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Chen, Hong

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Chen, Hong

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2017 - 20194

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Author's Publications: search.filters.isAuthorOfPublication.a4aa84d3-92cf-41c9-ad74-1b11c7bc800b

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Now showing 1 - 4 of 4
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    Cardiotoxicity of Anticancer Therapeutics
    (Frontiers Media S.A., 2018) Dong, Jerry; Chen, Hong
    As cancer therapeutics continues to improve and progress, the adverse side effects associated with anticancer treatments have also attracted more attention and have become extensively explored. Consequently, the importance of posttreatment follow-ups is becoming increasingly relevant to the discussion. Contemporary treatment methods, such as tyrosine kinase inhibitors, anthracycline chemotherapy, and immunotherapy regimens are effective in treating different modalities of cancers; however, these reagents act through interference with DNA replication or prevent DNA repair, causing endothelial dysfunction, generating reactive oxygen species, or eliciting non-specific immune responses. Therefore, cardiotoxic effects, such as hypertension, heart failure, and left ventricular dysfunction, arise posttreatment. Rising awareness of cardiovascular complications has led to meticulous attention for the evolution of treatment strategies and carefully monitoring between enhanced treatment effectiveness and minimization of adverse toxicity to the cardiovasculature, in which psychological assessments, early detection methods such as biomarkers, magnetic resonance imaging, and various drugs to reverse the damage from cardiotoxic events are more prevalent and their emphasis has increased tremendously. Fully understanding the mechanisms by which the risk factors action for various patients undergoing cancer treatment is also becoming more prevalent in preventing cardiotoxicity down the line.
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    Mimetic peptide of ubiquitin-interacting motif of epsin as a cancer therapeutic-perspective in brain tumor therapy through regulating VEGFR2 signaling
    (2018) Dong, Yunzhou; Wu, Hao; Dong, Jerry; Song, Kai; Rahman, Habibunnabi Ashiqur; Towner, Rheal; Chen, Hong
    Epsins, endocytic adaptor proteins required for internalization of ubiquitylated receptors, are generally upregulated in human cancers. It has been characterized that mice deficient of epsins in the endothelium inhibit tumor growth by dysregulating vascular endothelial growth factor receptor-2 (VEGFR2) signaling and non-productive tumor angiogenesis. Binding of the epsin ubiquitin (Ub)-interacting motif (UIM) with ubiquitylated VEGFR2 is a critical mechanism for epsin-dependent VEGFR2 endocytosis and degradation, indicative of epsin UIM as a potential therapeutic target. A Computer Assisted Drug Design approach was utilized to create the UIM mimetic peptides for the functional competition of epsin binding sites in ubiquitylated VEGFR2 in vivo. Specifically targeting VEGFR2 in the tumor vasculature, the chemically synthesized chimeric UIM peptide, UPI, causes non-functional tumor angiogenesis, retards tumor growth, and increases survival rates in several tumor models. The authors showed that UPI binds ubiquitylated VEGFR2 to form a supercomplex in an Ub-dependent fashion. Collectively, the UPI targeting strategy offers a potentially novel treatment for cancer patients who are resistant to current anti-angiogenic therapies. In this review, the authors outline the main points of this research specifically as a potential application for glioma tumor therapy.
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    Eating the Dead to Keep Atherosclerosis at Bay
    (Frontiers Media S.A., 2017) Brophy, Megan L.; Dong, Yunzhou; Wu, Hao; Rahman, H. N. Ashiqur; Song, Kai; Chen, Hong
    Atherosclerosis is the primary cause of coronary heart disease (CHD), ischemic stroke, and peripheral arterial disease. Despite effective lipid-lowering therapies and prevention programs, atherosclerosis is still the leading cause of mortality in the United States. Moreover, the prevalence of CHD in developing countries worldwide is rapidly increasing at a rate expected to overtake those of cancer and diabetes. Prominent risk factors include the hardening of arteries and high levels of cholesterol, which lead to the initiation and progression of atherosclerosis. However, cell death and efferocytosis are critical components of both atherosclerotic plaque progression and regression, yet, few currently available therapies focus on these processes. Thus, understanding the causes of cell death within the atherosclerotic plaque, the consequences of cell death, and the mechanisms of apoptotic cell clearance may enable the development of new therapies to treat cardiovascular disease. Here, we review how endoplasmic reticulum stress and cholesterol metabolism lead to cell death and inflammation, how dying cells affect plaque progression, and how autophagy and the clearance of dead cells ameliorates the inflammatory environment of the plaque. In addition, we review current research aimed at alleviating these processes and specifically targeting therapeutics to the site of the plaque.
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    Atypical Behaviour and Connectivity in SHANK3-Mutant Macaques
    (Springer Science and Business Media LLC, 2019-06) Zhou, Yang; Sharma, Jitendra; Yuan, Jingli; Chen, Hong; Aida, Tomomi; Yan, Ting; Zou, Ying; Xu, Dongdong; Parmar, Shivangi; Fanucci-Kiss, Adrian; Wang, Dongqing; Huang, Yan; Li, Yaqing; Bai, Yanyang; Ji, Wenjing; Lai, Xinqiang; Li, Weiqiang; Huang, Lihua; Lu, Zhonghua; Wang, Liping; Anteraper, Sheeba A.; Sur, Mriganka; Zhou, Huihui; Xiang, Andy Peng; Desimone, Robert; Feng, Guoping; Yang, Shihua; Ke, Qiong; Landman, Rogier; Hayden, David; Fisher, John; Jiang, Mingqing; Hyman, Julia; Meisner, Olivia; Menegas, William
    Mutation or disruption of the SHANK3 (SH3 domain and ankyrin repeat) gene represents a highly penetrant, monogenic risk-factor for Autism Spectrum Disorder (ASD) and is a cause of Phelan–McDermid syndrome (PMS). Recent advances in gene editing have enabled the creation of genetically engineered non-human primate (NHPs) models, which might better approximate the behavioral and neural abnormalities of ASD than rodent models and lead to more effective treatments. Here, we report CRISPR/Cas9-mediated generation of germline transmissible cynomolgus macaques and their F1 offspring carrying SHANK3 mutations. Genotyping of somatic cells and brain biopsies confirmed mutations in the SHANK3 gene and reduced SHANK3 proteins. Analysis of fMRI data revealed altered local and global connectivity patterns indicative of circuit abnormalities. The founder mutants exhibited sleep disturbances, motor deficits, and increased repetitive behaviors, as well as social and learning impairments. Together, these results parallel some aspects of the gene-circuit-behavior dysfunction in human ASD and PMS.