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Search Results: 1 - 10 of 80528 matches for " Mingyao Liu "
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Ventilator-induced lung injury and mechanotransduction: why should we care?
Mingyao Liu
Critical Care , 2007, DOI: 10.1186/cc6131
Abstract: As a professor in a clinical department, I am privileged to work with many clinician-investigator trainees. Recently, a new clinical research fellow told me that he had been reading many papers in order to decide which research project he should take. The more he reads, the more confused he feels. Many literatures sound contradictory. How to determine their clinical relevance is a challenge. In fact, this challenge is not only to new fellows, but also to experienced researchers.In this issue of Critical Care, Dr Li and Dr Quinn and their colleagues published a research article [1] exploring the molecular mechanisms of ventilator-induced lung injury (VILI). I would like to use this interesting article as an example, to lead readers who are not experts in this field through a translational process.Mechanical force-induced signal transduction (mechano-transduction) is responsible for many physiological processes in lung development [2], in maintaining lung functions [3], and in pathological conditions related to lung diseases, such as asthma, chronic obstructive pulmonary disease (COPD), and acute respiratory distress syndrome (ARDS), especially related to VILI [4]. However, very much like the routes in a city, both "good boys" and "bad boys" drive on the same streets. Many signal transduction pathways are shared by both the injury and repair processes.Neutrophil recruitment and activation is an important mechanism for lung tissue injury, which is mediated by a group of small molecules, namely chemokines, especially a subgroup of C-X-C chemokines. Interleukin-8 (IL-8) is the best example, which has been shown to be up-regulated by mechanical forces in human lung cells [5]. Rodents do not have the IL-8 gene, but produce macrophage inflammatory protein-2 (MIP-2) and other C-X-C chemokines. Mechanical stretch induced MIP-2 in rat lung cells [6]. Increased MIP-2 in murine lung was observed after high volume ventilation by Dr Li and co-workers [7]. They further questioned t
Roles of XB130, a novel adaptor protein, in cancer
Atsushi Shiozaki, Mingyao Liu
Journal of Clinical Bioinformatics , 2011, DOI: 10.1186/2043-9113-1-10
Abstract: Adaptor proteins are molecules of modular structures without enzymatic activity, composed of multiple protein-protein and/or protein-lipid interacting domains, through which they link signaling components to form macromolecular complexes and propagate cellular signals [1,2]. Depending on the functional role of the interacting partner and the specific biological event that is triggered by these interactions, adaptor proteins can participate in the regulation of different signaling pathways. A good example of how adaptor proteins are involved in signal transduction is the activation of c-Src protein-tyrosine kinases by adaptor proteins via protein-protein interactions. Adaptor proteins are also important to mediate signals initiated via receptor-tyrosine kinases in responses to extracellular stimuli [3,4], and together with non-receptor protein-tyrosine kinases to orchestrate the signal transduction elicited by either ligand receptor interactions or by cellular structure reorganization [5]. Further, a number of adaptor proteins have been demonstrated to regulate tumorigenesis. For example, actin filament associated protein (AFAP) is required for actin stress fiber formation and cell adhesion, and is critical for tumorigenic growth in prostate cancer [6,7]. Tyrosine kinase substrate 5 is a scaffolding adaptor protein with five Src homology (SH) 3 domains, co-localizes to podosomes and regulates migration and invasion of different human cancer cells [8,9]. These findings support a broader investigation of adaptor proteins on tumorigenesis and their potentiality as diagnostic biomarkers and therapeutic targets of cancer.During our studies aimed at the characterization of the AFAP [10-12], we cloned a novel 130 kDa protein, referred to as XB130 [13]. Our studies have indeed indicated that XB130 plays, as an adaptor, important roles in the regulation of signal transduction, cell proliferation, survival, motility and invasion [13-16]. In this review, we focus on studies rel
Hydroxyl radical induced structural changes of collagen
Helan Xiao,Guoping Cai,Mingyao Liu
Spectroscopy: An International Journal , 2007, DOI: 10.1155/2007/496174
Abstract: Extracellular matrix (ECM) plays an important role in cell differentiation, growth, migration and apoptosis. Collagen is the most abundant protein family in vivo, but its function has still not been clearly defined yet. Reactive oxygen species (ROS) have a central role in oxidative cell stress. Electron spin resonance (ESR) spectroscopy indicates that type I collagen could uniquely scavenge hydroxyl radicals in dose- and time-dependent manner; whereas BSA and gelatin (a denatured collagen) have no such an effect. However, the mechanism by which type I collagen scavenges hydroxyl radicals is different from that of GSH, a well-known free radical scavenger. Using a new method, two-dimensional FTIR correlation analysis, for the first time, we show that the order of functional group changes of type I collagen in this process is amide I earlier than amide II than amide III than –CH– than ν(C=O). The results indicates that the structure of the main chain of collagen changed first, followed by more residue group ν(C=O) exposed to hydroxyl radicals. The reaction with the carbonyl group in collagen causes the hydroxyl free radicals to be scavenged. Therefore, ECM can effectively scavenge ROS under normal physiological conditions. When the proteins of ECM were denatured in the same way as gelatin, they lost their function as a free radical scavenger. All of these results provide new insight into therapy or prevention of oxidative stress, apoptosis and ageing.
PKC Activation Induces Inflammatory Response and Cell Death in Human Bronchial Epithelial Cells
Hyunhee Kim, Ricardo Zamel, Xiao-Hui Bai, Mingyao Liu
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0064182
Abstract: A variety of airborne pathogens can induce inflammatory responses in airway epithelial cells, which is a crucial component of host defence. However, excessive inflammatory responses and chronic inflammation also contribute to different diseases of the respiratory system. We hypothesized that the activation of protein kinase C (PKC) is one of the essential mechanisms of inflammatory response in airway epithelial cells. In the present study, we stimulated human bronchial lung epithelial (BEAS-2B) cells with the phorbol ester Phorbol 12, 13-dibutyrate (PDBu), and examined gene expression profile using microarrays. Microarray analysis suggests that PKC activation induced dramatic changes in gene expression related to multiple cellular functions. The top two interaction networks generated from these changes were centered on NFκB and TNF-α, which are two commonly known pathways for cell death and inflammation. Subsequent tests confirmed the decrease in cell viability and an increase in the production of various cytokines. Interestingly, each of the increased cytokines was differentially regulated at mRNA and/or protein levels by different sub-classes of PKC isozymes. We conclude that pathological cell death and cytokine production in airway epithelial cells in various situations may be mediated through PKC related signaling pathways. These findings suggest that PKCs can be new targets for treatment of lung diseases.
Lgr4 in Ocular Development and Glaucoma
Stefan Siwko,Li Lai,Jinsheng Weng,Mingyao Liu
Journal of Ophthalmology , 2013, DOI: 10.1155/2013/987494
Abstract: The leucine-rich repeat-containing G protein-coupled receptor 4 (LGR4, also called GPR48) plays a key role in multiple developmental processes, and mice lacking Lgr4 display anterior segment dysgenesis leading to early-onset glaucomatous retinal ganglion cell loss as well as defective eyelid formation. This paper will review Lgr4 signaling and its regulation of the Axenfeld-Rieger syndrome gene Pitx2, a crucial developmental transcription factor. In addition, Wnt signaling plays an important role in eye development, with Norrin functioning to activate the Wnt receptor Frizzled 4 required for proper retinal vascularization. Recent discoveries identifying Lgr4 as a receptor for Norrin highlight the potential for Lgr4 function in retinal vascularization. Finally, several unanswered questions impeding a full understanding of Lgr4 in glaucoma are considered as avenues for further research. 1. Introduction Glaucoma is the second leading cause of blindness worldwide, but its etiology is complex and only partially understood. Frequently associated with elevated intraocular pressure (IOP) leading to a stereotypical pattern of retinal ganglion loss and cup excavation, glaucoma may result from closure of the iridocorneal angle, blockage of the trabecular meshwork responsible for aqueous humor outflow, pupil block of the space between the lens and iris necessary for humor circulation between the anterior and posterior chambers, and several other causes. Loss of the leucine-rich repeat domain-containing G protein-coupled receptor 4 (Lgr4, also called Gpr48) has been implicated in anterior segment dysgenesis including iridocorneal attachment and elevated intraocular pressure leading to early onset retinal ganglion cell loss in mice that is similar to glaucomatous damage in humans [1]. Recently published work identifies Lgr4 as a receptor for Norrin, a secreted protein with established roles in retinal neuron protection and retinal vascularization and therefore suggests an additional mechanism by which Lgr4 functions to prevent glaucoma [2]. This paper will provide an overview of Lgr4 signal transduction and its role in a wide variety of developmental processes, followed by a focus on recent developments in the role of Lgr4 in glaucoma. 2. Lgr4 Signaling The leucine-rich repeat domain-containing G protein-coupled receptors (LGRs) feature a large N-terminal extracellular domain containing multiple leucine-rich repeats and are subdivided into three groups. One group consists of the three glycoprotein hormone receptors: lutenizing hormone receptor, follicle-stimulating
Amelioration of Experimental Autoimmune Encephalomyelitis by Plumbagin through Down-Regulation of JAK-STAT and NF-κB Signaling Pathways
Yan Jia, Ji Jing, Yang Bai, Zhen Li, Lande Liu, Jian Luo, Mingyao Liu, Huaqing Chen
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0027006
Abstract: Plumbagin(PL), a herbal compound derived from roots of the medicinal plant Plumbago zeylanica, has been shown to have immunosuppressive properties. Present report describes that PL is a potent novel agent in control of encephalitogenic T cell responses and amelioration of mouse experimental autoimmune encephalomyelitis (EAE), through down-regulation of JAK-STAT pathway. PL was found to selectively inhibit IFN-γ and IL-17 production by CD4+ T cells, which was mediated through abrogated phosphorylation of JAK1 and JAK2. Consistent with IFN-γ and IL-17 reduction was suppressed STAT1/STAT4/T-bet pathway which is critical for Th1 differentiation, as well as STAT3/ROR pathway which is essential for Th17 differentiation. In addition, PL suppressed pro-inflammatory molecules such as iNOS, IFN-γ and IL-6, accompanied by inhibition of IκB degradation as well as NF-κB phosphorylation. These data give new insight into the novel immune regulatory mechanism of PL and highlight the great value of this kind of herb compounds in probing the complex cytokine signaling network and novel therapeutic targets for autoimmune diseases.
Gpr48 Deficiency Induces Polycystic Kidney Lesions and Renal Fibrosis in Mice by Activating Wnt Signal Pathway
Yongyan Dang, Bei Liu, Peng Xu, Pingya Zhu, Yimiao Zhai, Mingyao Liu, Xiyun Ye
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0089835
Abstract: G protein-coupled receptor 48 (Gpr48/Lgr4) is essential to regulate the development of multiple tissues in mice. The notion that Gpr48 functions in renal development prompted us to investigate the relation between Gpr48 and renal diseases. Using a Gpr48 knockout mice model, we observed that 66.7% Gpr48 null mice developed polycystic lesions in the kidney, while no cysts were observed in the kidneys of wild-type mice. Polycystic kidney disease 1 (PKD1) and PKD2 expressions were also markedly decreased in the Gpr48 knockout mice. Abnormal expressions of exra-cellular matrix protein lead to the progression of polycystic kidney disease and the formation of renal fibrosis in the Gpr48 null mice. The expressions of several Wnt molecules and its receptors were increased and marked β-catenin nuclear accumulation was observed in the Gpr48 null mice. The inhibitors of Wnt/β-catenin signal pathway such as GSK3β and axin2 were loss of function. The Wnt/PCP signaling pathway is also activated in Gpr48 null mice. However, TGF-β expression and phosphorylated Smad2/3 levels were not altered. Collectively, our results showed that Gpr48 null mice are at a greater risk of suffering from polycystic lesions and renal fibrosis. Moreover, the formation of polycystic lesions and renal fibrosis induced by Gpr48 deficiency involves the activation of Wnt signaling pathway but not the TGF-β/Smad pathway.
Norcantharidin Facilitates LPS-Mediated Immune Responses by Up-Regulation of AKT/NF-κB Signaling in Macrophages
Qufei Zhao,Yu Qian,Ruimei Li,Binghe Tan,Honghui Han,Mingyao Liu,Min Qian,Bing Du
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0044956
Abstract: Norcantharidin (NCTD), a demethylated analog of cantharidin, is a common used clinical drug to inhibit proliferation and metastasis of cancer cells. But the role of NCTD in modulating immune responses remains unknown. Here, we investigated the function and mechanism of NCTD in regulation of TLR4 associated immune response in macrophages. We evaluated the influence of NCTD on host defense against invaded pathogens by acute peritonitis mouse model, ELISA, Q-PCR, nitrite quantification, phagocytosis assay and gelatin zymography assay. Our data showed that the survival and the serum concentrations of IL-6 and TNF-α were all enhanced by NCTD significantly in peritonitis mouse model. Accordingly, LPS-induced cytokine, nitric oxide and MMP-9 production as well as the phagocytosis of bacteria were all up-regulated by NCTD in a dose dependent manner in both RAW264.7 cells and bone marrow-derived macrophages (BMMs). Then we further analyzed TLR4 associated signaling pathway by Western blot, Immunofluorescence and EMSA in the presence or absence of LPS. The phosphorylation of AKT and p65 at serine 536 but not serine 468 was enhanced obviously by NCTD in a dose dependent manner, whereas the degradation of IκBα was little effected. Consequently, the nuclear translocation and DNA binding ability of NF-κB was also increased by NCTD obviously in RAW264.7 cells. Our results demonstrated that NCTD could facilitate LPS-mediated immune response through promoting the phosphorylation of AKT/p65 and transcriptional activity of NF-κB, thus reprofiling the traditional anti-tumor drug NCTD as a novel immune regulator in promoting host defense against bacterial infection.
Bench-to-bedside review: Biotrauma and modulation of the innate immune response
Claudia C dos Santos, Haibo Zhang, Mingyao Liu, Arthur S Slutsky
Critical Care , 2005, DOI: 10.1186/cc3022
Abstract: The natural or innate immune system is present in some form in most living organisms and consists of mechanisms for defending the host against foreign invaders and for healing injured tissues. We now know that many of the mechanisms of resistance to infection are also involved in the individual's response to noninfectious foreign substances and environmental stresses, including mechanical stretch. Furthermore, mechanisms that normally protect individuals and eliminate foreign substances are themselves capable of causing tissue injury and disease. This inherent defense network includes anatomical, physical and chemical barriers, circulating molecules, cells with specific phagocytic or lytic abilities, and soluble mediators that orchestrate the activities of each component and their interactions with the acquired immune system. Normally, this is a well integrated system of host defense and preservation of self-integrity, in which numerous cells and molecules function cooperatively. However, dys-regulation of the fine balance between proinflammatory and anti-inflammatory stimuli may explain the pathophysiologic processes that underlie syndromes such as sepsis and acute lung injury (ALI) [1].Although patients undergoing positive pressure mechanical ventilation may have impaired lung function, and possibly impaired systemic immune defenses by virtue of their underlying lung pathology, further dysregulation of natural defenses occurs in these patients. The presence of an endotracheal tube bypassing natural upper airway defenses, decrease or loss of coughing, paralysis of bronchial ciliae, alterations in surfactant and phagocyte and epithelial defensins – a critical first line antibacterial defense mechanism – all contribute to impairment in host defense [2-4]. Apart from the direct effects of breaching pulmonary protective barriers, cyclic stretch generated during mechanical ventilation has been implicated in the modulation of the innate immune system. In this short revie
Revealing the missing expressed genes beyond the human reference genome by RNA-Seq
Geng Chen, Ruiyuan Li, Leming Shi, Junyi Qi, Pengzhan Hu, Jian Luo, Mingyao Liu, Tieliu Shi
BMC Genomics , 2011, DOI: 10.1186/1471-2164-12-590
Abstract: we used two RNA-Seq datasets from human brain tissues and 10 mixed cell lines to investigate the completeness of human reference genome. First, we demonstrated that in previously identified ~5 Mb Asian and ~5 Mb African novel sequences that are absent from the human reference genome of NCBI build 36, ~211 kb and ~201 kb of them could be transcribed, respectively. Our results suggest that many of those transcribed regions are not specific to Asian and African, but also present in Caucasian. Then, we found that the expressions of 104 RefSeq genes that are unalignable to NCBI build 37 in brain and cell lines are higher than 0.1 RPKM. 55 of them are conserved across human, chimpanzee and macaque, suggesting that there are still a significant number of functional human genes absent from the human reference genome. Moreover, we identified hundreds of novel transcript contigs that cannot be aligned to NCBI build 37, RefSeq genes and EST sequences. Some of those novel transcript contigs are also conserved among human, chimpanzee and macaque. By positioning those contigs onto the human genome, we identified several large deletions in the reference genome. Several conserved novel transcript contigs were further validated by RT-PCR.Our findings demonstrate that a significant number of genes are still absent from the incomplete human reference genome, highlighting the importance of further refining the human reference genome and curating those missing genes. Our study also shows the importance of de novo transcriptome assembly. The comparative approach between reference genome and other related human genomes based on the transcriptome provides an alternative way to refine the human reference genome.The latest version of the public human genome assembly NCBI build 37 (also known as GRCh37) has been released and is considered to be the successor to NCBI Build 36. Currently, different types of human genetic variation studies including single-nucleotide polymorphisms (SNPs), deleti
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