Publications by authors named "Yunpeng Tian"

11 Publications

  • Page 1 of 1

Corrigendum: Galectin-3 inhibition attenuates doxorubicin-induced cardiac dysfunction by upregulating the expression of peroxiredoxin-4.

Can J Physiol Pharmacol 2021 Mar 9;99(3):348. Epub 2021 Mar 9.

Department of Cardiology, Tongji Hospital of Tongji University, Shanghai 200003, People's Republic of China.

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http://dx.doi.org/10.1139/cjpp-2020-0752DOI Listing
March 2021

Sodium Houttuyfonate Ameliorates -amyloid-Induced Memory Impairment and Neuroinflammation through Inhibiting the NLRP3/GSDMD Pathway in Alzheimer's Disease.

Mediators Inflamm 2021 31;2021:8817698. Epub 2021 May 31.

Department of Pharmacy, Dongying People's Hospital, Dongying, Shandong 257091, China.

Objective: Our research is designed to explore the function of sodium houttuyfonate (SH) on Alzheimer's disease (AD) and its potential molecular mechanisms.

Methods: In our study, the Morris water maze (MWM) test was used to assess the role of SH on spatial learning and memory deficiency in amyloid- peptide (A)-induced AD mice. We explored the functions of SH on proinflammatory cytokines, neuron apoptosis, and damage and by using an enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (qRT-PCR), flow cytometry, western blot, and Nissl staining. Moreover, the effect of SH on oxidative stress and was also detected. To explore the underlying molecular mechanisms of SH on AD, the expressions of proteins and mRNA involved in the NOD-like receptor pyrin domain containing-3/gasdermin D (NLRP3/GSDMD) pathway were determined using western blot, immunofluorescence staining, and qRT-PCR.

Results: Our data demonstrated that SH ameliorated spatial learning and memory deficiency in A -induced AD mice. Moreover, SH significantly improved hippocampal neuron damage and inhibited oxidative stress, neuroinflammation, and neuron apoptosis in A -induced AD mice and PC12 cells. The results also revealed that SH protected A -induced AD through inhibiting the NLRP3/GSDMD pathway.

Conclusion: The present study demonstrated that SH could ameliorate A -induced memory impairment neuroinflammation and pyroptosis through inhibiting the NLRP3/GSDMD pathway in AD, suggesting that SH may be a potential candidate for AD treatment.
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http://dx.doi.org/10.1155/2021/8817698DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8195664PMC
May 2021

Equipping Natural Killer Cells with Cetuximab through Metabolic Glycoengineering and Bioorthogonal Reaction for Targeted Treatment of KRAS Mutant Colorectal Cancer.

ACS Chem Biol 2021 04 8;16(4):724-730. Epub 2021 Apr 8.

Department of Chemistry and Biomedical Engineering, Institute for Quantitative Health Science and Engineering, Michigan State University, East Lansing, Michigan 48824, United States.

While Cetuximab can be used to treat KRAS wild-type colon cancer cells by targeting EGFR and inhibiting the activation of downstream signaling pathways, it exhibits little therapeutic effect on KRAS mutant colon cancer cells. Natural killer (NK) cells are a class of powerful immune cells with anticancer activities. However, NK cells typically lack inherent tumor targeting abilities. Here, a new method is established to bestow NK-92 cells with tumor targeting abilities by installing cetuximab on the cell surface. Through metabolic glycoengineering, azide groups were introduced onto the surface of NK-92 cells. Bioorthogonal strain promoted the azide-alkyne cycloaddition click reaction of engineered NK-92 cells with alkyne modified cetuximab functionalized NK cells with the antibody. The resulting NK-92 cells were significantly more effective than the parent NK-92 cells in protecting against tumor development in a KRAS mutant mouse tumor model resistant to cetuximab treatment. Thus, NK cell functionalization with antibodies enabled by metabolic glycoengineering is a promising strategy to enhance anticancer immune therapy.
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http://dx.doi.org/10.1021/acschembio.1c00022DOI Listing
April 2021

Galectin-3 inhibition attenuates doxorubicin-induced cardiac dysfunction by upregulating the expression of peroxiredoxin-4.

Can J Physiol Pharmacol 2020 Oct 9;98(10):700-707. Epub 2020 Jun 9.

Department of Cardiology, Tongji Hospital of Tongji University, Shanghai 200003, People's Republic of China.

Doxorubicin (DOX) is a highly efficient chemotherapeutic drug limited by its cardiotoxicity. Galectin-3 (Gal-3) overexpression is associated with several cardiovascular diseases. In this study, the in vivo models of DOX-treated rats and the in vitro model of DOX-treated H9C2 cells were used. DOX induced cardiac injury and dysfunction accompanied with the upregulation of Gal-3 at the end of the experiment, while inhibition of Gal-3 with modified citrus pectin (MCP) exhibited a dramatic improvement in cardiac function of the DOX-treated rats, as manifested by increased left ventricular systolic pressure and ±d/d and decreased left ventricular end-diastolic pressure. The plasma levels of myocardial injury markers such as lactate dehydrogenase, creatine kinase, creatine kinase-MB, and cardiac troponin I were decreased after MCP treatment. In parallel, MCP attenuated myocardial tissue markers of oxidative stress such as hydrogen peroxide and malondialdehyde restored the activities of superoxide dismutase, catalase, and glutathione peroxidase and upregulated antioxidant peroxiredoxin-4 (Prx-4). To further verify the role of Prx-4, it was downregulated by siRNA-mediated knockdown in H9C2 cells. MCP could not reverse DOX-induced oxidative stress in Prx-4-knock-down cells. In conclusion, Gal-3 mediated DOX-induced cardiotoxicity and Gal-3 inhibition attenuated DOX-induced cardiac dysfunction by upregulating the expression of Prx-4 to reduce myocardial oxidative stress.
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http://dx.doi.org/10.1139/cjpp-2019-0700DOI Listing
October 2020

Synthesis of a New Water-Soluble Melatonin Derivative with Low Toxicity and a Strong Effect on Sleep Aid.

ACS Omega 2020 Mar 16;5(12):6494-6499. Epub 2020 Mar 16.

Cancer Research Center, Medical School, Xiamen University, Xiamen 361005, China.

A new melatonin sulfonate derivative sodium 4-(3-(2-acetamidoethyl)-5-methoxy-1-indol-1-yl) butane-1-sulfonate (MLTBS) with higher water solubility (695 times) and lower cytotoxicity than natural melatonin (MLT) was synthesized, yet with the same sleep aid function. The poor solubility of MLT in water has been improved with a simple chemical reaction, which solves the poor solubility of melatonin in water, overcoming the safety problem caused by adding organic reagents such as dimethyl sulfoxide (DMSO) and ethanol to increase the solubility. Moreover, the modified MLT still has the same sleep aid effect as the natural MLT and higher biological safety. As a novel potential drug for sleep aid, the new MLT derivative could also flourish the application and research of this molecule in medicine and biology.
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http://dx.doi.org/10.1021/acsomega.9b04120DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7114735PMC
March 2020

Glycoengineering of Natural Killer Cells with CD22 Ligands for Enhanced Anticancer Immunotherapy.

ACS Cent Sci 2020 Mar 5;6(3):382-389. Epub 2020 Mar 5.

Departments of Chemistry and Biomedical Engineering, Institute for Quantitative Health Science and Engineering, Michigan State University, East Lansing, Michigan 48824, United States.

Adoptive transfer of immune cells is being actively pursued for cancer treatment. Natural killer (NK) cells, a class of cytotoxic immune cells, generally lack inherent selectivities toward cancer. To bestow tumor-targeting abilities and enhance anticancer efficacy, a new strategy is established to glycoengineer NK cells. Carbohydrate-based ligands for CD22, a marker for B cell lymphoma, are introduced onto NK cells through either metabolic engineering or glyco-polymer insertion. Such NK cells exhibited greatly enhanced cytotoxicities toward CD22 lymphoma cells in a CD22-dependent manner. Importantly, both CD22 lymphoma cell lines and primary lymphoma cells from human cancer patients can be effectively killed by the engineered NK cells. Furthermore, glycoengineered NK cells provided significant protection to tumor-bearing mice. Thus, NK cell glycoengineering is an exciting new approach for cancer treatment complementing the current immune cell genetic engineering strategy.
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http://dx.doi.org/10.1021/acscentsci.9b00956DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7099595PMC
March 2020

LATS2 promotes cardiomyocyte H9C2 cells apoptosis via the Prx3-Mfn2-mitophagy pathways.

J Recept Signal Transduct Res 2019 Oct-Dec;39(5-6):470-478. Epub 2019 Dec 12.

Department of Cardiology, Shanghai Tongji Hospital, Shanghai, China.

The pathogenesis of cardiomyocyte death is closely associated with mitochondrial homeostasis poorly understood mechanisms. The aim of our study is to explore the contribution of large tumor suppressor kinase 2 (LATS2) to the apoptosis of cardiomyocyte H9C2 cells. Adenovirus-mediated LATS2 overexpression was carried out in H9C2 cells. The cell viability and apoptosis rate were measured an MTT assay, TUNEL staining, western blotting, an ELISA, and an LDH release assay. Mitophagy was quantified using immunofluorescence and western blotting. The overexpression of LATS2 in H9C2 cells drastically promoted cell death. Molecular investigations showed that LATS2 overexpression was associated with mitochondrial injury, as evidenced by increased mitochondrial ROS production, reduced antioxidant factor levels, increased cyt-c liberation into the nucleus and activated mitochondrial caspase-9-dependent apoptotic pathway activity. Furthermore, our results demonstrated that LATS2-mediated mitochondrial malfunction by repressing mitophagy and that the reactivation of mitophagy could sustain mitochondrial integrity and homeostasis in response to LATS2 overexpression. Furthermore, we found that LATS2 inhibited mitophagy by inactivating the Prx3-Mfn2 axis. The reactivation of Prx3-Mfn2 pathways abrogated the LATS2-mediated inhibition of mitochondrial apoptosis in H9C2 cells. The overexpression of LATS2 induces mitochondrial stress by repressing protective mitophagy in a manner dependent on Prx3-Mfn2 pathways, thus reducing the survival of H9C2 cells.
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http://dx.doi.org/10.1080/10799893.2019.1701031DOI Listing
June 2020

Redirecting immunity covalently incorporated immunogenic sialic acid on the tumor cell surface.

Chem Sci 2016 Jun 24;7(6):3737-3741. Epub 2016 Feb 24.

State Key Laboratory for Physical Chemistry of Solid Surfaces , Department of Chemical Biology , College of Chemistry and Chemical Engineering , The Key Laboratory for Chemical Biology of Fujian Province , The MOE Key Laboratory of Spectrochemical Analysis & Instrumentation, and Innovation Center for Cell Signaling Network , Xiamen University , Xiamen , 361005 , China . Email: ; Tel: +86-0592-2181728.

Techniques eliciting anti-tumor immunity are of interest for immunotherapy. We herein report the covalent incorporation of a non-self immunogen into the tumor glycocalyx by metabolic oligosaccharide engineering with 2,4-dinitrophenylated sialic acid (Sia). This enables marked suppression of pulmonary metastasis and subcutaneous tumor growth of B16F10 melanoma cells in mice preimmunized to produce anti-DNP antibodies. Located on the exterior glycocalyx, Sia is well-positioned to recruit antibodies. Given the high levels of natural anti-DNP antibodies in humans and ubiquitous sialylation across many cancers, Sia offers a simplified route to redirect immunity against diverse tumors without recourse to preimmunization.
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http://dx.doi.org/10.1039/c5sc04133cDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6008587PMC
June 2016

Optical tracking of phagocytosis with an activatable profluorophore metabolically incorporated into bacterial peptidoglycan.

Anal Chem 2015 Aug 5;87(16):8381-6. Epub 2015 Aug 5.

Phagocytosis is critical for immunity against pathogens. Prior imaging using dye-labeled synthetic beads or green fluorescent protein-expressing bacteria is limited by "always-on" signals which compromise discerning phagocytosed particles from adherent particles. Targeting cellular internalization of pathogens into acidic phagolysosomes, we herein report "turn-on" fluorescence imaging of phagocytosis with viable bacteria featuring peptidoglycans covalently modified with rhodamine-lactam responsive to acidic pH. Culturing of Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus) with d-lysine conjugated rhodamine-lactam and fluorescein isocyanate (FITC) leads to efficient metabolic incorporation of FITC and rhodamine-lactam into bacterial peptidoglycan. E. coli and S. aureus become red-emissive upon phagocytosis into Raw 264.7 macrophages. With FITC as the reference signal, the mono- and dual-color emission allow efficient in situ distinction of ingested bacteria from extracellular bacteria. Given the ease of optical peptidoglycan labeling, the prevalence of microbial peptidoglycan and preservation of microbial surface landscape, this approach would be of use for investigation on microbial pathogenesis and high-throughput screening of immunomodulators of phagocytosis.
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http://dx.doi.org/10.1021/acs.analchem.5b01633DOI Listing
August 2015

A fluorescently labelled sialic acid for high performance intraoperative tumor detection.

Biomater Sci 2014 Aug 1;2(8):1120-1127. Epub 2014 May 1.

Department of Chemical Biology, College of Chemistry and Chemical Engineering, The Key Laboratory for Chemical Biology of Fujian Province, The MOE Key Laboratory of Spectrochemical Analysis & Instrumentation, and Innovation Center for Cell Biology, Xiamen University, Xiamen, 361005, China.

Surgical resection is widely used for tumor treatment, necessitating approaches for the precise locating of elusive tumor foci. We report the high performance detection of tumors in mice with fluorescein-isothiocyanate (FITC) labelled sialic acid (FITC-SA), a fluorescent monosaccharide with low cytoxicity. Analysis of mice intravenously injected with FITC-SA revealed high target-to-background fluorescence ratios in subcutaneous tumors and liver tumor implants with 0.2-5 mm diameters, which are significantly below the clinical threshold of minimal residual cancer (∼1 cm clearance). Extracellular FITC-SA is quickly cleared from circulation whereas the intracellular FITC-SA could be metabolically incorporated into glycoproteins via a cellular sialylation pathway. Compared with FITC-SA-laden nanoparticles, free FITC-SA is preferentially and quickly taken up by tumors in mice and displays high tumor-to-background signal contrast, suggesting the potential for fluorescence directed surgical ablation of tumors.
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http://dx.doi.org/10.1039/c4bm00028eDOI Listing
August 2014

A targetable acid-responsive micellar system for signal activation based high performance surgical resolution of tumors.

Biomater Sci 2014 Jul 21;2(7):972-979. Epub 2014 Feb 21.

Department of Chemical Biology, College of Chemistry and Chemical Engineering, The Key Laboratory for Chemical Biology of Fujian Province, The MOE Key Laboratory of Spectrochemical Analysis & Instrumentation, and Innovation Center for Cell Biology, Xiamen University, Xiamen, 361005, China.

Tumor-reporting probes are valuable to guide surgical resection of tumor foci elusive to visual inspection. As tumors display distinct arrays of lectins, we herein report the construction and screening of a panel of glycan-displaying smart micelles for tumor illumination in mice. These micelles consist of cores of rhodamine-sultam (RST) responsive to lysosomal acidity and a corona of poly[styrene-alter-(maleic acid)] glycosylated with d-glucosamine, d-mannosamine or d-galactosamine. These nanoscale micelles are nonfluorescent extracellularly and become luminescent within acidic lysosomes, enabling optical tracking of tumor endocytosis of the micelles. In vivo screening revealed high-efficiency uptake and fluorescence activation of galactosylated micelles ([email protected]) by subcutaneous tumor and disseminated liver tumor foci with diameters of 0.1-10 mm, which is significantly below minimal residual cancer (a minimum of 1 cm clearance). This system is readily adapted to illuminate different tumors by expanding the diversity of glycans on the shell. Given the robustness and high performance of this system, lectin-targeted responsive micelles are attractive for diagnosis or surgical ablation of tumors.
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http://dx.doi.org/10.1039/c4bm00007bDOI Listing
July 2014
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