Genetic Diversity and Structure of Cordyceps sinensis Populations from Extensive Geographical Regions in China as Revealed by Inter-Simple Sequence Repeat Markers

Hong-Hui Liang,Zhou Cheng,Xiao-Ling Yang,Shan Li,Zu-Quan Ding,Tong-Shui Zhou,Wen-Ju Zhang,Jia-Kuan Chen 한국미생물학회 2008 The journal of microbiology Vol.46 No.5

Cordyceps sinensis is one of the most valuable medicinal caterpillar fungi native to China. However, its productivity is extremely limited and the species is becoming endangered. The genetic diversity of eighteen C. sinensis populations across its major distributing regions in China was evaluated by inter-simple sequence repeat (ISSR) markers. A total of 141 markers were produced in 180 individuals from the 18 populations, of which 99.3% were polymorphic. The low average of Shannon (0.104) and Nei index (0.07) of the 18 populations indicates that there are little genetic variations within populations. For all 18 populations, estimates of total gene diversity (HT), gene diversity within populations (HS), coefficient of genetic differentiation (GST), and gene flow (Nm) were 0.170, 0.071, 0.583, and 0.357, respectively. This pattern suggests that the genetic diversity of C. sinensis is low and most of the ISSR variations are found among populations with little gene exchange. The 18 populations are divided into five groups based on the genetic distance and the grouping pattern matches with the geographic distribution along the latitudinal gradient. The five groups show obvious difference in the GST and Nm values. Therefore, the genetic diversification of C. sinensis populations may be determined by geographic isolation and the combined effects of life history characters and the interaction with host insect species. The information illustrated by this study is useful for selecting in situ conservation sites of C. sinensis.

Acupuncture reduces nicotine-induced norepinephrine release in the hypothalamus via the solitary NMDA receptor/NOS pathway

Liu, Hong Feng,Zhao, ZhengLin,Zhang, Jie,Wu, Yi Yan,Jiao, Yu,Wu, Tong,Kim, Sang Chan,Lee, Bong Hyo,Fan, Yu,Lee, Chul Won,Kim, Young Woo,Yang, Chae Ha,Zhu, Xiao Dong,Zhao, Rong Jie Elsevier 2019 Neuroscience Letters Vol.705 No.-

<P><B>Abstract</B></P> <P>Noradrenergic projections from the nucleus tractus solitarius (NTS) to the hypothalamic paraventricular nucleus (PVN) are involved in nicotine (Nic) dependence. Nic induces hypothalamic norepinephrine (NE) release through <I>N</I>-methyl-<SMALL>D</SMALL>-aspartate receptors (NMDARs) and nitric oxide in the NTS. However, acupuncture attenuates Nic withdrawal-induced anxiety. Therefore, this study investigated the effects of acupuncture on Nic-induced hypothalamic NE release. Rats received an intravenous infusion of Nic (90 μg/kg, over 60 s) and extracellular NE levels in the PVN were determined by in vivo microdialysis. Immediately after Nic administration, the rats were bilaterally treated with acupuncture at acupoint HT7 (Shen-Men) or PC6 (Nei-Guan), or a non-acupoint (tail) for 60 s. Acupuncture at HT7, but not at PC6 or the tail, significantly reduced Nic-induced NE release. However, this was abolished by a post-acupuncture infusion of either NMDA or sodium nitroprusside into the NTS. Additionally, acupuncture at HT7, but not the control points, prevented Nic-induced plasma corticosterone secretion and inhibited Nic-induced increases in the phosphorylation of neuronal nitric oxide synthase (nNOS) and endothelial NOS in the NTS. These findings suggest that acupuncture at HT7 reduces Nic-induced NE release in the PVN via inhibition of the solitary NMDAR/NOS pathway.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Acupuncture inhibited nicotine-induced hypothalamic norepinephrine release. </LI> <LI> Acupuncture diminished nicotine-induced plasma corticosterone secretion. </LI> <LI> Acupuncture reversed nicotine-induced phosphorylation of solitary nNOS and eNOS. </LI> <LI> NMDA abolished acupunctural effects on nicotine-induced norepinephrine release. </LI> <LI> NO abolished acupunctural effects on nicotine-induced norepinephrine release. </LI> </UL> </P>

Inhibitory effects of osteoprotegerin on osteoclast formation and function under serum-free conditions

Ying-Xiao Fu,Jian-Hong Gu,Yi-Ran Zhang,Xi-Shuai Tong,Hong-Yan Zhao,Yan Yuan,Xue-Zhong Liu,Jian-Chun Bian,Zong-Ping Liu 대한수의학회 2013 Journal of Veterinary Science Vol.14 No.4

The purpose of this study was to determine whether osteoprotegerin (OPG) could affect osteoclat differentiation and activation under serum-free conditions. Both duck embryo bone marrow cells and RAW264.7 cells were incubated with macrophage colony stimulatory factor (M-CSF) and receptor activator for nuclear factor κB ligand (RANKL) in serum-free medium to promote osteoclastogenesis. During cultivation, 0,10, 20, 50, and 100 ng/mL OPG were added to various groups of cells. Osteoclast differentiation and activation were monitored via tartrate-resistant acid phosphatase (TRAP) staining,filamentous-actin rings analysis, and a bone resorption assay. Furthermore, the expression osteoclast-related genes, such as TRAP and receptor activator for nuclear factor κB (RANK),that was influenced by OPG in RAW264.7 cells was examined using real-time polymerase chain reaction. In summary,findings from the present study suggested that M-CSF with RANKL can promote osteoclast differentiation and activation,and enhance the expression of TRAP and RANK mRNA in osteoclasts. In contrast, OPG inhibited these activities under serum-free conditions.

PREPARATION AND ANTI-CORROSION PERFORMANCE OF ZINC PHOSPHATE NANOCRYSTALS BY ULTRASONIC – HYDROTHERMAL SYNERGISTIC ROUTE

CHANG LIU,HONG-ZHEN XIE,QIN TONG,JIAN-DONG WANG,JIN-KU LIU,XIAO-HONG YANG 성균관대학교(자연과학캠퍼스) 성균나노과학기술원 2014 NANO Vol.9 No.6

The zinc phosphate nanocrystals were synthesized by the ultrasonic – hydrothermal synergisticroute. The ultrasonic – hydrothermal synergistic route can not only decrease the size of the zincphosphate material, but also improve the crystallinity of the product. The transmission electronmicroscopy (TEM) image showed that the needle-like zinc phosphate product was 200 – 300 nmin length and 70 – 80 nm in width. The anti-corrosion tests revealed that the salt atmosphere-resistant time about 1056 h was longer than 768 h common zinc phosphate materials in themarket. The mechanisms of ultrasonic – hydrothermal synergistic route and anti-corrosion werediscussed.

Elevated FBXL6 expression in hepatocytes activates VRK2-transketolase-ROS-mTOR-mediated immune evasion and liver cancer metastasis in mice

Zhang Jie,Lin Xiao-Tong,Yu Hong-Qiang,Fang Lei,Wu Di,Luo Yuan-Deng,Zhang Yu-Jun,Xie Chuan-Ming 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-

Metastatic hepatocellular carcinoma (HCC) is the most lethal malignancy and lacks effective treatment. FBXL6 is overexpressed in human hepatocellular carcinoma (HCC), but whether this change drives liver tumorigenesis and lung metastasis in vivo remains unknown. In this study, we aimed to identify FBXL6 (F-Box and Leucine Rich Repeat Protein 6) as a key driver of HCC metastasis and to provide a new paradigm for HCC therapy. We found that elevated FBXL6 expression in hepatocytes drove HCC lung metastasis and was a much stronger driver than Kras mutation (KrasG12D/+;Alb-Cre), p53 haploinsufficiency (p53+/-) or Tsc1 loss (Tsc1fl/fl;Alb-Cre). Mechanistically, VRK2 promoted Thr287 phosphorylation of TKT and then recruited FBXL6 to promote TKT ubiquitination and activation. Activated TKT further increased PD-L1 and VRK2 expression via the ROS-mTOR axis, leading to immune evasion and HCC metastasis. Targeting or knockdown of TKT significantly blocked FBXL6-driven immune evasion and HCC metastasis in vitro and in vivo. Notably, the level of active TKT (p-Thr287 TKT) was increased and was positively correlated with the FBXL6 and VRK2 expression levels in HCC patients. Our work provides novel mechanistic insights into FBXL6-driven HCC metastasis and suggests that targeting the TKT-ROS-mTOR-PD-L1/VRK2 axis is a new paradigm for treating patients with metastatic HCC with high FBXL6 expression.

Activated Protein C Protects Myocardium Via Activation of Anti-apoptotic Pathways of Survival in Ischemia-reperfused Rat Heart

Jia-Wang Ding,Xiao-Hong Tong,Jun Yang,Zhao-Qi Liu,Yan Zhang,Jian Yang,Song Li,Li Li 대한의학회 2010 Journal of Korean medical science Vol.25 No.11

Activated protein C (APC) is known to be beneficial on ischemia reperfusion injury in myocardium. However, the protection mechanism of APC is not fully understood. The purpose of this study was to investigate the effects and possible mechanisms of APC on myocardial ischemic damage. Artificially ventilated anaesthetized Sprague-Dawley rats were subjected to a 30 min of left anterior descending coronary artery occlusion followed by 2 hr of reperfusion. Rats were randomly divided into four groups; Sham, I/R, APC preconditioning and postconditioning group. Myocardial infarct size, apoptosis index, the phosphorylation of ERK1/2, Bcl-2, Bax and cytochrome c genes and proteins were assessed. In APC-administrated rat hearts, regardless of the timing of administration, infarct size was consistently reduced compared to ischemia/reperfusion (I/R) rats. APC improved the expression of ERK1/2 and anti-apoptotic protein Bcl-2 which were significantly reduced in the I/R rats. APC reduced the expression of pro-apoptotic genes, Bax and cytochrome c. These findings suggest that APC produces cardioprotective effect by preserving the expression of proteins and genes involved in anti-apoptotic pathways, regardless of the timing of administration.

Self-assembly and Mechanism of L-Alanine-based Dihydrazide Derivative as Excellent Gelator of Organic Solvents

Wang, Chuan-Sheng,Wang, Xiao-Hong,Li, Zhi-Yuan,Wei, Wei,Shi, Zhong-Liang,Sui, Zhi-Tong Korean Chemical Society 2011 Bulletin of the Korean Chemical Society Vol.32 No.4

A new organogelator, L-Alanine dihydrazide derivative can self-assemble in various organic solvents and turned them into thermally reversible physical supramolecular organogels at extremely low concentrations (< 2 wt %). The gel-sol phase transition temperatures ($T_{GS}$) were determined as a function of gelator concentration and the corresponding enthalpies (${\Delta}H_g$) were extracted. Scanning electron microscopy (SEM) measurements revealed that the interspaces of fiber-like network structures were diminished with the increasing of the LMOG concentration. FT-IR spectroscopy studies revealed that hydrogen-bonding and hydrophobic interaction were the driving forces for the formation of the gels. Based on the data of XRD and molecular modeling, the possible packing modes for the formation of organogelator aggregates were proposed.

Transcriptome analysis of rice leaves in response to Rhizoctonia solani infection and reveals a novel regulatory mechanism

De Peng Yuan,Xiao Feng Xu,Hong Woo-Jong,Si Ting Wang,Xin Tong Jia,Yang Liu,Shuang Li,Zhi Min Li,Qian Sun,Qiong Mei,Shuai Li,정기홍,Song Hong Wei,Yuan Hu Xuan 한국식물생명공학회 2020 Plant biotechnology reports Vol.14 No.5

Sheath blight disease (ShB) severely afects rice production; however, the details of defense against ShB remain unclear. To understand the rice defense mechanism against ShB, an RNA sequencing analysis was performed using Rhizoctonia solani inoculated rice leaves after 48 h of inoculation. Among them, 3417 genes were upregulated and 2532 were downregulated when compared with the control group (>twofold or<1/2). In addition, the diferentially expressed genes were classifed via Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and MapMan analyses. Fifty-nine GO terms and seven KEGG pathways were signifcantly enriched. A MapMan analysis demonstrated that the phytohormone and metabolic pathways were signifcantly altered. Interestingly, the expression levels of 359 transcription factors, including WRKY, MYB, and NAC family members, as well as 239 transporter genes, including ABC, MFS, and SWEET, were signifcantly changed in response to R. solani AG1-IA inoculation. Additionally, OsWRKY53 and OsAKT1 negatively regulate the defense response in rice against R. solani via gain of function study for OsWRKY53 and loss of function study for OsAKT1, respectively. Furthermore, several diferentially expressed genes contain R. solani-responsive cis acting regulatory elements in their promoter regions. Taken together, our analyses provide valuable information for the additional study of the defense mechanisms against ShB, and the candidate genes identifed in this study will be useful resource for future breeding to enhance resistance against ShB.

Elevated expression of WSB2 degrades p53 and activates the IGFBP3-AKT-mTOR-dependent pathway to drive hepatocellular carcinoma

Li Xun,Zhang Cheng-Cheng,Lin Xiao-Tong,Zhang Jie,Zhang Yu-Jun,Yu Hong-Qiang,Liu Ze-Yu,Gong Yi,Zhang Lei-Da,Xie Chuan-Ming 생화학분자생물학회 2024 Experimental and molecular medicine Vol.56 No.-

Dysregulation of wild-type p53 turnover is a key cause of hepatocellular carcinoma (HCC), yet its mechanism remains poorly understood. Here, we report that WD repeat and SOCS box containing protein 2 (WSB2), an E3 ubiquitin ligase, is an independent adverse prognostic factor in HCC patients. WSB2 drives HCC tumorigenesis and lung metastasis in vitro and in vivo. Mechanistically, WSB2 is a new p53 destabilizer that promotes K48-linked p53 polyubiquitination at the Lys291 and Lys292 sites in HCC cells, leading to p53 proteasomal degradation. Degradation of p53 causes IGFBP3-dependent AKT/mTOR signaling activation. Furthermore, WSB2 was found to bind to the p53 tetramerization domain via its SOCS box domain. Targeting mTOR with everolimus, an oral drug, significantly blocked WSB2-triggered HCC tumorigenesis and metastasis in vivo. In clinical samples, high expression of WSB2 was associated with low wild-type p53 expression and high p-mTOR expression. These findings demonstrate that WSB2 is overexpressed and degrades wild-type p53 and then activates the IGFBP3-AKT/mTOR axis, leading to HCC tumorigenesis and lung metastasis, which indicates that targeting mTOR could be a new therapeutic strategy for HCC patients with high WSB2 expression and wild-type p53.

Endothelial Aquaporin-1 (AQP1) Expression Is Regulated by Transcription Factor Mef2c

Jiang, Yong,Liu, He,Liu, Wen-jing,Tong, Hai-bin,Chen, Chang-jun,Lin, Fu-gui,Zhuo, Yan-hang,Qian, Xiao-zhen,Wang, Zeng-bin,Wang, Yu,Zhang, Peng,Jia, Hong-liang Korean Society for Molecular and Cellular Biology 2016 Molecules and cells Vol.39 No.4

Aquaporin 1 (AQP1) is expressed in most microvasculature endothelial cells and forms water channels that play major roles in a variety of physiologic processes. This study aimed to delineate the transcriptional regulation of AQP1 by Mef2c in endothelial cells. Mef2c cooperated with Sp1 to activate human AQP1 transcription by binding to its proximal promoter in human umbilical cord vein endothelial cells (HUVEC). Over-expression of Mef2c, Sp1, or Mef2c/Sp1 increased HUVEC migration and tube-forming ability, which can be abolished AQP1 knockdown. These data indicate that AQP1 is a direct target of Mef2c in regulating angiogenesis and vasculogenesis of endothelial cells.