CCN4 Regulates Vascular Smooth Muscle Cell Migration and Proliferation

Hao Liu,Zhengjun Liu,Wenpeng Dong,Zhiqi Lin,Jingbo Lu,Heng Wan,Zhongxin Zhou 한국분자세포생물학회 2013 Molecules and cells Vol.36 No.2

The migration and proliferation of vascular smooth muscle cells (VSMCs) are essential elements during the development of atherosclerosis and restenosis. An increasing number of studies have reported that extracellular matrix (ECM) proteins, including the CCN protein family, play a significant role in VSMC migration and proliferation. CCN4 is a member of the CCN protein family, which controls cell development and survival in multiple systems of the body. Here, we sought to determine whether CCN4 is involved in VSMC migration and proliferation. We examined the effect of CCN4 using rat cultured VSMCs. In cultured VSMCs, CCN4 stimulated the adhesion and migration of VSMCs in a dose-dependent manner, and this effect was blocked by an antibody for integrin 51. CCN4 expression was en-hanced by the pro-inflammatory cytokine tumor necrosis factor  (TNF-). Furthermore, knockdown of CCN4 by siRNA significantly inhibited the VSMC proliferation. CCN4 also could up-regulate the expression level of marker proteins of the VSMCs phenotype. Taken together, these results suggest that CCN4 is involved in the migration and proliferation of VSMCs. Inhibition of CCN4 may provide a promising strategy for the prevention of restenosis after vascular interventions.

Error-constrained Coordinated Tracking Control for High-order Multiagent Systems Based on Barrier Lyapunov Function

Yunbiao Jiang,Zhongxin Liu,Zengqiang Chen,Feng Duan 제어·로봇·시스템학회 2022 International Journal of Control, Automation, and Vol.20 No.4

In this paper, the coordinated tracking problem of high-order multiagent systems with preset error constraints is studied. Based on the barrier Lyapunov function method, two novel distributed error-constrained consensus controllers are proposed: time-invariant symmetric error-constrained controller and time-varying asymmetric error-constrained controller. The first controller can meet the requirement of a fixed preset error bound for the system, and the system errors converge with the exponential rate. Then, the second controller is designed based on an error-constrained function and error transformation, which can not only meet the time-varying error constraint but also guarantee the lower bound of the convergence rate of the consensus error. That is, the transient performance of the system is guaranteed. Then, the effectiveness of the two controllers is verified and compared by a simulation example. Furthermore, a full-order error-constrained controller is designed by combining the above two methods, and its effectiveness is verified by the coordinated depth tracking simulation of multiple underwater vehicles.

Inhibiting Cytochrome C Oxidase Leads to Alleviated Ischemia Reperfusion Injury

Zhaoyun Yang,Zhongxin Duan,Tian Yu,Junmei Xu,Lei Liu 대한심장학회 2017 Korean Circulation Journal Vol.47 No.2

Background and Objectives: The overall purpose of this study was to investigate the role of cytochrome C oxidase (CcO) in preventing ischemia reperfusion-induced cardiac injury through gaseous signaling molecule pathways. Materials and Methods: We used CcO inhibitor, potassium cyanide (KCN) to mimic the pre-treatment of gaseous signaling molecules in a global ischemia/reperfusion (IR) injury model in rats. Intracellular reactive oxygen species (ROS) was determined by measuring mitochondrial H2O2 and mitochondrial complex activity. Results: KCN pre-treatment led to decreased infarction area after IR injury and improved cardiac function. KCN pre-treated group challenged with IR injury was associated with reduced ROS production through inhibition of activity and not downregulation of CcO expression. In addition, KCN pre-treatment was associated with enhanced expression and activity of mitochondrial antioxidase, suggesting the role of CcO in regulating IR injury through oxidative stress. Conclusion: KCN pre-treatment reduced the severity of IR injury. The potential mechanism could be increased endogenous anti-oxidase activity and consequently, the enhanced clearance of ROS.

Cisplatin-induced PANDAR-Chemo-EVs contribute to a more aggressive and chemoresistant ovarian cancer phenotype through the SRSF9-SIRT4/ SIRT6 axis

Hao Wang,Yinuo Liu,Yanan Wang,Xiumin Shang,Zhongxin Yan,Shengli Li,Wei Bao 대한부인종양학회 2024 Journal of Gynecologic Oncology Vol.35 No.2

Objective: We previously elucidated that long non-coding RNA Promoter of CDKN1A AntisenseDNA damage Activated RNA (PANDAR) as a p53-dependent oncogene to promote cisplatinresistance in ovarian cancer (OC). Intriguingly, high level of p53-independent PANDAR wasfound in cisplatin-resistant patients with p53 mutation. Here, our study probed the new rolesand the underlying mechanisms of PANDAR in p53-mutant OC cisplatin-resistance. Methods: A2780 and A2780-DDP cells were ser ved as OC cisplatin-sensitive and cisplatin-resistant cells. HO-8910PM cells were subjected to construct chemotherapy-inducedextracellular vesicles (Chemo-EVs). Transmission electron microscopy (TEM) and nanoparticletracking analysis were employed to evaluate Chemo-EVs. Cell viability was assessed using cellcounting kit-8 and colony formation assays. Cell apoptosis was assessed using Annexin V andpropidium iodide staining. The relationships between PANDAR, serine and arginine-rich pre-mRNA splicing factor 9 (SRSF9) were verified by RNA immunoprecipitation and fluorescencein situ hybridization. Tumor xenograft experiment was employed to evaluate the effects ofPANDAR-Chemo-EVs on OC cisplatin-resistance in vivo. Immunofluorescent staining andimmunohistochemistr y were performed in tumor tissue. Results: PANDAR level increased in OC patients with p53-mutation. PANDAR efflux enactedvia exosomes under cisplatin conditions. Additionally, exosomes from OC cell lines carriedPANDAR, which significantly increased cell sur vival and chemoresistance in vitro and tumorprogression and metastasis in vivo. During cisplatin-induced stress, SRSF9 was recruited tonuclear bodies by increased PANDAR and muted apoptosis in response to cisplatin. Besides,SRSF9 significantly increased the ratio of SIRT4/SIRT6 mRNA in OC. Conclusion: Cisplatin-induced exosomes transfer PANDAR and lead to a rapid adaptation ofOC cell sur vival through accumulating SRSF9 following cisplatin stress exposure.

Underwater superoleophobic copper mesh coated with block nano protrusion hierarchical structure for efficient oil/water separation

Xinyu Qi,Zhuwei Gao,Chengxin Li,Shihao Wang,Xin Zou,Lan He,Zhongxin Liu 한국공업화학회 2023 Journal of Industrial and Engineering Chemistry Vol.119 No.-

Compared with monolayer nanosheet membranes, multilayer nanosheet membranes have low energyconsumption and can be mass-produced for industrial applications. Herein, a multi-layer nanostructuredmembrane, nickel-doped brochantite/Cu(OH)2 nano protrusion structure coated copper meshes(NBCPCMs), were successfully prepared. Firstly, the surface of the copper mesh was etched by chemicaloxidation to form a disordered copper hydroxide nanosheet layer. Secondly, the etched copper mesh surfacewas coated with nickel-controlled brochantite block-like protrusions by hydrothermal synthesismethod, and nickel-doped brochantite/Cu(OH)2 nanosheets were generated by high pressure. The resultsshowed that NBCPCM-4 had excellent hydrophilic/underwater superoleophobicity, the oil–water separationefficiency of immiscible cyclohexane/water mixture was the highest, about 98.54%, and still had avery high flux (>60 (kL/(hm2))) after multiple cycles of separation. In addition to ultra-high separationefficiency, NBCPCM-4 also had super durability. The copper mesh maintained good underwater superoleophobicityin different aqueous solutions. Therefore, NBCPCM-4 is a potential high-efficiency and sustainableoil–water separation membrane material. It is expected that the developed technology is usefulfor sea transportation and marine environment management, along with other industries.