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Dive into the research topics where Chang-Min Liang is active.

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Featured researches published by Chang-Min Liang.


PLOS ONE | 2014

Autophagy activation is involved in 3,4-methylenedioxymethamphetamine ('ecstasy')--induced neurotoxicity in cultured cortical neurons.

I-Hsun Li; Kuo-Hsing Ma; Shao-Ju Weng; Shiang-Suo Huang; Chang-Min Liang; Yuahn-Sieh Huang

Autophagic (type II) cell death, characterized by the massive accumulation of autophagic vacuoles in the cytoplasm of cells, has been suggested to play pathogenetic roles in cerebral ischemia, brain trauma, and neurodegenerative disorders. 3,4-Methylenedioxymethamphetamine (MDMA or ecstasy) is an illicit drug causing long-term neurotoxicity in the brain. Apoptotic (type I) and necrotic (type III) cell death have been implicated in MDMA-induced neurotoxicity, while the role of autophagy in MDMA-elicited neurotoxicity has not been investigated. The present study aimed to evaluate the occurrence and contribution of autophagy to neurotoxicity in cultured rat cortical neurons challenged with MDMA. Autophagy activation was monitored by expression of microtubule-associated protein 1 light chain 3 (LC3; an autophagic marker) using immunofluorescence and western blot analysis. Here, we demonstrate that MDMA exposure induced monodansylcadaverine (MDC)- and LC3B-densely stained autophagosome formation and increased conversion of LC3B-I to LC3B-II, coinciding with the neurodegenerative phase of MDMA challenge. Autophagy inhibitor 3-methyladenine (3-MA) pretreatment significantly attenuated MDMA-induced autophagosome accumulation, LC3B-II expression, and ameliorated MDMA-triggered neurite damage and neuronal death. In contrast, enhanced autophagy flux by rapamycin or impaired autophagosome clearance by bafilomycin A1 led to more autophagosome accumulation in neurons and aggravated neurite degeneration, indicating that excessive autophagosome accumulation contributes to MDMA-induced neurotoxicity. Furthermore, MDMA induced phosphorylation of AMP-activated protein kinase (AMPK) and its downstream unc-51-like kinase 1 (ULK1), suggesting the AMPK/ULK1 signaling pathway might be involved in MDMA-induced autophagy activation.


Investigative Ophthalmology & Visual Science | 2015

Protective Effects of Glucosamine on Oxidative-Stress and Ischemia/Reperfusion-Induced Retinal Injury

Ying-Jen Chen; Yuahn-Sieh Huang; Jiann-Torng Chen; Yi-Hao Chen; Ming-Cheng Tai; Ching-Long Chen; Chang-Min Liang

PURPOSE To investigate the protective effects of glucosamine (GlcN) using oxidative stress and rat models of ischemia-reperfusion (I/R) injury and to determine the antiapoptotic and anti-inflammatory mechanisms of GlcN treatment. METHODS We determined the effects of GlcN and the levels of O-linked N-acetylglucosamine (O-GlcNAc) in in vitro retinal ganglion cells (RGCs) treated with or without H₂O₂. The survival and apoptosis rates of RGCs were compared after the addition of GlcN, glucose, or O-(2-acetamido-2-deoxy-Dglucopyranosylidene) amino-N-phenylcarbamate (PUGNAc). Retinal I/R injury was induced in Sprague-Dawley rats by elevating the IOP to 110 mm Hg for 60 minutes. An intraperitoneal injection of GlcN (1000 mg/kg) or normal saline was administered in the different groups, including a control group, a GlcN group, an I/R group, a GlcN+I/R group (1000 mg/kg GlcN 24 hours before I/R injury), and an I/R+GlcN group (7-day period of 1000 mg/kg GlcN 24 hours after I/R injury). The rats were killed 7 days after the I/R injury, and the retinas were collected from each rat for thickness measurements. Quantitative analysis of RGC survival was further determined using labeling with FluoroGold. RESULTS The GlcN increased levels of O-GlcNAc in a dose-dependent manner in the RGCs treated with or without H₂O₂. The GlcN resulted in increased cell survival and reduced apoptosis in the RGCs under oxidative stress conditions. In the rat model of I/R injury, GlcN significantly protected against I/R-induced retinal thinning and suppressed the I/R-induced reductions in a- and b-wave amplitudes of the ERG. In terms of RGC survival, significant incremental density of RGCs was found in the I/R+GlcN group compared with the I/R group. Notably, the use of GlcN in the rat retina decreased apoptosis and the formation of reactive oxygen species (ROS) after I/R injury. We also found that mitogen-activated protein kinase signal pathways played a critical role in the GlcN-mediated attenuation of ROS-induced damage in vitro and I/R injury in vivo. CONCLUSIONS Glucosamine treatment provides multiple levels of retinal protection, including antiapoptotic, anti-inflammatory, and antioxidative benefits. More research on the role of GlcN as a potential agent for the prevention and treatment of glaucoma is warranted.


Brain & Development | 2012

Involvement of SHP2 in focal adhesion, migration and differentiation of neural stem cells

Yuahn-Sieh Huang; Cheng-Yi Cheng; Sheau-Huei Chueh; Dueng-Yuan Hueng; Yu-Fen Huang; Chun-Ming Chu; Sheng-Tang Wu; Ming-Cheng Tai; Chang-Min Liang; Mei-Hsiu Liao; Chia-Chieh Chen; Lie-Hang Shen; Kuo-Hsing Ma

OBJECTIVES SHP2 (Src-homology-2 domain-containing protein tyrosine phosphatase) plays an important role in cell adhesion, migration and cell signaling. However, its role in focal adhesion, differentiation and migration of neural stem cells is still unclear. METHODS In this study, rat neurospheres were cultured in suspension and differentiated neural stem cells were cultured on collagen-coated surfaces. RESULTS The results showed that p-SHP2 co-localized with focal adhesion kinase (FAK) and paxillin in neurospheres and in differentiated neural precursor cells, astrocytes, neurons, and oligodendrocytes. Suppression of SHP2 activity by PTP4 or siRNA-mediated SHP2 silencing caused reduction in the cell migration and neurite outgrowth, and thinning of glial cell processes. Differentiation-induced activation of FAK, Src, paxillin, ERK1/2, and RhoA was decreased by SHP2 inactivation. CONCLUSIONS These results indicate that SHP2 is recruited in focal adhesions of neural stem cells and regulates focal adhesion formation. SHP2-mediated regulation of neural differentiation and migration may be related to formation of focal adhesions and RhoA and ERK1/2 activation.


Journal of Tissue Engineering and Regenerative Medicine | 2015

Mesenchymal stem cells from rat olfactory bulbs can differentiate into cells with cardiomyocyte characteristics.

Yuahn-Sieh Huang; I-Hsun Li; Sheau-Huei Chueh; Dueng-Yuan Hueng; Ming-Cheng Tai; Chang-Min Liang; Shiu-Bii Lien; Huey-Kang Sytwu; Kuo-Hsing Ma

Mesenchymal stromal/stem cells (MSCs) are widely distributed in different tissues such as bone marrow, adipose tissues, peripheral blood, umbilical cord and amnionic fluid. Recently, MSC‐like cells were also found to exist in rat olfactory bulb and are capable of inducing differentiation into mesenchymal lineages – osteocytes, chondrocytes and adipocytes. However, whether these cells can differentiate into myocardial cells is not known. In this study, we examined whether olfactory bulb‐derived MSCs could differentiate into myocardial cells in vitro. Fibroblast‐like cells isolated from the olfactory bulb of neonatal rats were grown under four conditions: no treatment; in the presence of growth factors (neuregulin‐1, bFGF and forskolin); co‐cultured with cardiomyocytes; and co‐cultured with cardiomyocytes plus neuregulin‐1, bFGF and forskolin. Cell differentiation into myocardial cells was monitored by RT–PCR, light microscopy immunofluorescence, western blot analysis and contractile response to pharmacological treatments. The isolated olfactory bulb‐derived fibroblast‐like cells expressed CD29, CD44, CD90, CD105, CD166 but not CD34 and CD45, consistent with the characteristics of MSCs. Long cylindical cells that spontaneously contracted were only observed following 7 days of co‐culture of MSCs with rat cardiomyocytes plus neuregulin‐1, bFGF and forskolin. RT–PCR and western blot analysis indicated that the cylindrical cells expressed myocardial markers, such as Nkx2.5, GATA4, sarcomeric α‐actinin, cardiac troponin I, cardiac myosin heavy chain, atrial natriuretic peptide and connexin 43. They also contained sarcomeres and gap junction and were sensitive to pharmacological treatments (adrenal and cholinergic agonists and antagonists). These findings indicate that rat olfactory bulb‐derived fibroblast‐like cells with MSC characteristics can differentiate into myocardial‐like cells. Copyright


Cytotherapy | 2014

Neurotrophic and neuroprotective potential of human limbus-derived mesenchymal stromal cells

Chang-Min Liang; Shao-Ju Weng; Tung-Han Tsai; I-Hsun Li; Pin-Hui Lu; Kuo-Hsing Ma; Ming-Cheng Tai; Jiann-Torng Chen; Cheng-Yi Cheng; Yuahn-Sieh Huang

BACKGROUND AIMS The purpose of this study was to examine neurotrophic and neuroprotective effects of limbus stroma-derived mesenchymal stromal cells (L-MSCs) on cortical neurons in vitro and in vivo. METHODS Cultured L-MSCs were characterized by flow cytometry and immunofluorescence through the use of specific MSC marker antibodies. Conditioned media were collected from normoxia- and hypoxia-treated L-MSCs to assess neurotrophic effects. Neuroprotective potentials were evaluated through the use of in vitro hypoxic cortical neuron culture and in vivo rat focal cerebral ischemia models. Neuronal morphology was confirmed by immunofluorescence with the use of anti-MAP2 antibody. Post-ischemic infarct volume and motor behavior were assayed by means of triphenyltetrazolium chloride staining and open-field testing, respectively. Human growth antibody arrays and enzyme-linked immunoassays were used to analyze trophic/growth factors contained in conditioned media. RESULTS Isolated human L-MSCs highly expressed CD29, CD90 and CD105 but not CD34 and CD45. Mesenchymal lineage cell surface expression pattern and differentiation capacity were identical to MSCs derived form human bone marrow and adipose tissue. The L-MSC normoxic and hypoxic conditioned media both promoted neurite outgrowth in cultured cortical neurons. Hypoxic conditioned medium showed superior neurotrophic function and neuroprotective potential with reduced ischemic brain injury and improved functional recovery in rat focal cerebral ischemia models. Human growth factor arrays and enzyme-linked immunoassays measurements showed neuroprotective and growth-associated cytokines (vascular endothelial growth factor [VEGF], VEGFR3, brain-derived neurotrophic factor, insulin-like growth factor -2 and hepatocyte growth factor) contained in conditioned media. Hypoxic exposure caused VEGF and brain-derived neurotrophic factor upregulation, possibly contributing to neurotrophic and neuroprotective effects. CONCLUSIONS L-MSCs can secrete various neurotrophic factors stimulating neurite outgrowth and protecting neurons against brain ischemic injury through paracrine mechanism.


PLOS ONE | 2017

Silibinin treatment prevents endotoxin-induced uveitis in rats in vivo and in vitro

Ching-Long Chen; Jiann-Torng Chen; Chang-Min Liang; Ming-Cheng Tai; Da-Wen Lu; Yi-Hao Chen; Partha Mukhopadhyay

Uveitis, an intraocular inflammatory disease, occurs mostly in young people and can result in the loss of socioeconomic capabilities. Silibinin has been shown to exert anti-inflammatory effects in human retinal pigment epithelial (RPE) cells. The present study investigated the anti-inflammatory effect of silibinin pretreatment on endotoxin-induced uveitis (EIU) in rats and the mechanisms by which it exerts these effects. Uveitis was induced via injection of lipopolysaccharides (LPS) into Lewis rats. Twenty-four hours after the LPS injection, histological examination showed that silibinin decreased inflammatory cell infiltration in the anterior segment of the eyes of LPS-treated rats. Analyses of the aqueous humor showed that silibinin decreased cell infiltration, protein concentration, nitric oxide (NO), and prostaglandin (PG)-E2 production. Western blot analysis indicated that silibinin decreased the expression of inducible NO synthase (iNOS), cyclooxygenase (COX-2), and phosphorylated IkB in the iris-ciliary body (ICB). Immunohistochemistry showed that silibinin decreased intercellular adhesion molecule (ICAM-1) expression in the ICB. In addition, western blot analysis showed that silibinin attenuated the expression of iNOS, COX-2, ICAM-1, and nuclear p65 in LPS-treated RAW cells. In conclusion, silibinin pretreatment prevents EIU and the subsequent production of proinflammatory mediators and ICAM-1, at least in part, by blocking the NF-κB–dependent signaling pathway both in vivo and in vitro. These effects may contribute to the silibinin-mediated preventive effects on intraocular inflammatory diseases such as acute uveitis.


PLOS ONE | 2016

Silibinin Inhibits Platelet-Derived Growth Factor-Driven Cell Proliferation via Downregulation of N-Glycosylation in Human Tenon's Fibroblasts in a Proteasome-Dependent Manner.

Yi-Hao Chen; Ching-Long Chen; Da-Wen Lu; Chang-Min Liang; Ming-Cheng Tai; Jiann-Torng Chen

The objective of this study was to evaluate the effects of silibinin on cell proliferation in platelet-derived growth factor (PDGF)-treated human Tenons fibroblasts (HTFs). The effect of silibinin on cell proliferation in PDGF-treated HTFs was determined by examining the expression of proliferating cell nuclear antigen (PCNA) and performing WST-1 assays. Cell cycle progression was evaluated using flow cytometry. The related cyclins and cyclin-dependent kinases (CDKs) were also analyzed using western blot. A modified rat trabeculectomy model was established to evaluate the effect of silibinin on cell proliferation in vivo. Western blot analysis was carried out to determine the effect of silibinin on the expression of PDGF receptor and on the downstream signaling pathways regulated by PDGF receptor. PDGF elevated the expression of PCNA in HTFs, and this elevation was inhibited by silibinin. The inhibitory effect of silibinin on cell proliferation was also confirmed via WST-1 assay. PDGF-stimulated cell cycle in HTFs was delayed by silibinin, and the related cyclin D1 and CDK4 were also suppressed by silibinin. In the rat model of trabeculectomy, silibinin reduced the expression of PCNA at the site of blebs in vivo. The effects of silibinin on PDGF-stimulated HTFs were mediated via the downregulation of PDGF receptor-regulated signaling pathways, such as ERKs and STATs, which may be partially caused by the downregulation of N-glycosylation of PDGF receptor beta (PDGFRβ). The effect of silibinin on modulation of N-glycosylation of PDGFRβ was mediated in a proteasome-dependent manner. Silibinin inhibited cell proliferation and delayed cell cycle progression in PDGF-treated HTFs in vitro. PDGF also modulated the process of N-glycosylation of the PDGFRβ in a proteasome-dependent manner. Our findings suggest that silibinin has potential therapeutic applications in glaucoma filtering surgery.


Journal of The Chinese Medical Association | 2018

Impact of hypoxic and mesopic environments on visual acuity, contrast sensitivity and accommodation in subjects with LASIK surgery and aircrew candidate

Hsin-Ting Lin; Hui-Ju Chan; Cheng-Wen Ho; Ming-Cheng Tai; Jiann-Torng Chen; Chang-Min Liang

Background: The safety of Laser‐assisted in situ keratomileusis (LASIK) in aircrew was unclear, in addition, LASIK was not yet approved for aircrew of Taiwan Air Force. This study was aimed to evaluate visual performance in LASIK eyes in hypoxic and twilight environment. Methods: 48 myopic eyes of 24 subjects enrolled in this study were divided into LASIK group and control group. Subjects were exposed in hypoxic (15% O2) and mesopic (3 cd/m2) environment. Visual performance was evaluated using the Early Treatment of Diabetic Retinopathy Study (ETDRS) visual chart, and Functional Acuity Contrast Test (FACT) before and after the expirement. Physiological parameters of all subjects were measured and recorded throughout the experiment. Results: There was no significant difference of the two groups regarding their age, height, weight, and BMI. There is significant difference of preoperative spherical refractive error between the two groups. The results of physiological parameters were similar between two groups. Under normoxic conditions, there were no significant difference regarding distant vision in photopic and mesopic environments, so as for near vision. As a whole, the contrast sensitivity of the LASIK group were lowered than that of the control group about 35%, under whether normoxic or hypoxic conditions; photopic or mesopic circumstances. Under normoxic conditions, the measured accommodation of the LASIK group were 21% lowered than that of the control group and 31% lowered under hypoxic circumstances. Conclusion: There was no significant difference of visual acuity between the two groups regarding hypoxic and mesopic environment, but reduced contrast sensitivity was significant in LASIK group as compared to those of the control group. Accommodation was significantly lowered in LASIK group, compared with control group, in hypoxic environment. Whether postoperative visual performance after LASIK in aircrew during flying duty is safe might need further investigation.


Journal of The Chinese Medical Association | 2017

Effect of microgravity on the mesenchymal stem cell characteristics of limbal fibroblasts

Shu-I Pao; Ke-Hung Chien; Hsin-Ting Lin; Ming-Cheng Tai; Jiann-Torng Chen; Chang-Min Liang

Background Mesenchymal stem cells (MSCs) are important for regenerative medicine. Limbal fibroblasts (LFs), present in the corneal limbus, have been shown to possess MSC characteristics, and can differentiate into other cell types. The current study sought to investigate the effect of microgravity on the proliferation and differentiation of LFs, and identify culture conditions to obtain a high proportion of LFs possessing MSC characteristics. Methods A rotary cell culture system was used to generate microgravity. Cellular proliferation and MSC marker (CD14, CD45, CD90, CD105, and SSEA4) expression were evaluated by WST‐1 test and flow cytometry, respectively. Differentiation of LFs into adipocytes, osteocytes, and chondrocytes was examined. The effects of LF‐conditioned medium on limbal stem cell differentiation were assessed. Results The cellular proliferation rates under microgravity were significantly lower than those under normal gravity (0.44 vs. 0.18 at 24 h, and 0.70 vs. 0.44 at 48 h, both P ≤ 0.004). Higher proportions of cells expressed CD90 (95.33% vs 81.69%), CD105 (95.32% vs 87.96%), and SSEA4 (68.26% vs 26.13%) under microgravity than under normal gravity. The differentiation potential of LFs was more prominent under microgravity. The LF‐conditioned medium attenuated the differentiation of limbal corneal epithelial stem cells. Conclusion Under microgravity, LFs showed a higher proportion of MSC characteristics and were easily induced into different linage cells. Culture in a microgravity environment may allow harvesting a greater number of MSC‐like LFs for stem cell therapy in ocular surface reconstruction.


Medicine | 2018

Orbital apex syndrome secondary to aspergilloma masquerading as a paranasal sinus tumor: A case report and literature review

Yu-Min Chang; Yun-Hsiang Chang; Ke-Hung Chien; Chang-Min Liang; Ming-Cheng Tai; Shin Nieh; Ying-Jen Chen

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Ming-Cheng Tai

National Defense Medical Center

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Jiann-Torng Chen

National Defense Medical Center

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Yuahn-Sieh Huang

National Defense Medical Center

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Kuo-Hsing Ma

National Defense Medical Center

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I-Hsun Li

National Defense Medical Center

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Ching-Long Chen

National Defense Medical Center

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Dueng-Yuan Hueng

National Defense Medical Center

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Hsin-Ting Lin

National Defense Medical Center

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Ke-Hung Chien

National Defense Medical Center

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Shao-Ju Weng

National Defense Medical Center

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