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Transcriptomic Features of Echinococcus granulosus Protoscolex during the Encystation Process
Junjie Fan,Hongye Wu,Kai Li,Xunuo Liu,Qingqing Tan,Wenqiao Cao,Bo Liang,Bin Ye 대한기생충학ㆍ열대의학회 2020 The Korean Journal of Parasitology Vol.58 No.3
Cystic echinococcosis (CE) is a zoonotic infection caused by Echinococcus granulosus larvae. It seriously af- fects the development of animal husbandry and endangers human health. Due to a poor understanding of the cystic fluid formation pathway, there is currently a lack of innovative methods for the prevention and treatment of CE. In this study, the protoscoleces (PSCs) in the encystation process were analyzed by high-throughput RNA sequencing. A total of 32,401 transcripts and 14,903 cDNAs revealed numbers of new genes and transcripts, stage-specific genes, and differ- ently expressed genes. Genes encoding proteins involved in signaling pathways, such as putative G-protein coupled re- ceptor, tyrosine kinases, and serine/threonine protein kinase, were predominantly up-regulated during the encystation process. Antioxidant enzymes included cytochrome c oxidase, thioredoxin glutathione, and glutathione peroxidase were a high expression level. Intriguingly, KEGG enrichment suggested that differentially up-regulated genes involved in the va- sopressin-regulated water reabsorption metabolic pathway may play important roles in the transport of proteins, carbo- hydrates, and other substances. These results provide valuable information on the mechanism of cystic fluid production during the encystation process, and provide a basis for further studies on the molecular mechanisms of growth and de- velopment of PSCs.
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STING Negatively Regulates Double-Stranded DNA-Activated JAK1-STAT1 Signaling via SHP-1/2 in B Cells
Dong, Guanjun,You, Ming,Ding, Liang,Fan, Hongye,Liu, Fei,Ren, Deshan,Hou, Yayi Korean Society for Molecular and Cellular Biology 2015 Molecules and cells Vol.38 No.5
Recognition of cytosolic DNA initiates a series of innate immune responses by inducing IFN-I production and subsequent triggering JAK1-STAT1 signaling which plays critical roles in the pathogenesis of infection, inflammation and autoimmune diseases through promoting B cell activation and antibody responses. The stimulator of interferon genes protein (STING) has been demonstrated to be a critical hub of type I IFN induction in cytosolic DNA-sensing pathways. However, it still remains unknown whether cytosolic DNA can directly activate the JAK1-STAT1 signaling or not. And the role of STING is also unclear in this response. In the present study, we found that dsDNA directly triggered the JAK1-STAT1 signaling by inducing phosphorylation of the Lyn kinase. Moreover, this response is not dependent on type I IFN receptors. Interestingly, STING could inhibit dsDNA-triggered activation of JAK1-STAT1 signaling by inducing SHP-1 and SHP-2 phosphorylation. In addition, compared with normal B cells, the expression of STING was significantly lower and the phosphorylation level of JAK1 was significantly higher in B cells from MRL/lpr lupus-prone mice, highlighting the close association between STING low-expression and JAK1-STAT1 signaling activation in B cells in autoimmune diseases. Our data provide a molecular insight into the novel role of STING in dsDNA-mediated inflammatory disorders.
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Chunyun Hou,Jiangwei Yu,Jin-Rui Ding,Weiqiang Fan,Hongye Bai,Dongbo Xu,Wei-dong Shi 한국공업화학회 2021 Journal of Industrial and Engineering Chemistry Vol.104 No.-
The unsatisfactory solar light absorption of WO3 and poor charge separation of BiVO4 are main limits fortheir use in photoelectrochemical (PEC) water oxidation. Coupling WO3 with BiVO4 has been consideredas a feasible way to improve PEC performance by taking complementary advantages of them. In thiswork, we obtained nanoflake-structured WO3 by hydrothermal growth with post-annealing. The effectof process variables on morphology and resultant performance were investigated. Electrodepositiongrowth was utilized to deposit BiVO4 onto WO3 forming WO3/BiVO4 heterojunction thin films. PorousBiVO4 with wormlike morphology was tightly coupled and well-distributed onto WO3 nanoflakes. Theoptimized best-performing WO3/BiVO4 photoanode exhibits higher photocurrent density than that summationof bare WO3 and BiVO4 over entire range of applied potential. This enhancement is mainly attributedto the effective charge separation at WO3/BiVO4 interface, which is confirmed throughelectrochemical impedance spectra (EIS) measurements, respectively. Our work provides a referableapproach for the growth of WO3/BiVO4 heterojunction photoanode with enhanced PEC performance.
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STING Negatively Regulates Double-Stranded DNA-Activated JAK1-STAT1 Signaling via SHP-1/2 in B Cells
Yayi Hou,Guanjun Dong,Ming You,Liang Ding,Hongye Fan,Fei Liu,Deshan Ren 한국분자세포생물학회 2015 Molecules and cells Vol.38 No.5
Recognition of cytosolic DNA initiates a series of innate immune responses by inducing IFN-I production and subsequent triggering JAK1-STAT1 signaling which plays critical roles in the pathogenesis of infection, inflammation and autoimmune diseases through promoting B cell activation and antibody responses. The stimulator of interferon genes protein (STING) has been demonstrated to be a critical hub of type I IFN induction in cytosolic DNA-sensing pathways. However, it still remains unknown whether cytosolic DNA can directly activate the JAK1-STAT1 signaling or not. And the role of STING is also unclear in this response. In the present study, we found that dsDNA directly triggered the JAK1-STAT1 signaling by inducing phosphorylation of the Lyn kinase. Moreover, this response is not dependent on type I IFN receptors. Interestingly, STING could inhibit dsDNA-triggered activation of JAK1-STAT1 signaling by inducing SHP-1 and SHP-2 phosphorylation. In addition, compared with normal B cells, the expression of STING was significantly lower and the phosphorylation level of JAK1 was significantly higher in B cells from MRL/lpr lupus-prone mice, highlighting the close association between STING low-expression and JAK1-STAT1 signaling activation in B cells in autoimmune diseases. Our data provide a molecular insight into the novel role of STING in dsDNA-mediated inflammatory disorders.
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