内最重要的信号系统之一,在细胞增殖、生长、发育、分化、凋亡以及应激、炎症等多种生理和病理过程发挥十分重要的调节作用,主要是通过MAPKKK/MAPKK/MAP级联系统传递信号.已经在多种细胞中研究发现,NO与MAPK信号转导途径之间有着密切的相互调节关系.因此,加深对信号传导通路各个环节两者调控机理的认识,对某些疾病病理机制的阐明和治疗有重要理论意义和应用价值,因而也受到广泛的关注.文中根据此前的报道,结合该实验室的研究结果,综述了NO与MAPK信号转导途径之间的相互调节关系.     

大鼠主动脉球囊内皮剥脱对血小板活化功能的影响

目的：观察大鼠主动脉球囊内皮剥脱对血小板活化的影响。方法：在大鼠主动脉球囊内皮剥脱模型上，分别于术后7、14和21天观察球囊内皮剥脱对血小板活化的影响。结果：大鼠球囊内皮剥脱术后，于7、14、21天时，血小板聚集明显增强，蛋白激酶（PKC）活性明显增高，环磷酸腺苷（cAMP）活性明显降低，均以7天组最为明显。结论：临床PTCA后较长时间应用抗栓剂是必要的。     

应力导致的细胞内信号转导和基因表达变化

阐述了应力与细胞的紧密关系.综述了应力作用细胞后引起的生化反应及其细胞骨架介导的信号转导和相关基因表达的变化,系统列举了一些应力诱导的基因表达变化,如即早基因、细胞因子、酶、胞外基质分子等;并针对细胞应力响应,提出了目前这一领域存在的一些问题,希望应力与细胞响应的分子机制得到进一步发展,为解决应力引起的生物体生理和病理变化提供理论基础.     

一氧化氮与植物的逆境响应

综述了植物体内一氧化氮(NO)的来源及形成途径(即一氧化氮合酶途径、硝酸还原酶途径、亚硝酸还原酶途径和非酶途径),在生物和非生物胁迫条件下NO与过氧化氢,脱落酸,水杨酸等信号分子之间的相互关系及其信号转导途径等方面的研究进展。     

MAPK信号转导通路与HCMV感染

MAPK信号转导通路参与了HCMV的感染过程.MAPK通路中的ERK和p38通路在HCMV复制周期中起重要作用,它通过磷酸化转录因子引起病毒及宿主相关基因的转录,从而调控HCMV的复制.HCMV的包膜糖蛋白及其他多种基因表达产物可通过不同的机制以一定时序激活MAPK通路,调节自身及宿主细胞相应基因表达,以利于病毒完成其生活周期,并参与病毒的致病过程.深入研究MAPK信号转导通路与HCMV感染的关系可为治疗HCMV感染引起的疾病提供新的治疗靶点.     

细胞因子受体介导的信号转导途径研究进展

细胞对外界刺激发生生物学效应是与细胞内信号传递分不开的。细胞在生长、增殖、分化等过程中，酪氨酸蛋白激酶(Tyrosine protein kinases，TPK)具有重要的调节作用。细胞内的TPK包括两类：第一类为位于细胞质膜上的TPK，称为受体型TPK，如胰岛素受体、表皮生长因子受体，这些受体具有催化活性；第二类为位于胞浆中的TPK，称为非受体型TPK，如一些底物酶和某些原癌基因(src、yes等)编码的TPK，它们与无催化活性的受体偶联而发挥生理作用。有的细胞因子受体本身无酪氨酸激酶活性、不能依靠受体的活性而活化其它信号分子，但其胞浆存在非跨膜型蛋白酪氨酸激酶(nontransmemberane protein tyrosine kinases，NM-PTKs)介导细胞因子与其受体结合后的信号转导。     

气孔运动调控中过氧化氢和一氧化氮信号途径的交叉作用

用NO荧光指示剂DAF-2DA测定了H 2 O 2 对蚕豆和鸭跖草气孔保卫细胞NO的影响;以蚕豆幼苗为材料研究了H 2 O 2 和NO在调控气孔运动中的相互关系.结果表明,H 2 O 2 能够诱导保卫细胞胞质NO的形成,其诱导作用可以被2-苯-4,4,5,5-四甲基咪唑-1-氧-3-氧化物(PTIO)所清除和N G -氮-L-精氨酸-甲酯(L-NAME)所阻断.推测保卫细胞中可能存在一氧化氮合酶(NOS)类似物.H 2 O 2 主要是通过NOS途径诱导产生NO.在10～100μmol/L范围内,NO的供体硝普钠(SNP)和H 2 O 2 都可诱导气孔关闭,并具明显的浓度效应.H 2 O 2 清除剂过氧化氢酶(CAT)能够完全抵消NO的诱导气孔关闭作用;H 2 O 2 合成抑制剂二苯基碘(DPI)可部分减弱NO诱导的气孔关闭.NO合酶抑制剂L-NAME和NO的清除剂与H 2 O 2 共处理时,H 2 O 2 诱导气孔关闭的作用被大大减弱.结果说明,在调控气孔运动中H 2 O 2 和NO具有相互依赖性,H 2 O 2 和NO信号分子具有信号自身放大功能,共同参与了对气孔运动的调控.     

钙——钙调素热激信号转导途径研究进展

植物细胞内存在一条新的热激信号转导途径.热激引起细胞内自由钙离子浓度([Ca2+];)迅速上升,而磷脂酶C/1,3,5-三磷酸肌醇(PLC/IP3)信号系统的参与是热激引起[Ca2+]i升高的因素之一.热激也提高钙调素(CaM)基因表达和CaM蛋白的积累,钙调素基因AtCaM3是Ca2+-CaM热激信号转导途径中的重要成员.钙调素下游信号分子研究表明:AtCaM3通过CaM结合的蛋白激酶AtcBK3或CaM结合的蛋白磷酸酶AtPP7改变热激因子AtHSFAla的磷酸化状态以调节AtHSFAla的活性,进而影响热激蛋白基因的表达,最终影响植株的耐热性.     

细菌环二鸟苷酸介导的信号转导途径研究进展

环二鸟苷酸(c-di-GMP)是在细菌中广泛存在的第二信使分子,它介导的信号转导途径涉及调控细菌的运动、致病性、生物膜形成、细胞周期进程和有机溶剂耐受性等多种重要功能.该文主要从c-di-GMP的合成与降解、c-di-GMP的效应子及c-di-GMP的生理作用3方面对c-di-GMP介导的信号转导途径进行总结,并对该信号转导途径的研究前景进行了展望.     

Regulation between nitric oxide and MAPK signal transduction in mammals

Nitric oxide (NO) is an important biological messenger in the regulation of tissue homeostasis. It exhibits a wide range of effects during physiological and pathophysiological processes. Typical beneficial properties of NO include the regulation of vascular tone,the protection of cells against apoptosis, the modulation of immune responses, and the killing of microbial pathogens. On the other hand,NO may cause severe vasodilation and myocardial depression during bacterial sepsis or act as a cytotoxic and tissue-damaging molecule in autoimmune diseases. Mitogen-activated protein kinase (MAPK) is a family of serine/threonine protein kinases that are widely distributed in mammalian cells. MAPK cascade plays pivotal roles in gene expression, cell proliferation, differentiation, neuronal survival and programmed cell death under a variety of experimental conditions. MAPKs transduce the signal for the cellular response to extracellular stresses or stimuli. The relation between them, however, has never been reviewed. Based on our researches and other reports in the field, we review their reciprocal regulatory functions.     

Involvement of nitric oxide in the signal transduction of salicylic acid regulating stomatal movement

The effects and the relationship between sali-cylic acid(SA)and nitric oxide(NO) on Vicia faba L.stomatal movement were studied.The results here showed that exogenous SA and NO induced stomatal closure,100μmol/L SA induced a rapid and striking NO increase in the cytosol of guard cells.This phenomenon was largely prevented by 2000μmol/L 2-phenyl-4,4,5,5-tetramethylimidazoline-l-oxyl-3-oxide(PTIO),a specific NO scavenger,and 25μmol/L N^G-nitro-L-Arg-methyl eater (L-NAME),an inhibitor of NO synthase(NOS) in mammalian cells that also inhibits plant NOS.In addition,SA-induced stomatal closure was largely prevented by PTIO and L-NAME.These results provide evidence that guard cells generate NO in response to SA via NOS-like activity,and that such NO production is required for full stomatal closure in response to SA.H-(1,2,4)-oxadiazole-[4,3-α]quinoxalin-l-one(ODQ),an inhibitor of guanylate cyclase,and nicotinamide,an antagonist of cADPR production,inhibited the effects of SA-and NO-induced stomatal closure.It suggests that both cGMP and cADPR might mediate the signal transduction of SA and NO-induced stomatal closure.     

Nitric oxide involved in signal transduction of Jasmonic acid-induced stomatal closure of Vicia faba L.

Nitric oxide (NO) and Jasmonic acid (JA) are two key signaling molecules involved in many and diverse biological pathways in plants. Growing evidence suggested that NO signaling interacts with JA signaling. In this work, Our experiment showed that NO exists in guard cell of Vicia faba L., and NO is involved in signal transduction of JAinduced stomata closuring: ( i ) JA enhances NO synthesis in guard cell; ( ii ) both JA and NO induced stomatal closure, and had dose response to their effects; ( iU ) there are synergetic correlation between JA and lower NO concentration in regulation of stomatal movement; (iV) JA-induced stomatal closure was largely prevented by 2-phenyl-4,4,5,5-tetramethylimidazoline-l-oxyl-3-oxide (PTIO), a specific NO scavenger. An inhibitor of NO synthase (NOS) in mammalian cells, N^G-nitro-L-Arg-methyl eater (L-NAME) also inhibits plant NOS, repressing JA-induced NO generation and JA-induced stomatal closure. We presumed that NO mainly comes from NOS after JA treatment.     

Regulation of mouse blastocyst adhesion,outgrowth and secretion of matrix metalloproteinase-2 by cGMP and nitric oxide <Emphasis Type="Italic">in vitro</Emphasis>

Nitric oxide (NO) is a multifunctional messenger molecule produced through oxidation of L-arginine to L-citrulline by enzyme NO synthase (NOS). In the current study, mouse blastocysts were cultured in the different media, and the implantation capacity of blastocyst was evaluated by evaluating the percentage of embryos adhesion and outgrowth after culture for 12, 24 or 48 h. Matrix metalloproteinase-2 (MMP-2) mRNA was detected by RT-PCR, and MMP-2 protein was detected by gelatin zymography. Inhibition of blastocyst adhesion and outgrowth was observed in embryo cultured with 500 μmol/L NOS inhibitor N^G-mono-methyI-L-arginine (L-NMMA) alone; however, 100 μmol/L S-nitroso-N-acetylpenicillamine (SNAP), a NO donor, and 20μmol/L cGMP analogue, 8-Br-cGMP could block this inhibition. The expression and production of MMP-2 in the blastocysts were suppressed by L-NMMA, and SNAP or 8-br-cGMP could reverse this suppression. These results suggest that NO induces embryo implantation by cGMP signaling pathway.     

蓝藻真核型蛋白质激酶与信号传导

对最近10年在蓝藻中找到大量编码Ser／Thr基因的研究结果进行了综述,并对这些蛋白质激酶在信号传导中的作用模式做了讨论．     

Regulation of embryo implantation by nitric oxide in mouse

Intrauterine injection and zymography were used to investigate the effect of nitric oxide (NO) on embryo implantation in mice. On day 3, one uterine horn of female pregnant mice was injected intraluminally with various doses of nitric oxide synthase (NOS) inhibitor, N-nitro-L-arginine methyl ester (L-NAME), while the contralateral horn served as control. Animals were sacrificed by cervical dislocation on day 7 of gestation, and the number of implanted embryos in each horn was calculated. The results showed that lower doses (0.05 mg L-NAME) did not inhibit implantation significantly (P > 0.05), but high doses (0.2 mg L- NAME) resulted in a significant reduction in the number of implanted embryos (P < 0.05). Co-administration of SNP, a generator of NO, with L-NAME would reverse the antiimplantation effect of L-NAME. To further understand the precise mechanism of NO in implantation, matrix metalloproteinase (MMPs) activities were detected by gelatin zymography. The reduction in the number of implanted embryos in 0.2 mg L-NAME treated group was associated with decreased MMP-9 activity but a stable MMP-2 activity. The activities of MMP-2 and MMP-9 were not changed in L-NAME and SNP treated group. These data suggest that NO acts as a mediator to regulate the activity of MMP-9, and facilitates embryo implantation.     

大鼠端脑神经元型一氧化氮合酶免疫阳性神经元的分布

目的 :观察大鼠端脑神经元型一氧化氮合酶 (nNOS)免疫阳性神经元的分布。方法 :ABC免疫细胞化学法显示大鼠端脑nNOS阳性神经元。结果 :nNOS阳性神经元呈棕褐色 ,胞体的形态多样化 ,呈梭形、三角形、圆形等多种形状 ,突起有一个或多个 ;阳性纤维呈棕色串珠状 ,个别脑区阳性纤维相互交织成网。端脑nNOS免疫阳性神经元主要分布于嗅结节 (包括海马回 )、梨状区 (包括梨状皮质和梨状核 )、斜角带、隔区、杏仁复合体、海马结构、尾壳核和苍白球 ,以及大脑皮质等各个部位 ,其中以大脑皮质、梨状区和斜角带、尾壳核等部位最为丰富。结论 :大鼠端脑内分布有丰富的nNOS阳性神经元 ,它们可能通过调节神经递质的分泌 ,参与脑的高级整合功能。     

Nitric oxide mediates the fungal elicitor-induced Taxol biosynthesis of Taxus chinensis suspension cells through the reactive oxygen species-dependent and -independent signal pathways

Taxol (paclitaxel, NSC-125973), a secondary me- tabolite of the Taxus species, has been recognized as one of the best anticancer drugs emerging in the last decade[1]. The production of Taxol by various Taxus spp. cells in culture has been one of the most …     

Cell cycle and cell signal transduction in marine phytoplankton

tAs unicellular phytoplankton, the growth of a marine phytoplankton population results directly from the completion of a cell cycle, therefore, cell-environment communication is an important way which involves signal transduction pathways to regulate cell cycle progression and contribute to growth, metabolism and primary production and respond to their surrounding environment in marine phytoplankton. Cyclin-CDK and CaM/Ca²⁺ are essentially key regulators in control of cell cycle and signal transduction pathway, which has important values on both basic research and applied biotechnology. This paper reviews progress made in this research field, which involves the identification and characterization of cyclins and cell signal transduction system, cell cycle-control mechanisms in marine phytoplankton cells, cell cycle proteins as a marker of a terminal event to estimate the growth rate of phytoplankton at the species level, cell cycle-dependent toxin production of toxic algae and cell cycle progression regulated by environmental factors.