Sphingosine kinase type 1 induces G12/13-mediated stress fiber formation,yet promotes growth and survival independent of G protein-coupled receptors

Sphingosine 1-phosphate (S1P) is the ligand for a family of specific G protein-coupled receptors (GPCRs) that regulate a wide variety of important cellular functions, including growth, survival, cytoskeletal rearrangements, and cell motility. However, whether it also has an intracellular function is still a matter of great debate. Overexpression of sphingosine kinase type 1, which generated S1P, induced extensive stress fibers and impaired formation of the Src-focal adhesion kinase signaling complex, with consequent aberrant focal adhesion turnover, leading to inhibition of cell locomotion. We have dissected biological responses dependent on intracellular S1P from those that are receptor-mediated by specifically blocking signaling of Galphaq, Galphai, Galpha12/13, and Gbetagamma subunits, the G proteins that S1P receptors (S1PRs) couple to and signal through. We found that intracellular S1P signaled "inside out" through its cell-surface receptors linked to G12/13-mediated stress fiber formation, important for cell motility. Remarkably, cell growth stimulation and suppression of apoptosis by endogenous S1P were independent of GPCRs and inside-out signaling. Using fibroblasts from embryonic mice devoid of functional S1PRs, we also demonstrated that, in contrast to exogenous S1P, intracellular S1P formed by overexpression of sphingosine kinase type 1 promoted growth and survival independent of its GPCRs. Hence, exogenous and intracellularly generated S1Ps affect cell growth and survival by divergent pathways. Our results demonstrate a receptor-independent intracellular function of S1P, reminiscent of its action in yeast cells that lack S1PRs.     

alpha-Melanocyte-stimulating hormone inhibits lipopolysaccharide-induced tumor necrosis factor-alpha production in leukocytes by modulating protein kinase A,p38 kinase,and nuclear factor kappa B signaling pathways

The neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) inhibits inflammation by down-regulating the expression of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha) in leukocytes via stimulation of alpha-MSH cell surface receptors. However, the signaling mechanism of alpha-MSH action has not yet been clearly elucidated. Here, we have investigated signaling pathways by which alpha-MSH inhibits lipopolysaccharide (LPS)-induced TNF-alpha production in leukocytes such as THP-1 cells. We focused on the possible roles of protein kinase A (PKA), p38 kinase, and nuclear factor kappa B (NF kappa B) signaling. In THP-1 cells, LPS is known to activate p38 kinase, which in turn activates NF kappa B to induce TNF-alpha production. We found that pretreatment of cells with alpha-MSH blocked LPS-induced p38 kinase and NF kappa B activation as well as TNF-alpha production. This response was proportional to alpha-MSH receptor expression levels, and addition of an alpha-MSH receptor antagonist abolished the inhibitory effects. In addition, alpha-MSH treatment activated PKA, and PKA inhibition abrogated the inhibitory effects of alpha-MSH on p38 kinase activation, NF kappa B activation, and TNF-alpha production. Taken together, our results indicate that stimulation of PKA by alpha-MSH causes inhibition of LPS-induced activation of p38 kinase and NF kappa B to block TNF-alpha production.     

SEK1-dependent JNK1 activation prolongs cell survival during G-Rh2-induced apoptosis

We provide here evidence that c-Jun N-terminal protein kinase 1 (JNK1) activity is differentially up-regulated during apoptosis of SK-HEP-1 cells after treatment with ginsenoside Rh2 (G-Rh2). The G-Rh2-mediated JNK1 activation that occurred for the first 10-30min was associated with SEK1 activity, but thereafter, the sustained activation was associated not with SEK1 activity, but with proteolytic cleavage of JNK1-associated p21(WAF1/CIP1). Supporting this is that the expression of the dominant negative SEK1 mutant effectively blocked the early JNK1 activation phase but did not alter the sustained activation phase or apoptosis. Furthermore, expression of p21D112N, an uncleavable mutant of p21(WAF1/CIP1), suppressed the later JNK1 activation. Moreover, the stable overexpression of ectopic JNK1 suppressed apoptosis while expression of the dominant negative JNK1 mutant promoted it. We propose that the early SEK1-associated JNK1 activation phase acts to prolong cell survival in response to apoptosis-inducing agents, thereby serving as an intervening checkpoint prior to the commitment to apoptosis.     

Role of apoptosis-inducing factor in myocardial cell death by ischemia-reperfusion

Although apoptosis contributes to myocardial cell death in the ischemia-reperfused heart, the molecular basis of apoptosis is poorly understood. Apoptosis-inducing factor (AIF) has been characterized as a caspase-independent death effector. Upon the induction of apoptosis, mitochondrial AIF is released to the cytoplasm and then enters the nucleus, in which it induces chromatin condensation and 50 kbp DNA fragmentation. In the present study, we examined the role of AIF in ischemia-reperfusion injury in isolated rat hearts. AIF was detected in the cytosolic and nuclear fractions of hearts subjected to ischemia-reperfusion, whereas it was detected only in the mitochondria of control hearts. Moreover, AIF release increased in a reperfusion time-dependent manner. Pulse field gel electrophoresis revealed that 50 kbp DNA fragments were produced by ischemia/reperfusion. In contrast, cytochrome c release and the activation of caspase-3 did not occur to a significant extent. Moreover, ischemic preconditioning attenuated the AIF release and the 50 kbp DNA fragmentation. These results suggest that AIF-dependent apoptosis is likely to attribute to myocardial cell death in the ischemia-reperfused heart and that it is related with the protective effect of ischemic preconditioning.     

南极地区苔藓剖面中地球化学元素的营养运移特征

对采自南极的苔藓剖面上各层苔藓的地球化学元素含量进行分析,得到以下的初步结论：地球化学元素在苔藓剖面上的分布具有很强的继承性;不同地球化学元素在苔藓剖面上的分布特征不同,这与元素在苔藓中的营养特征有关,研究发现元素Ca在苔藓体内,异常活跃,它极易被累积在新鲜苔藓体内,Zn也是苔藓易吸收的元素;地球化学元素在老新苔藓中的转移能力不同;底层苔藓的元素转移能力很低,中层苔藓中元素维持在基本平衡的状态,上层苔藓中元素的转移系数较大。     

舞草种子的蚂蚁传播

舞草(Codariocalyx motorius)由于其小叶具有自身"摆动"的功能,从而具有较高的观赏价值.在长期的演化过程中,舞草与蚂蚁形成了互惠共生的关系舞草种子生成了附生其上的能吸引蚂蚁的油质体,蚂蚁在搬运取食中,使舞草种子得以传播.舞草种子最重要的传播者是圆叶铺道蚁(Tetramorium cyclolobium Xu et Zheng)和布立毛蚁(Paratrechina bourbonica Forel).另外长足光结蚁(Anoplolepis gracilipes Smith)和两种大头蚁(Pheidole sp.1和sp.2)也搬运其种子.野外试验表明,圆叶铺道蚁日搬运活动与气温呈显著正相关,即y(搬运种子数)=-9.5038+0%5608X(气温)(r=0.7196**,n=33,P＜0.01),中午搬运效率达到高峰.布立毛蚁日搬运活动在上、下午各有一个高峰,上午的高峰出现时间不稳定,下午的高峰出现在1 600～1800.舞草种子上附生的油质体是吸引蚂蚁并产生搬运行为的主要物质.化学分析表明,油质体富含蚂蚁生长发育所必需的10种氨基酸和多种无机元素.样地采用陷阱诱捕蚂蚁的调查显示,5种搬运者中,圆叶铺道蚁数量最大,分别占蚂蚁总量的8.26%和搬运蚂蚁总量的48%.这说明圆叶铺道蚁在舞草种子的搬运中起着主要作用.     

试论生态分类系统在我国天然林保护与经营中的应用

我国林业的发展正面临前所未有的机遇和挑战,现有资料表明,一方面,我国林业的宏观政策以及森林的采伐更新过程缺乏基本生态学原理的支持;另一方面,仅研究生态学理论还不够,还要研究生态学理论转化为生产力的工具,生产态分类系统是确定、描述和纵制生态系统类型图的方法。应用这种多层次系统的目的是用图的形式是把森景观的生物和环境特征抽象化,综合化、标准化和整体化,以实现生态系统管理的目标。通过纵绘制各种景观特征、林业人员可以根据土地承载力及适应性 确定森林的经营方向和经营措施,生态分类系统在吉林省东部针阔混交林区试验应用。     

浸提条件对小麦秸秆中化感物质检测结果的影响

通过对比不同浸提条件下小麦秸秆中化感物质的检测结果,发现浸提温度和时间对化感物质的最终结果有很大的影响,在室温条件下,化感物质的量随着浸提时间的延长而增长,但在50℃时,随着浸提时间的延长,化感物质的量反而降低。化感物质最大量在50℃,24h浸提条件下得到。在高温高压条件下提取到的化感物质的量多于多数条件下得到的量（除少于50℃,24h浸提条件下得到的量）。试验结果表明随着漫提温度升高,植物材料中的化感物质在水中的溶解速度加快,但是性质不稳定,容易分解变性。     

南极地区苔藓地衣植物的地球化学元素营养富集特征

研究南极苔藓地衣中地球化学元素的营养富集特征,发现K,Ca为苔藓地衣中最活跃元素,主要以主动吸收的方式累积于苔藓地衣植物中,P极易富集在地衣的藻层,参与藻类的有机合成过程,苔藓容易富集环境中的S,Al,Si以被动吸收的方式累积于地衣中,同时Fe,Mg以被动吸收的方式累积于苔藓体内,根据元素的含量和营养作用,研究认为K,Ca苔地衣的大量无机营养元素,S,P为苔藓地衣的中等营养元素,Al,Si为苔藓地衣的环境累积元素。     

Isolation of novel human fetal brain cDNAs mapped to human chromosome bands, 1q25 and 8q24.1

We isolated chromosome band-specific human fetal brain cDNAs by the microdissection mediated cDNA capture method, and localized these cDNA using in situ hybridization histochemistry with developing rat brain sections. Uni-Amp cDNAs were prepared from an 18-week old human fetal brain, and hybridized to human metaphase chromosomes. Eight Uni-Amp cDNAs, hybridized to chromosome band 1q25 or 8q24.1, were recovered by microdissection and PCR amplification with Uni-Amp primers. Among these cDNAs, two novel genes (FB113 of 8q24.1 and FB134 of 1q25) showed a temporospatially interesting expression pattern in the developing rat brains. The expression of FB113 was under dynamic regulation in the developing granule cells of cerebellum and dentate gyrus. FB134 showed a nervous tissue specific expression pattern and an exclusively prominent expression in the developing presubiculum and parasubiculum. By the fluorescence in situ hybridization using human genomic DNAs, FB113 and FB134 were mapped back to the human chromosome bands 8q24.1 and 1q25, respectively. These results indicate that combined application of the microdissection mediated cDNA capture method and in situ hybridization histochemistry can be used for the isolation of chromosomal band-specific genes related to brain development or human genetic diseases.