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Start Over Author "Chen, Mei" Journal international journal of molecular sciences
35 results on '"Chen, Mei"'

1. Isorhamnetin Regulates Programmed Death Ligand-1 Expression by Suppressing the EGFR–STAT3 Signaling Pathway in Canine Mammary Tumors

Author

Chen Mei, Xue Zhang, Yan Zhi, Zhixuan Liang, Haojun Xu, Zhenyi Liu, Ying Liu, Yanli Lyu, and Hongjun Wang

Subjects
canine mammary tumor, isorhamnetin, surface plasmon resonance (SPR), target protein, programmed death ligand-1 (PD-L1), EGFR-STAT3 signaling pathway, Biology (General), QH301-705.5, Chemistry, QD1-999
Abstract

Programmed death ligand-1 (PD-L1) is highly expressed in a variety of cancer cells and suggests a poorer prognosis for patients. The natural compound isorhamnetin (ISO) shows promise in treating cancers and causing damage to canine mammary tumor (CMT) cells. We investigated the mechanism of ISO in reducing PD-L1 expression in CMT cells. Clustered, regularly interspaced short palindromic repeat-associated protein 9 (CRISPR/Cas9) was used to mediate CD274 knockout in U27 cells. Then, monoclonal cells were screened and cultured. Nucleotide sequencing and expression of PD-L1 were detected. Additionally, we examined cell migration, invasion, and damage. Immunofluorescent staining of PD-L1 was examined in U27 cells. The signaling pathways were measured by Western blotting. Murine xenotransplantation models and murine immunocompetent allograft mammary tumor models were established to evaluate the effect of ISO therapy. Expression of Ki-67, caspase3, and PD-L1 were analyzed by immunohistochemistry. A pull-down assay was used to explore which proteins could bind to ISO. Canine EGFR protein was purified and used to detect whether it directly binds to ISO using a surface plasmon resonance assay. ISO inhibited the EGFR-STAT3-PD-L1 signaling pathway and blocked cancer growth, significantly increasing the survival rate of healthy cells. The cell membrane receptor EGFR was identified as a direct target of ISO. ISO could be exploited as an antineoplastic treatment of CMT by targeting EGFR to suppress PD-L1 expression.

Published
2024
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2. Dual-Specificity Phosphatase 6 Deficiency Attenuates Arterial-Injury-Induced Intimal Hyperplasia in Mice

Author

Candra D. Hamdin, Meng-Ling Wu, Chen-Mei Chen, Yen-Chun Ho, Wei-Cheng Jiang, Pei-Yu Gung, Hua-Hui Ho, Huai-Chia Chuang, Tse-Hua Tan, and Shaw-Fang Yet

Subjects
DUSP6, vascular remodeling, VSMC, proliferation, migration, Biology (General), QH301-705.5, Chemistry, QD1-999
Abstract

In response to injury, vascular smooth muscle cells (VSMCs) of the arterial wall dedifferentiate into a proliferative and migratory phenotype, leading to intimal hyperplasia. The ERK1/2 pathway participates in cellular proliferation and migration, while dual-specificity phosphatase 6 (DUSP6, also named MKP3) can dephosphorylate activated ERK1/2. We showed that DUSP6 was expressed in low baseline levels in normal arteries; however, arterial injury significantly increased DUSP6 levels in the vessel wall. Compared with wild-type mice, Dusp6-deficient mice had smaller neointima. In vitro, IL-1β induced DUSP6 expression and increased VSMC proliferation and migration. Lack of DUSP6 reduced IL-1β-induced VSMC proliferation and migration. DUSP6 deficiency did not affect IL-1β-stimulated ERK1/2 activation. Instead, ERK1/2 inhibitor U0126 prevented DUSP6 induction by IL-1β, indicating that ERK1/2 functions upstream of DUSP6 to regulate DUSP6 expression in VSMCs rather than downstream as a DUSP6 substrate. IL-1β decreased the levels of cell cycle inhibitor p27 and cell–cell adhesion molecule N-cadherin in VSMCs, whereas lack of DUSP6 maintained their high levels, revealing novel functions of DUSP6 in regulating these two molecules. Taken together, our results indicate that lack of DUSP6 attenuated neointima formation following arterial injury by reducing VSMC proliferation and migration, which were likely mediated via maintaining p27 and N-cadherin levels.

Published
2023
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9. Exposure to Zinc Oxide Nanoparticles Disrupts Endothelial Tight and Adherens Junctions and Induces Pulmonary Inflammatory Cell Infiltration

Author

Chen-Mei Chen, Meng-Ling Wu, Yen-Chun Ho, Pei-Yu Gung, Ming-Hsien Tsai, Alexander N. Orekhov, Igor A. Sobenin, Pinpin Lin, and Shaw-Fang Yet

Subjects
zinc oxide nanoparticles, pulmonary infiltration, endothelial barrier, tight junctions, adherens junctions, Biology (General), QH301-705.5, Chemistry, QD1-999
Abstract

Zinc oxide nanoparticles (ZnONPs) are frequently encountered nanomaterials in our daily lives. Despite the benefits of ZnONPs in a variety of applications, many studies have shown potential health hazards of exposure to ZnONPs. We have shown that oropharyngeal aspiration of ZnONPs in mice increases lung inflammation. However, the detailed mechanisms underlying pulmonary inflammatory cell infiltration remain to be elucidated. Endothelium functions as a barrier between the blood stream and the blood vessel wall. Endothelial barrier dysfunction may increase infiltration of immune cells into the vessel wall and underlying tissues. This current study examined the effects of ZnONPs exposure on endothelial barriers. ZnONPs exposure increased leukocyte infiltration in the mouse lungs. In endothelial cells, ZnONPs reduced the continuity of tight junction proteins claudin-5 and zonula occludens-1 (ZO-1) at the cell junctions. ZnONPs induced adherens junction protein VE-cadherin internalization from membrane to cytosol and dissociation with β-catenin, leading to reduced and diffused staining of VE-cadherin and β-catenin at cell junctions. Our results demonstrated that ZnONPs disrupted both tight and adherens junctions, compromising the integrity and stability of the junction network, leading to inflammatory cell infiltration. Thus, ZnONPs exposure in many different settings should be carefully evaluated for vascular effects and subsequent health impacts.

Published
2020
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13. Epithelial-Mesenchymal Transition and Senescence in the Retinal Pigment Epithelium of NFE2L2/PGC-1α Double Knock-Out Mice

Author

Blasiak, Janusz, Koskela, Ali, Pawlowska, Elzbieta, Liukkonen, Mikko, Ruuth, Johanna, Toropainen, Elisa, Hyttinen, Juha M T, Viiri, Johanna, Eriksson, John E, Xu, Heping, Chen, Mei, Felszeghy, Szabolcs, and Kaarniranta, Kai

Subjects
lcsh:Chemistry, senescence, lcsh:Biology (General), lcsh:QD1-999, NFE2L2/PGC-1α dKO mice, epithelial-mesenchymal transition, sense organs, AMD, age-related macular degeneration, lcsh:QH301-705.5, eye diseases
Abstract

Age-related macular degeneration (AMD) is the most prevalent form of irreversible blindness worldwide in the elderly population. In our previous studies, we found that deficiencies in the nuclear factor, erythroid 2 like 2 (NFE2L2) and peroxisome proliferator-activated receptor gamma coactivator 1-α (PGC-1α) genes caused AMD-like pathological phenotypes in mice. In the present work, we show hijacked epithelial-mesenchymal transition (EMT) due to the common loss of PGC-1α and NFE2L2 (double knock-out, dKO) genes in aged animals. The implanted area was assessed by histology, immunohistochemistry and transmission electron microscopy. Confocal microscopy revealed altered regions in the filamentous actin ring. This contrasted with hexagonal RPE morphology in wild-type mice. The ultrastructural RPE features here illustrated loss of apical microvilli, alteration of cell-cell contact, loss of basal in-folding with deposits on Bruch’s membrane, and excessive lipofuscin deposition in dKO samples. We also found the expression of epithelial-mesenchymal transition transcription factors, such as Snail, Slug, collagen 1, vimentin and OB-cadherin, to be significantly different in dKO RPEs. An increased immunoreactivity of senescence markers p16, DEC1 and HMGB1 was also noted. These findings suggest that EMT and senescence pathways may intersect in the retinas of dKO mice. Both processes can be activated by damage to the RPE, which may be caused by increased oxidative stress resulting from the absence of NFE2L2 and PGC-1α genes, important for antioxidant defense. This dKO model may provide useful tools for studying AMD pathogenesis and evaluating novel therapies for this disease.

Published
2021

17. Exposure to Zinc Oxide Nanoparticles Disrupts Endothelial Tight and Adherens Junctions and Induces Pulmonary Inflammatory Cell Infiltration

Author

Shaw-Fang Yet, Pinpin Lin, Chen-Mei Chen, Ming-Hsien Tsai, Pei-Yu Gung, Yen-Chun Ho, Meng-Ling Wu, Igor A. Sobenin, and Alexander N. Orekhov

Subjects
0301 basic medicine, tight junctions, endothelial barrier, Oropharynx, zinc oxide nanoparticles, 010501 environmental sciences, 01 natural sciences, Cell junction, lcsh:Chemistry, Mice, Leukocytes, Claudin-5, lcsh:QH301-705.5, Spectroscopy, Tight junction, Chemistry, General Medicine, Adherens Junctions, Computer Science Applications, Cell biology, medicine.anatomical_structure, medicine.symptom, Zinc Oxide, Infiltration (medical), Blood vessel, Endothelium, pulmonary infiltration, Inflammation, Catalysis, Article, Inorganic Chemistry, Adherens junction, 03 medical and health sciences, Immune system, medicine, Animals, Humans, Physical and Theoretical Chemistry, Molecular Biology, 0105 earth and related environmental sciences, Organic Chemistry, Pneumonia, medicine.disease, 030104 developmental biology, lcsh:Biology (General), lcsh:QD1-999, Zonula Occludens-1 Protein, Blood Vessels, Nanoparticles
Abstract

Zinc oxide nanoparticles (ZnONPs) are frequently encountered nanomaterials in our daily lives. Despite the benefits of ZnONPs in a variety of applications, many studies have shown potential health hazards of exposure to ZnONPs. We have shown that oropharyngeal aspiration of ZnONPs in mice increases lung inflammation. However, the detailed mechanisms underlying pulmonary inflammatory cell infiltration remain to be elucidated. Endothelium functions as a barrier between the blood stream and the blood vessel wall. Endothelial barrier dysfunction may increase infiltration of immune cells into the vessel wall and underlying tissues. This current study examined the effects of ZnONPs exposure on endothelial barriers. ZnONPs exposure increased leukocyte infiltration in the mouse lungs. In endothelial cells, ZnONPs reduced the continuity of tight junction proteins claudin-5 and zonula occludens-1 (ZO-1) at the cell junctions. ZnONPs induced adherens junction protein VE-cadherin internalization from membrane to cytosol and dissociation with &beta, catenin, leading to reduced and diffused staining of VE-cadherin and &beta, catenin at cell junctions. Our results demonstrated that ZnONPs disrupted both tight and adherens junctions, compromising the integrity and stability of the junction network, leading to inflammatory cell infiltration. Thus, ZnONPs exposure in many different settings should be carefully evaluated for vascular effects and subsequent health impacts.

Published
2020

21. Future Aspects of CDK5 in Prostate Cancer: From Pathogenesis to Therapeutic Implications

Author

Oner, Muhammet, primary, Lin, Eugene, additional, Chen, Mei-Chih, additional, Hsu, Fu-Ning, additional, Shazzad Hossain Prince, G M, additional, Chiu, Kun-Yuan, additional, Teng, Chieh-Lin Jerry, additional, Yang, Tsung-Ying, additional, Wang, Hsin-Yi, additional, Yue, Chia-Herng, additional, Yu, Ching-Han, additional, Lai, Chih-Ho, additional, Hsieh, Jer-Tsong, additional, and Lin, Ho, additional

Published
2019
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29. The Prognostic Role of STEAP1 Expression Determined via Immunohistochemistry Staining in Predicting Prognosis of Primary Colorectal Cancer: A Survival Analysis

Author

Lee, Ching-Hsiao, primary, Chen, Sung-Lang, additional, Sung, Wen-Wei, additional, Lai, Hung-Wen, additional, Hsieh, Ming-Ju, additional, Yen, Hsu-Heng, additional, Su, Tzu-Cheng, additional, Chiou, Yu-Hu, additional, Chen, Chia-Yu, additional, Lin, Cheng-Yu, additional, Chen, Mei-Ling, additional, and Chen, Chih-Jung, additional

Published
2016
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