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.

Networks of MicroRNAs and Genes in Retinoblastomas

Li, Jie,Xu, Zhi-Wen,Wang, Kun-Hao,Wang, Ning,Li, De-Qiang,Wang, Shang Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.11

Through years of effort, researchers have made notable progress in gene and microRNA fields about retinoblastoma morbidity. However, experimentally validated data for genes, microRNAs (miRNAs) and transcription factors (TFs) can only be found in a scattered form, which makes it difficult to conclude the relationship between genes and retinoblastoma systematically. In this study, we regarded genes, miRNAs and TFs as elements in the regulatory network and focused on the relationship between pairs of examples. In this way, we paid attention to all the elements macroscopically, instead of only researching one or several. To show regulatory relationships over genes, miRNAs and TFs clearly, we constructed 3 regulatory networks hierarchically, including a differentially expressed network, a related network and a global network, for analysis of similarities and comparison of differences. After construction of the three networks, important pathways were highlighted. We constructed an upstream and downstream element table of differentially expressed genes and miRNAs, in which we found self-adaption relations and circle-regulation. Our study systematically assessed factors in the pathogenesis of retinoblastoma and provided theoretical foundations for gene therapy researchers. In future studies, especial attention should be paid to the highlighted genes and miRNAs.

Integrin-linked Kinase Functions as a Tumor Promoter in Bladder Transitional Cell Carcinoma

Wang, De-Lin,Lan, Jian-Hua,Chen, Liang,Huang, Biao,Li, Zeng,Zhao, Xiu-Min,Ma, Qiang,Sheng, Xia,Li, Wen-Bin,Tang, Wei-Xue Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.6

The aim of this study was to elucidate the role of the integrin-linked kinase (ILK) gene in development of human bladder transitional cell carcinoma (BTCC). Expression of ILK protein and ILK mRNA in 56 cases of human BTCC tissue and in 30 cases of adjacent normal bladder tissue was detected by immunohistochemistry S-P and reverse transcription polymerase chain reaction (RT-PCR), respectively. Four specific miRNA RNAi vectors targeting human ILK were synthesized and transfected into BIU-87 cells by liposome to obtain stable expression cell strains. The influence of ILK on proliferation of BTCC was detected by MTT, FCM on athymic mouse tumorigenesis. The positive rate of ILK protein in BTCC tissue (53.6%) was much higher than adjacent normal bladder tissue (10.0%) (p<0.05). Similarly, expression of ILK mRNA in BTCC tissue ($0.540{\pm}0.083$) was significantly higher than in adjacent normal bladder tissue ($0.492{\pm}0.070$) (p<0.05). MTT showed that the proliferation ability of miRNA-ILK transfected group was clearly decreased (p<0.05), the cell cycle being arrested in G0/G1-S, an tumorigenesis in vivo was also significantly reduced (p<0.05). ILK gene transcription and protein expression may be involved in the development of BTCC, so that ILK might be the new marker for early diagnosis and the new target for gene treatment.

Risk Factors for Anxiety in Major Depressive Disorder Patients

Li-Min Xin,Lin Chen,Zhen-Peng Ji,Suo-Yuan Zhang,Jun Wang,Yan-Hong Liu,Da-Fang Chen,Fu-De Yang,Gang Wang,Yi-Ru Fang,Zheng Lu,Hai-Chen Yang,Jian Hu,Zhi-Yu Chen,Yi Huang,Jing Sun,Xiao-Ping Wang,Hui-Chun 대한정신약물학회 2015 CLINICAL PSYCHOPHARMACOLOGY AND NEUROSCIENCE Vol.13 No.3

Objective: To analyze the sociodemographic and clinical factors related to anxiety in patients with major depressive disorder (MDD). Methods: This study involved a secondary analysis of data obtained from the Diagnostic Assessment Service for People with Bipolar Disorders in China (DASP), which was initiated by the Chinese Society of Psychiatry (CSP) and conducted from September 1, 2010 to February 28, 2011. Based on the presence or absence of anxiety-related characteristics, 1,178 MDD patients were classified as suffering from anxious depression (n=915) or non-anxious depression (n=263), respectively. Results: Compared with the non-anxious group, the anxious-depression group had an older age at onset (t=−4.39, p<0.001), were older (t=−4.69, p<0.001), reported more lifetime depressive episodes (z=−3.24, p=0.001), were more likely to experience seasonal depressive episodes (χ2=6.896, p=0.009) and depressive episodes following stressful life events (χ2=59.350, p <0.001), and were more likely to have a family history of psychiatric disorders (χ2=6.091, p=0.014). Their positive and total scores on the Mood Disorder Questionnaire (MDQ) and the 32-item Hypomania Checklist (HCL-32) (p<0.05) were also lower. The logistic regression analysis indicated that age (odds ratio [OR]=1.03, p<0.001), a lower total MDQ score (OR=0.94, p=0.011), depressive episodes following stressful life events (OR=3.04, p<0.001), and seasonal depressive episodes (OR=1.75, p=0.039) were significantly associated with anxious depression. Conclusion: These findings indicate that older age, fewer subclinical bipolar features, an increased number of depressive episodes following stressful life events, and seasonal depressive episodes may be risk factors for anxiety-related characteristics in patients with MDD.

Implantation of Bone Marrow Mesenchymal Stem Cells into Small Intestinal Submucosa Improves Bile Duct Injury in Rabbits

Li Ying,Wang Piao,Hu Xiao-dong,Zeng Jing-da,Fang Cheng,Gan Yu,Peng Fang-yi,Yang Xiao-li,Luo De,Li Bo,Su Song 한국조직공학과 재생의학회 2021 조직공학과 재생의학 Vol.18 No.5

BACKGROUND: Bile duct injury (BDI), which may occur during cholecystectomy procedures and living-donor liver transplantation, leads to life-altering complications and significantly increased mortality and morbidity. Tissue engineering, as an emerging method, has shown great potential to treat BDI. Here, we aimed to explore the application of small intestinal submucosa (SIS) matrix composites with bone marrow mesenchymal stem cells (BMSCs) to treat BDI in a rabbit model. METHODS: Rabbit-derived BMSCs were used as seed cells. Porcine SIS was used as the support material. Five centimetres of the common bile duct was dissected, and 1/3–1/2 of the anterior wall diameter was transversely incised to construct the rabbit BDI model. Then, SIS materials without/with BMSCs were inserted into the common bile duct of the BDI rabbits. After 1, 2, 4, and 8 weeks of implantation, the common bile duct was removed. Haematoxylin and eosin (HE) staining was used to assess pathological alterations in the common bile duct, while immunohistochemical staining and western blotting were used to detect expression of the epithelial cell markers CK19 and E-cadherin. Scanning electron microscopy was used to evaluate BMSC growth. RESULTS: Compared with BMSCs alone, SIS-attached BMSCs had increased growth. HE staining showed that the injured bile duct healed well and that the complex gradually degraded as the time from implantation increased. Immunohistochemical staining and western blotting showed that compared with the control group, the in vivo complex group had significantly elevated expression levels of CK19 and E-cadherin. CONCLUSION: BMSC implantation into SIS could improve BDI in rabbits, which might have clinical value for BDI treatment. BACKGROUND: Bile duct injury (BDI), which may occur during cholecystectomy procedures and living-donor liver transplantation, leads to life-altering complications and significantly increased mortality and morbidity. Tissue engineering, as an emerging method, has shown great potential to treat BDI. Here, we aimed to explore the application of small intestinal submucosa (SIS) matrix composites with bone marrow mesenchymal stem cells (BMSCs) to treat BDI in a rabbit model. METHODS: Rabbit-derived BMSCs were used as seed cells. Porcine SIS was used as the support material. Five centimetres of the common bile duct was dissected, and 1/3–1/2 of the anterior wall diameter was transversely incised to construct the rabbit BDI model. Then, SIS materials without/with BMSCs were inserted into the common bile duct of the BDI rabbits. After 1, 2, 4, and 8 weeks of implantation, the common bile duct was removed. Haematoxylin and eosin (HE) staining was used to assess pathological alterations in the common bile duct, while immunohistochemical staining and western blotting were used to detect expression of the epithelial cell markers CK19 and E-cadherin. Scanning electron microscopy was used to evaluate BMSC growth. RESULTS: Compared with BMSCs alone, SIS-attached BMSCs had increased growth. HE staining showed that the injured bile duct healed well and that the complex gradually degraded as the time from implantation increased. Immunohistochemical staining and western blotting showed that compared with the control group, the in vivo complex group had significantly elevated expression levels of CK19 and E-cadherin. CONCLUSION: BMSC implantation into SIS could improve BDI in rabbits, which might have clinical value for BDI treatment.

Fibulin2: a negative regulator of BMSC osteogenic differentiation in infected bone fracture healing

Li Shi-Dan,Xing Wei,Wang Shao-Chuan,Li You-Bin,Jiang Hao,Zheng Han-Xuan,Li Xiao-Ming,Yang Jing,Guo De-Bin,Xie Xiao-Yu,Jiang Ren-Qing,Fan Chao,Li Lei,Xu Xiang,Fei Jun 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-

Bone fracture remains a common occurrence, with a population-weighted incidence of approximately 3.21 per 1000. In addition, approximately 2% to 50% of patients with skeletal fractures will develop an infection, one of the causes of disordered bone healing. Dysfunction of bone marrow mesenchymal stem cells (BMSCs) plays a key role in disordered bone repair. However, the specific mechanisms underlying BMSC dysfunction caused by bone infection are largely unknown. In this study, we discovered that Fibulin2 expression was upregulated in infected bone tissues and that BMSCs were the source of infection-induced Fibulin2. Importantly, Fibulin2 knockout accelerated mineralized bone formation during skeletal development and inhibited inflammatory bone resorption. We demonstrated that Fibulin2 suppressed BMSC osteogenic differentiation by binding to Notch2 and inactivating the Notch2 signaling pathway. Moreover, Fibulin2 knockdown restored Notch2 pathway activation and promoted BMSC osteogenesis; these outcomes were abolished by DAPT, a Notch inhibitor. Furthermore, transplanted Fibulin2 knockdown BMSCs displayed better bone repair potential in vivo. Altogether, Fibulin2 is a negative regulator of BMSC osteogenic differentiation that inhibits osteogenesis by inactivating the Notch2 signaling pathway in infected bone.

ADAPTIVE SLIDING MODE CONTROL OF LATERAL STABILITY OF FOUR WHEEL HUB ELECTRIC VEHICLES

Shou-Tao Li,Hui Liu,Di Zhao,Qiu-Yuan Li,Yantao Tian,De-Jun Wang,Ding-Li Yu 한국자동차공학회 2020 International journal of automotive technology Vol.21 No.3

Some physical parameters of a hub motor-driven four-wheel electric vehicle will change when the vehicle turns or maneuvers and the parameter change is caused by the change of the driving conditions. An adaptive sliding mode control is proposed in this paper to maintain the vehicle’s stability by compensating for the change of these parameters. The control parameter being adapted is the converging rate of the system state towards the sliding mode. As the Lyapunov method is used, so both the vehicle stability and adaptive rate convergence are guaranteed. Moreover, the hierarchical control structure is adopted for this vehicle stability control system. The above adaptive sliding model control forms the upper-layer; while the lower-layer control is to distribute the upper torque to the four wheels in an optimal way, subject to several constraints. In addition, the best feasible reference of the yaw rate and the vehicle side slip angle are obtained and used in the control system. The developed method is simulated under the CarSim/MATLAB co-simulation environment to evaluate the system performance. The simulation results are compared with the non-adaptive existing sliding mode control, and show that the proposed method is superior under different conditions.

Study in the Mechanisms of Formation of Transfer Film under the Condition of Wear of Steel AISI1020 by Natural Rubber

DE-GUO WANG,SI-WEI ZHANG,REN-YANG HE,MING-YUAN LI 한국트라이볼로지학회 2002 한국트라이볼로지학회 학술대회 Vol.2002 No.10

The mechanisms of formation of transfer film under the condition of wear of Steel AISI1020 by natural rubber were investigated. The transfer film was observed and the formation mechanisms were clarified. The formation process of transfer film on the worn surface of the steel could be divided into two stages. Firstly, the adhesive layer emerged on the worn surface of the steel by adhesion of natural rubber, in which the macromolecular chains of natural rubber joined to the surface of the steel by Van der Waals' force. And then, the iron atom and metal oxide reacted with the macroradicals of natural rubber in the adhesive layer and produced Fe-polymer compound. As a result, the transfer film was formed on the worn surface of the steel. The transfer film was joined to the worn surface of the steel by the chemical bonds and electrostatic force.

Expression and Significance of Twist and E-cadherin in Ovarian Cancer Tissues

Wang, Wen-Shuang,Yu, Shou-Li,Yang, Xing-Sheng,Chang, Shu-De,Hou, Jian-Qing Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.2

Objective: To investigate the expression of Twist and E-cadherin in ovarian cancer tissues as well as the role of epithelial-mesenchymal transformation (EMT) in ovarian cancer metastasis. Method: The expressions of Twist and E-cadherin in 54 cases of ovarian cancer and paracancerous tissues were detected by Western blottin g and reverse transcriptase polymerase chain reaction. We used RNA interference to silence Twist expression in human ovarian cancer cell line, and detected E-cadherin expression using Western blotting. Results: There was an increase in the relative abundance of Twist proteins and a decrease in E-cadherin in ovarian cancer compared with normal ovary tissues (P < 0.05). The expression levels of Twist and E-cadherin mRNA were $1.49{\pm}0.53$ and $0.82{\pm}0.24$ in ovarian cancer, and $1.14{\pm}0.38$ and $1.08{\pm}0.19$ in paracancerous tissues, respectively. The difference between the indicators in ovarian cancer and in paracancerous tissues was statistically significant (P < 0.05). When the Twist expression was silenced in an ovarian cancer cell line, the expression of the E-cadherin protein increased (P<0.05). Conclusion: The expression of Twist is upregulated, whereas that of E-cadherin is downregulated in ovarian cancer. EMT, mediated by Twist, may be correlated with ovarian cancer metastasis.

Fucoidan inhibits LPS-induced acute lung injury in mice through regulating GSK-3β-Nrf2 signaling pathway

De-Zhang Zhu,Yan-Ting Wang,Yan-Li Zhuo,Kong-Juan Zhu,Xiang-Zhen Wang,Ai-Jie Liu 대한약학회 2020 Archives of Pharmacal Research Vol.43 No.6

The purpose of this study was to investigatethe protective eff ects of fucoidan on Lipopolysaccharide(LPS)-induced acute lung injury (ALI) in mice. The micewere divided into the control, LPS, and LPS + fucoidan(20, 40, or 80 mg/kg) groups. LPS was given by intrachealinstillation and fucoidan was given 1 h before LPS treatment. Myeloperoxidase (MPO) activity, malondialdehyde(MDA), superoxide dismutase (SOD), reactive oxygen species(ROS), glutathione (GSH) contents, and infl ammatorycytokine production were detected. The results showed thatLPS-induced TNF-α, IL-1β, and IL-6 production, lung wet/dry (W/D) ratio, ROS, MDA content, and MPO activity weresuppressed by fucoidan. The levels of SOD and GSH wereincreased by fucoidan. Meanwhile, LPS-induced nuclearfactor kappa-B (NF-κB) activation was dose-dependentlyattenuated by fucoidan. Furthermore, fucoidan increasedthe expression of nuclear factor erythroid-2 related factor2 (Nrf2), Glycogen synthase kinase3β (GSK-3β), and hemeoxygenase (HO-1). In vitro, the results demonstrated thatfucoidan or GSK-3β inhibitor signifi cantly inhibited LPSinducedTNF-α production in A549 cells. And the inhibitionof fucoidan on TNF-α production was blocked by Nrf2siRNA. This study showed fucoidan protected mice againstLPS-induced ALI through inhibiting inflammatory andoxidative responses via regulating GSK-3β-Nrf2 signalingpathway.