富营养化水体中N、P浓度对浮游植物生长繁殖速率和生物量的影响

在浮游植物生长繁殖的高峰期（7—10月份）对3个富营养化水体的总氮、总磷和浮游植物生物量进行调查,统计分析了生物量与氮和磷浓度的关系。利用3种水样和梯度稀释的东湖水样培养玫瑰拟衣藻（Chloromonas rosae）,研究了氮、磷浓度对生长繁殖速率的影响。结果表明磷是生长繁殖速率的限制因子,求出了生长繁殖速率与磷浓度的对数回归方程y=0．08061nx＋0．4658,当磷浓度小于0．05mg／L时,生长繁殖速率随着磷浓度的升高而直线上升,当磷浓度进一步升高,生长繁殖速率仍然随之增加,但增加的幅度越来越小,当磷浓度达到0．2mg／L时,生长繁殖速率基本不再随着磷浓度的增加而升高。计算出生长速率为零时磷的浓度是0．003mg／L,接近贫营养化湖泊磷浓度的下限,计算结果与坂本的调查统计结果相吻合,说明回归方程具有代表性。在凋查的3个富营养化水体中,浮游植物中的氮占全部氮元素的53％,磷占全部磷元素的85％,是氮、磷存在的主要形式,所以,评价水体的营养程度,必须同时考虑水中溶解的氮、磷和生物体内的氮、磷。统计分析表明,3个富营养化水体中浮游植物的生物量由氮（溶解氮＋胞内氮）和磷（溶解磷＋胞内磷）的浓度共同决定,生物量与氮浓度的直线回归方程y=10．687x-7．8304,生物量与磷浓度的直线回归方程y=122．11x-12．069。实验结果为根据氮、磷浓度以Redfield值判断浮游植物限制性营养元素的相对性和绝对性提供了例证。对3个富营养化水体的比较表明,防止水体富营养的唯一办法是维持水体氮、磷等主要营养元素收支平衡,治理富营养化的根本办法是从水体中移走过量的氮、磷等主要营养元素。     

Role of Rbp1 in the acquired chill-light tolerance of cyanobacteria

Synechocystis sp. strain PCC 6803 cultured at 30°C losses viability quickly under chill (5°C)-light stress but becomes highly tolerant to the stress after conditioning at 15°C (Y. Yang, C. Yin, W. Li, and X. Xu, J. Bacteriol. 190:1554-1560, 2008). Hypothetically, certain factors induced during preconditioning are involved in acquisition of chill-light tolerance. In this study, Rbp1 (RNA-binding protein 1) rather than Rbp2 was found to be accumulated during preconditioning, and the accumulation of Rbp1 was correlated with the increase of chill-light tolerance. Inactivation of its encoding gene rbp1 led to a great reduction in the acquired chill-light tolerance, while ectopic expression of rbp1 enabled the cyanobacterium to survive the chill-light stress without preconditioning. Microarray analyses suggested that the Rbp1-dependent chill-light tolerance may not be based on its influence on mRNA abundance of certain genes. Similarly to that in Synechocystis, the Rbp1 homologue(s) can be accumulated in Microcystis cells collected from a subtropic lake in low-temperature seasons. Rbp1 is the first factor shown to be both accumulated early during preconditioning and directly involved in development of chill-light tolerance in Synechocystis. Its accumulation may greatly enhance the overwintering capability in certain groups of cyanobacteria.     

Combination of rapamycin and IL-2 do not affect antigen presentation ability of rat B cell and could promote Tregs proliferation and inhibitory activity

Rapamycin (RPM), a powerful agent used clinically in transplant recipients, induces CD4⁺CD25⁺ regulatory T cells (Tregs) which play an important role in induction of immune tolerance. However, long-term use of RPM has negative side effects. In this report, we found that combination with the low dose RPM and high dose IL-2 did not affect antigen presentation of rat B cells to Tregs, and could efficiently promote Tregs proliferation and enhance their inhibitory activities in vitro. In addition, the combination of low dose RPM and high dose IL-2 enhanced mRNA expression of Foxp3, TGF-β1 and Pim-2 in Tregs but not in CD4⁺CD25⁻ T effector cells (Teffs). The Tregs inhibitory activity is positively associated with mRNA expressions of TGF-β1 and Pim-2 while unrelated to the Foxp3 mRNA expression. Our present study offers one approach to expand functional Tregs in vitro, which maybe used for clinical immune tolerance induction.     

Hydrogen sulfide protects against chemical hypoxia-induced cytotoxicity and inflammation in HaCaT cells through inhibition of ROS/NF-κB/COX-2 pathway

Hydrogen sulfide (H(2)S) has been shown to protect against oxidative stress injury and inflammation in various hypoxia-induced insult models. However, it remains unknown whether H(2)S protects human skin keratinocytes (HaCaT cells) against chemical hypoxia-induced damage. In the current study, HaCaT cells were treated with cobalt chloride (CoCl(2)), a well known hypoxia mimetic agent, to establish a chemical hypoxia-induced cell injury model. Our findings showed that pretreatment of HaCaT cells with NaHS (a donor of H(2)S) for 30 min before exposure to CoCl(2) for 24 h significantly attenuated CoCl(2)-induced injuries and inflammatory responses, evidenced by increases in cell viability and GSH level and decreases in ROS generation and secretions of IL-1β, IL-6 and IL-8. In addition, pretreatment with NaHS markedly reduced CoCl(2)-induced COX-2 overexpression and PGE(2) secretion as well as intranuclear NF-κB p65 subunit accumulation (the central step of NF-κB activation). Similar to the protective effect of H(2)S, both NS-398 (a selective COX-2 inhibitor) and PDTC (a selective NF-κB inhibitor) depressed not only CoCl(2)-induced cytotoxicity, but also the secretions of IL-1β, IL-6 and IL-8. Importantly, PDTC obviously attenuated overexpression of COX-2 induced by CoCl(2). Notably, NAC, a ROS scavenger, conferred a similar protective effect of H(2)S against CoCl(2)-induced insults and inflammatory responses. Taken together, the findings of the present study have demonstrated for the first time that H(2)S protects HaCaT cells against CoCl(2)-induced injuries and inflammatory responses through inhibition of ROS-activated NF-κB/COX-2 pathway.     

Asparaginyl endopeptidase protects against podocyte injury in diabetic nephropathy through cleaving cofilin-1

Podocyte injury and loss are critical events in diabetic nephropathy (DN); however, the underlying molecular mechanisms remain unclear. Here, we demonstrate that asparaginyl endopeptidase (AEP) protects against podocyte injury through modulating the dynamics of the cytoskeleton. AEP was highly upregulated in diabetic glomeruli and hyperglycemic stimuli treated-podocytes; however, AEP gene knockout and its compound inhibitor treatment accelerated DN in streptozotocin-induced diabetic mice, whereas specific induction of AEP in glomerular cells attenuated podocyte injury and renal function deterioration. In vitro, elevated AEP was involved in actin cytoskeleton maintenance and anti-apoptosis effects. Mechanistically, we found that AEP directly cleaved the actin-binding protein cofilin-1 after the asparagine 138 (N138) site. The protein levels of endogenous cofilin-1 1-138 fragments were upregulated in diabetic podocytes, consistent with the changes in AEP levels. Importantly, we found that cofilin-1 1-138 fragments were remarkably unphosphorylated than full-length cofilin-1, indicating the enhanced cytoskeleton maintenance activity of cofilin-1 1-138. Then we validated cofilin-1 1-138 could rescue podocytes from cytoskeleton disarrangement and injury in diabetic conditions. Taken together, our data suggest a protective role of elevated AEP in podocyte injury during DN progression through cleaving cofilin-1 to maintain podocyte cytoskeleton dynamics and defend damage.Subject terms: Cell death, Kidney diseases