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Search Results: 1 - 10 of 2560 matches for " Hsi-Lung Hsieh "
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Calmodulin kinase II-dependent transactivation of PDGF receptors mediates astrocytic MMP-9 expression and cell motility induced by lipoteichoic acid
Hui-Hsin Wang, Hsi-Lung Hsieh, Chuen-Mao Yang
Journal of Neuroinflammation , 2010, DOI: 10.1186/1742-2094-7-84
Abstract: The goal of this study was to examine whether LTA-induced cell migration is mediated by calcium/calmodulin (CaM)/CaM kinase II (CaMKII)-dependent transactivation of the PDGFR pathway in rat brain astrocytes (RBA-1 cells).Expression and activity of MMP-9 induced by LTA was evaluated by zymographic, western blotting, and RT-PCR analyses. MMP-9 regulatory signaling pathways were investigated by treatment with pharmacological inhibitors or using dominant negative mutants or short hairpin RNA (shRNA) transfection, and chromatin immunoprecipitation (ChIP)-PCR and promoter activity reporter assays. Finally, we determined the cell functional changes by cell migration assay.The data show that c-Jun/AP-1 mediates LTA-induced MMP-9 expression in RBA-1 cells. Next, we demonstrated that LTA induces MMP-9 expression via a calcium/CaM/CaMKII-dependent transactivation of PDGFR pathway. Transactivation of PDGFR led to activation of PI3K/Akt and JNK1/2 and then activated c-Jun/AP-1 signaling. Activated-c-Jun bound to the AP-1-binding site of the MMP-9 promoter, and thereby turned on transcription of MMP-9. Eventually, up-regulation of MMP-9 by LTA enhanced cell migration of astrocytes.These results demonstrate that in RBA-1 cells, activation of c-Jun/AP-1 by a CaMKII-dependent PI3K/Akt-JNK activation mediated through transactivation of PDGFR is essential for up-regulation of MMP-9 and cell migration induced by LTA. Understanding the regulatory mechanisms underlying LTA-induced MMP-9 expression and functional changes in astrocytes may provide a new therapeutic strategy for Gram-positive bacterial infections in brain disorders.Bacterial infections are responsible for a number of inflammatory diseases including brain inflammation [1]. Gram-positive bacterial infections of the central nervous system (CNS) occur either as bacterial meningitis or as brain abscess, being localized to the membranes surrounding the brain or in its parenchyma, respectively [2]. Lipoteichoic acid (LTA), an amph
Intracellular Signaling Mechanisms Underlying the Expression of Pro-inflammatory Mediators in Airway Diseases
Chuen-Mao Yang,Hsi-Lung Hsieh,Chiang-Wen Lee
Chang Gung Medical Journal , 2005,
Abstract: asthma and airway inflammation mechanisms. Elevated levels of proinflammatorycytokines including tumor necrosis factor-α and interleukin-1β in the bronchoalveolar lavage fluid have been detected inasthmatic patients. Cytokines exert as potent stimuli in inflammatoryresponses through up-regulation of many gene expressions, includingcytokines, chemokines, cytosolic phospholipase A2, cyclooxygenase,adhesion molecules and matrix metalloproteinases. The extent of thesegene expressions is correlated with the severity of inflammation.However, the intracellular signaling mechanisms underlying theexpression of target proteins regulated by these factors are elusive. Themechanisms underlying actions by cytokines may be integrated to thesignaling networks that augment airway inflammation by recruitingleukocytes and leading to airway remodeling. Although cytokines havebeen reported to activate mitogen-activated protein kinases includingp42/p44 and p38, and c-Jun N-terminal kinase, the relationship between the activation ofthese pathways and expression of inflammatory genes remains unknown. Moreover, manygenes regulated by mitogen-activated protein kinases are dependent on NF-κB for transcription.NF-κB has also been shown to be involved in target protein expression at the transcriptionallevel in various cell types. We review the mechanisms underlying the intracellular signalinginvolved in several target protein expressions induced by cytokines in airway residentcells. Conclusion: Increased understanding of signal transduction mechanisms underlyingtarget protein gene expression will create opportunities for the development of anti-inflammationtherapeutic strategies
c-Src-dependent EGF receptor transactivation contributes to ET-1-induced COX-2 expression in brain microvascular endothelial cells
Hsi-Lung Hsieh, Chin-Chung Lin, Hui-Ju Chan, Caleb M Yang, Chuen-Mao Yang
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-152
Abstract: The goal of this study was to examine whether ET-1-induced COX-2 expression and prostaglandin E2 (PGE2) release were mediated through a c-Src-dependent transactivation of epidermal growth factor receptor (EGFR) pathway in brain microvascular endothelial cells (bEnd.3 cells).The expression of COX-2 induced by ET-1 was evaluated by Western blotting and RT-PCR analysis. The COX-2 regulatory signaling pathways were investigated by pretreatment with pharmacological inhibitors, short hairpin RNA (shRNA) or small interfering RNA (siRNA) transfection, chromatin immunoprecipitation (ChIP), and promoter activity reporter assays. Finally, we determined the PGE2 level as a marker of functional activity of COX-2 expression.First, the data showed that ET-1-induced COX-2 expression was mediated through a c-Src-dependent transactivation of EGFR/PI3K/Akt cascade. Next, we demonstrated that ET-1 stimulated activation (phosphorylation) of c-Src/EGFR/Akt/MAPKs (ERK1/2, p38 MAPK, and JNK1/2) and then activated the c-Jun/activator protein 1 (AP-1) via Gq/i protein-coupled ETB receptors. The activated c-Jun/AP-1 bound to its corresponding binding sites within COX-2 promoter, thereby turning on COX-2 gene transcription. Ultimately, upregulation of COX-2 by ET-1 promoted PGE2 biosynthesis and release in bEnd.3 cells.These results demonstrate that in bEnd.3 cells, c-Src-dependent transactivation of EGFR/PI3K/Akt and MAPKs linking to c-Jun/AP-1 cascade is essential for ET-1-induced COX-2 upregulation. Understanding the mechanisms of COX-2 expression and PGE2 release regulated by ET-1/ETB system on brain microvascular endothelial cells may provide rational therapeutic interventions for brain injury and inflammatory diseases.
NADPH oxidase-mediated redox signal contributes to lipoteichoic acid-induced MMP-9 upregulation in brain astrocytes
Hsi-Lung Hsieh, Chih-Chung Lin, Ruey-Horng Shih, Li-Der Hsiao, Chuen-Mao Yang
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-110
Abstract: Herein we explored whether LTA-induced MMP-9 expression was mediated through redox signals in rat brain astrocytes (RBA-1 cells).Upregulation of MMP-9 by LTA was evaluated by zymographic and RT-PCR analyses. Next, the MMP-9 regulatory pathways were investigated by pretreatment with pharmacological inhibitors or transfection with small interfering RNAs (siRNAs), Western blotting, and chromatin immunoprecipitation (ChIP)-PCR and promoter activity reporter assays. Moreover, we determined the cell functional changes by migration assay.These results showed that LTA induced MMP-9 expression via a PKC(α)-dependent pathway. We further demonstrated that PKCα stimulated p47phox/NADPH oxidase 2 (Nox2)-dependent reactive oxygen species (ROS) generation and then activated the ATF2/AP-1 signals. The activated-ATF2 bound to the AP-1-binding site of MMP-9 promoter, and thereby turned on MMP-9 gene transcription. Additionally, the co-activator p300 also contributed to these responses. Functionally, LTA-induced MMP-9 expression enhanced astrocytic migration.These results demonstrated that in RBA-1 cells, activation of ATF2/AP-1 by the PKC(α)-mediated Nox(2)/ROS signals is essential for upregulation of MMP-9 and cell migration enhanced by LTA.Matrix metalloproteinases (MMPs) comprise a family of calcium- and zinc-dependent proteinases, and are involved in normal development and wound healing as well as in pathological conditions such as atherosclerosis and metastasis. In brain, MMP-9 has been shown to be upregulated during various CNS diseases [1,2]. Previous reports have indicated that a series of functional element-binding sites have been identified, including NF-κB, Ets and AP-1 within the MMP-9 promoter [3], which can be regulated by diverse stimuli. Moreover, proinflammatory factors including cytokines, endotoxins and oxidative stress have been reported to upregulate MMP-9 in astrocytes in vitro [4-6], implying that MMP-9 activity may be regulated by diverse factors in the CNS du
Transforming growth factor-β1 induces matrix metalloproteinase-9 and cell migration in astrocytes: roles of ROS-dependent ERK- and JNK-NF-κB pathways
Hsi-Lung Hsieh, Hui-Hsin Wang, Wen-Bin Wu, Po-Ju Chu, Chuen-Mao Yang
Journal of Neuroinflammation , 2010, DOI: 10.1186/1742-2094-7-88
Abstract: Rat brain astrocytes (RBA-1) were used. MMP-9 expression was analyzed by gelatin zymography and RT-PCR. The involvement of signaling molecules including MAPKs and NF-κB in the responses was investigated using pharmacological inhibitors and dominant negative mutants, determined by western blot and gene promoter assay. The functional activity of MMP-9 was evaluated by cell migration assay.Here we report that TGF-β1 induces MMP-9 expression and enzymatic activity via a TGF-β receptor-activated reactive oxygen species (ROS)-dependent signaling pathway. ROS production leads to activation of extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun-N-terminal kinase (JNK) and then activation of the NF-κB transcription factor. Activated NF-κB turns on transcription of the MMP-9 gene. The rat MMP-9 promoter, containing a NF-κB cis-binding site, was identified as a crucial domain linking to TGF-β1 action.Collectively, in RBA-1 cells, activation of ERK1/2- and JNK-NF-κB cascades by a ROS-dependent manner is essential for MMP-9 up-regulation/activation and cell migration induced by TGF-β1. These findings indicate a new regulatory pathway of TGF-β1 in regulating expression of MMP-9 in brain astrocytes, which is involved in physiological and pathological tissue remodeling of central nervous system.Matrix metalloproteinases (MMPs) are a large family of zinc-dependent endopeptidases that play an important role in the turnover of extracellular matrix (ECM) and function in physiological and pathological processes [1]. In the central nervous system (CNS), MMPs, and MMP-9 especially, are implicated in development, morphogenesis, wounding healing, neurite outgrowth, and immune cell migration [2]. In addition, they also participate in the pathogenesis of several CNS diseases such as stroke, Alzheimer's disease, neuroinflammation, and malignant glioma [3]. Among members of the MMP family, MMP-9 has been shown to be elevated in various brain disorders [4-6]. Moreover, several pro-infla
NADPH oxidase 2-derived reactive oxygen species signal contributes to bradykinin-induced matrix metalloproteinase-9 expression and cell migration in brain astrocytes
Chih-Chung Lin, Hsi-Lung Hsieh, Ruey-Horng Shih, Pei-Ling Chi, Shin-Ei Cheng, Jin-Chung Chen, Chuen-Mao Yang
Cell Communication and Signaling , 2012, DOI: 10.1186/1478-811x-10-35
Abstract: In the study, we first demonstrated that reactive oxygen species (ROS) plays a crucial role in BK-induced MMP-9 expression in cultured brain astrocytes (in vitro) and animal brain tissue (in vivo) models. Next, BK-induced MMP-9 expression is mediated through a Ca2+-mediated PKC-α linking to p47phox/NADPH oxidase 2 (Nox2)/ROS signaling pathway. Nox2-dependent ROS generation led to activation and up-regulation of the downstream transcriptional factor AP-1 (i.e. c-Fos and c-Jun), which bound to MMP-9 promoter region, and thereby turned on transcription of MMP-9 gene. Functionally, BK-induced MMP-9 expression enhanced astrocytic migration.These results demonstrated that in RBA-1 cells, activation of AP-1 (c-Fos/c-Jun) by the PKC-α-mediated Nox2/ROS signals is essential for up-regulation of MMP-9 and cell migration enhanced by BK.Matrix metalloproteinases (MMPs) is a large family of zinc-dependent endopeptidases, which play an important role in the turnover of extracellular matrix (ECM) and pathophysiological processes [1]. In the central nervous system (CNS), MMPs, in particular MMP-9, have been shown to be involved in morphogenesis, wounding healing, and neurite outgrowth, [2]. Up-regulation of MMP-9 has been induced by various brain injuries, which may participate in the pathogenesis of brain diseases [3]. Moreover, cytokines and lipopolysaccharide (LPS) have been shown to induce MMP-9 expression and activity in culture rat brain astrocytes [4,5]. These studies demonstrated that MMP-9 may be involved in brain inflammation and injury.Reactive oxygen species (ROS) are produced by various enzymatic and chemical processes or directly inhaled, including O2-, ·OH, and hydrogen peroxide (H2O2). The ROS at low level have physiological roles as signaling molecules in various cellular and developmental processes [6,7] and killing of invading microorganisms [8]. In contrast, recent report indicated that oxidative stress plays an important role in the progression of various disea
Up-regulation of COX-2/PGE2 by endothelin-1 via MAPK-dependent NF-κB pathway in mouse brain microvascular endothelial cells
Chih-Chung Lin, Hsi-Lung Hsieh, Ruey-Horng Shih, Pei-Ling Chi, Shin-Ei Cheng, Chuen-Mao Yang
Cell Communication and Signaling , 2013, DOI: 10.1186/1478-811x-11-8
Abstract: The data obtained with Western blotting, RT-PCR, and immunofluorescent staining analyses showed that ET-1-induced COX-2 expression was mediated through an ETB-dependent transcriptional activation. Engagement of Gi- and Gq-protein-coupled ETB receptors by ET-1 led to phosphorylation of ERK1/2, p38 MAPK, and JNK1/2 and then activated transcription factor NF-κB. Moreover, the data of chromatin immunoprecipitation (ChIP) and promoter reporter assay demonstrated that the activated NF-κB was translocated into nucleus and bound to its corresponding binding sites in COX-2 promoter, thereby turning on COX-2 gene transcription. Finally, up-regulation of COX-2 by ET-1 promoted PGE2 release in these cells.These results suggested that in mouse bEnd.3 cells, activation of NF-κB by ETB-dependent MAPK cascades is essential for ET-1-induced up-regulation of COX-2/PGE2 system. Understanding the mechanisms of COX-2 expression and PGE2 release regulated by ET-1/ETB system on brain microvascular endothelial cells may provide rationally therapeutic interventions for brain injury or inflammatory diseases.Cerebral capillary and microvascular endothelial cells play an active role in maintaining cerebral blood flow, microvascular tone and blood-brain barrier (BBB) functions [1]. In the development of various vascular diseases, an early finding is dysfunction of the vascular endothelium that is closely related to clinical events in patients with atherosclerosis and hypertension [2,3]. The vasoactive mediators such as endothelin (ET) could be produced by endothelial cells to maintain hemodynamic responses. Production and release of ETs from cultured endothelial cells are regulated at transcription and translation levels by a variety of chemical and physical stimuli and the levels of ET, ET-1 especially, are elevated in shock, myocardial infarction, and kidney failure indicative of enhanced formation in these diseases [4]. Moreover, the bioactivity of ET-1 triggers vasoconstriction and pro-infl
An Adaptive Particle Filter Based Method for Real Time Face Tracking  [PDF]
Wei-Ming Chen, Yi-Lung Lin, Ya-Hsiung Hsieh
Journal of Software Engineering and Applications (JSEA) , 2013, DOI: 10.4236/jsea.2013.65B001
Abstract: The video surveillance systems of recent years, usually major focus on the Human-Face of observation and detection. Human-Face is the most characteristic and prominent feature of a human, therefore, detection and tracking of Human-Face has become an important indicator of the study. This paper discusses video surveillance of public places and majors in automated face detection and face tracking. The main detection method is the use of Haar-Like Feature-based and through the Cascade classifier of the Adaboost face detection. In the tracking mechanism is based on particle filter and we modified SURF (Speeded Up Robust Features) particle filter tracking, and thus enhance the detection and tracking accuracy.
Alternative Fuzzy Switching Regression
Kuo Lung Wu,Miin Shen Yang,June Nan Hsieh
Lecture Notes in Engineering and Computer Science , 2009,
Abstract:
Tracking single particles on supported lipid membranes: multi-mobility diffusion and nanoscopic confinement
Chia-Lung Hsieh,Susann Spindler,Jens Ehrig,Vahid Sandoghdar
Physics , 2013, DOI: 10.1021/jp412203t
Abstract: Supported lipid bilayers have been studied intensively over the past two decades. In this work, we study the diffusion of single gold nanoparticles (GNPs) with diameter of 20 nm attached to GM1 ganglioside or DOPE lipids at different concentrations in supported DOPC bilayers. The indefinite photostability of GNPs combined with the high sensitivity of interferometric scattering microscopy (iSCAT) allows us to achieve 1.9 nm spatial precision at 1 ms temporal resolution, while maintaining long recording times. Our trajectories visualize strong transient confinements within domains as small as 20 nm, and the statistical analysis of the data reveals multiple mobilities and deviations from normal diffusion. We present a detailed analysis of our findings and provide interpretations regarding the effect of the supporting substrate and GM1 clustering. We also comment on the use of high-speed iSCAT for investigating diffusion of lipids, proteins or viruses in lipid membranes with unprecedented spatial and temporal resolution.
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