Publications by authors named "Wenyu Su"

6 Publications

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Comparative Analysis of Chemical Constituents in Different Parts of Lotus by UPLC and QToF-MS.

Molecules 2021 Mar 25;26(7). Epub 2021 Mar 25.

School of Pharmaceutical Sciences, Jilin University, Fujin Road 1266, Changchun 130021, China.

Six parts of lotus (seeds, leaves, plumule, stamens, receptacles and rhizome nodes) are herbal medicines that are listed in the Chinese Pharmacopoeia. Their indications and functions have been confirmed by a long history of clinical practice. To fully understand the material basis of clinical applications, UPLC-QToF-MS combined with the UNIFI platform and multivariate statistical analysis was used in this study. As a result, a total of 171 compounds were detected and characterized from the six parts, and 23 robust biomarkers were discovered. The method can be used as a standard protocol for the direct identification and prediction of the six parts of lotus. Meanwhile, these discoveries are valuable for improving the quality control method of herbal medicines. Most importantly, this was the first time that alkaloids were detected in the stamen, and terpenoids were detected in the cored seed. The stamen is a noteworthy part because it contains the greatest diversity of flavonoids and terpenoids, but research on the stamen is rather limited.
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http://dx.doi.org/10.3390/molecules26071855DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8036816PMC
March 2021

γδ T Cells Promote Steatohepatitis by Orchestrating Innate and Adaptive Immune Programming.

Hepatology 2020 02 31;71(2):477-494. Epub 2019 Dec 31.

Department of Surgery, S.A. Localio Laboratory, New York University School of Medicine, New York, NY.

Background And Aims: The recruitment and activation of inflammatory cells in the liver delineates the transition from hepatic steatosis to steatohepatitis (SH).

Approach And Results: We found that in SH, γδT cells are recruited to the liver by C-C chemokine receptor (CCR) 2, CCR5, and nucleotide-binding oligomerization domain-containing protein 2 signaling and are skewed toward an interleukin (IL)-17A phenotype in an inducible costimulator (ICOS)/ICOS ligand-dependent manner. γδT cells exhibit a distinct Vγ4 , PD1 , Ly6C CD44 phenotype in SH. Moreover, γδT cells up-regulate both CD1d, which is necessary for lipid-based antigens presentation, and the free fatty acid receptor, CD36. γδT cells are stimulated to express IL-17A by palmitic acid and CD1d ligation. Deletion, depletion, and targeted interruption of γδT cell recruitment protects against diet-induced SH and accelerates disease resolution.

Conclusions: We demonstrate that hepatic γδT cells exacerbate SH, independent of IL-17 expression, by mitigating conventional CD4 T-cell expansion and modulating their inflammatory program by CD1d-dependent vascular endothelial growth factor expression.
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http://dx.doi.org/10.1002/hep.30952DOI Listing
February 2020

Targeting SYK signaling in myeloid cells protects against liver fibrosis and hepatocarcinogenesis.

Oncogene 2019 06 11;38(23):4512-4526. Epub 2019 Feb 11.

S.A. Localio Laboratory, Departments of Surgery, New York University School of Medicine, 450 East 29th Street, New York, NY, 10016, USA.

Liver fibrosis and fibrosis-associated hepatocarcinogenesis are driven by chronic inflammation and are leading causes of morbidity and death worldwide. SYK signaling regulates critical processes in innate and adaptive immunity, as well as parenchymal cells. We discovered high SYK expression in the parenchymal hepatocyte, hepatic stellate cell (HSC), and the inflammatory compartments in the fibrotic liver. We postulated that targeting SYK would mitigate hepatic fibrosis and oncogenic progression. We found that inhibition of SYK with the selective small molecule inhibitors Piceatannol and PRT062607 markedly protected against toxin-induced hepatic fibrosis, associated hepatocellular injury and intra-hepatic inflammation, and hepatocarcinogenesis. SYK inhibition resulted in increased intra-tumoral expression of the p16 and p53 but decreased expression of Bcl-xL and SMAD4. Further, hepatic expression of genes regulating angiogenesis, apoptosis, cell cycle regulation, and cellular senescence were affected by targeting SYK. We found that SYK inhibition mitigated both HSC trans-differentiation and acquisition of an inflammatory phenotype in T cells, B cells, and myeloid cells. However, in vivo experiments employing selective targeted deletion of SYK indicated that only SYK deletion in the myeloid compartment was sufficient to confer protection against fibrogenic progression. Targeting SYK promoted myeloid cell differentiation into hepato-protective TNFα CD206 phenotype downregulating mTOR, IL-8 signaling and oxidative phosphorylation. Collectively, these data suggest that SYK is an attractive target for experimental therapeutics in treating hepatic fibrosis and oncogenesis.
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http://dx.doi.org/10.1038/s41388-019-0734-5DOI Listing
June 2019

RIP1 Kinase Drives Macrophage-Mediated Adaptive Immune Tolerance in Pancreatic Cancer.

Cancer Cell 2018 11;34(5):757-774.e7

S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 435 East 30th Street, 4th Floor, New York, NY 10016, USA.

Pancreatic ductal adenocarcinoma (PDA) is characterized by immune tolerance and immunotherapeutic resistance. We discovered upregulation of receptor-interacting serine/threonine protein kinase 1 (RIP1) in tumor-associated macrophages (TAMs) in PDA. To study its role in oncogenic progression, we developed a selective small-molecule RIP1 inhibitor with high in vivo exposure. Targeting RIP1 reprogrammed TAMs toward an MHCIITNFαIFNγ immunogenic phenotype in a STAT1-dependent manner. RIP1 inhibition in TAMs resulted in cytotoxic T cell activation and T helper cell differentiation toward a mixed Th1/Th17 phenotype, leading to tumor immunity in mice and in organotypic models of human PDA. Targeting RIP1 synergized with PD1-and inducible co-stimulator-based immunotherapies. Tumor-promoting effects of RIP1 were independent of its co-association with RIP3. Collectively, our work describes RIP1 as a checkpoint kinase governing tumor immunity.
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http://dx.doi.org/10.1016/j.ccell.2018.10.006DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6836726PMC
November 2018

Upregulation of ASAP3 contributes to colorectal carcinogenesis and indicates poor survival outcome.

Cancer Sci 2017 Aug 14;108(8):1544-1555. Epub 2017 Jun 14.

Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai Institute of Digestive Disease, Shanghai Jiao Tong University, Shanghai, China.

The function and clinical implication of ArfGAP with SH3 domain, ankyrin repeat, and PH domain 3 (ASAP3) in colorectal cancer (CRC) remains undefined. In the present study, we showed that the expression level of ASAP3 was dramatically increased in CRC and its upregulation was associated with American Joint Committee on Cancer stage (P < 0.001) and poor prognosis (P = 0.0022). The combination of stage and ASAP3 expression improved the prediction of survival in CRC patients. Suppression of ASAP3 inhibited cell proliferation by inducing G phase arrest without influencing apoptosis. ASAP3 promoted growth of colon tumors in mice with colitis, and accelerated cell invasion and migration in vitro. Increased ASAP3 was associated with activation of the nuclear factor-κB (NF-κB) canonical pathway in CRC. Upregulation of ASAP3 increased the phosphorylation and nuclear translocation of the p65 NF-κB subunit. Mechanistically, ASAP3 interacts with NF-κB essential modulator (NEMO) and could reduce the polyubiquitinylation of NEMO. Overall, ASAP3 might regulate NF-κB via binding to NEMO. ASAP3 acts as an oncogene in colonic cancer and could be a potential biomarker of colon carcinogenesis.
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http://dx.doi.org/10.1111/cas.13281DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5543456PMC
August 2017
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