Yin Chen
Assistant Professor, BIO5 Institute
Associate Professor, Pharmacology and Toxicology
Primary Department
(520) 626-4715
Research Interest
Yin Chen, PhD. is an Assistant Professor in Pharmacology and Toxicology in the College of Pharmacy at UA. Dr. Chen’s research focus is on epithelial biology. He was a research faculty in University of California, Davis and an Assistant Investigator in Chemical Industry Institute of Toxicology (former CIIT and later Hamner Institute). His long-term research objective is to understand the dysfunction of airway epithelial mucosa in the pathogenesis of a variety of acute and chronic airway diseases. His current research programs are: a) understanding the molecular mechanisms underlying airway mucous cell development and mucous cell metaplasia in chronic diseases including cancer, COPD and asthma; (b) understanding the function and regulation of novel COPD associated genes and developing novel compounds to treat COPD; (c) understanding the impact of fungal exposure on airway innate immunity and its contribution to the development and exacerbation of asthma. Dr. Chen has more than 30 publications including peer-reviewed research articles, reviews and book chapters. He has served as the PI on one R01, two R21, one Flight Attendant Medical Institute (FAMRI) Innovative Clinical Award and one Arizona Biomedical Research Commission Award. He has also served as co-PI on two R01 and one P01 grants. He has built a long productive track record in studying airway mucus production and respiratory viral infection using primary airway epithelial cell model. He routinely cultivate and use primary epithelial cells from eye, salivary gland, airway surface and submucosal gland in different species (e.g. human, monkey, pig, rat and mouse) as our in vitro model to study mucin genes. The differentiated primary culture model demonstrates pseudostratified morphology, is composed of ciliated, non-ciliated, and goblet cells, and has a transepithelial barrier with high electro-resistance. He has also established in vivo exposure system to study the pulmonary effect of the exposure to particulates, pathogens and gases. Using this system, he has developed various airway disease models including CS-induced COPD model, ovalbumin-induced asthma model, fungal-induced asthma model and several infection models such as H1N1, rhinovirus, Aspergillus, and Alternaria.


Deng, J., Chen, Y., & Reen, W. u. (2000). Induction of cell cornification and enhanced squamous-cell marker SPRR1 gene expression by phorbol ester are regulated by different signaling pathways in human conducting airway epithelial cells. American Journal of Respiratory Cell and Molecular Biology, 22(5), 597-603.

PMID: 10783132;Abstract:

Phorbol ester is a strong inducer for both cell cornification and squamous-cell marker SPRR1 gene expression in conducting airway epithelial cells. However, the signaling pathways involved in the regulation of both events have not been completely elucidated. The current study focuses on the common and divergent pathways involved in the induction of these two activities by phorbol-13-myristate-12-acetate (PMA). Using a protein kinase (PK) C inhibitor, bisindolylmaleimide I, PMA-induced cell cornification and SPRR1 gene expression were abolished. Further, a PKC activator, indolactam V, induced cell cornification in the absence of PMA treatment. These results suggest a PKC-dependent signaling pathway for both gene induction and enhanced cell cornification by PMA. However, a mitogen-activated protein kinase-specific inhibitor, PD98059, could only block the gene induction event but failed to prevent cell cornification induced by PMA. These results suggest that diverse signaling pathways after PKC activation by PMA are involved in the regulation of these two events.

Lee, W., Chen, Y., Wang, W., & Mosser, A. (2015). Infectivity assays of human rhinovirus-A and -B serotypes. Methods in molecular biology (Clifton, N.J.), 1221, 71-81.

Infectivity is a fundamental property of viral pathogens such as human rhinoviruses (HRVs). This chapter describes two methods for measuring the infectivity of HRV-A and -B serotypes: end point dilution (TCID50) assay and plaque assay. End point dilution assay is a quantal, not quantitative, assay that determines the dilution of the sample at which 50 % of the aliquots have infectious virus. It can be used for all the HRV-A and -B serotypes and related clinical isolates that grow in cell culture and induce cytopathic effect (CPE), degenerative changes in cells that are visible under a microscope. Plaque assay is a quantitative assay that determines the number of infectious units of a virus in a sample. After an infectious unit of virus infects one cell, the infected cell produces progeny viruses that then infect and kill a circle of adjacent cells. This circle of dead cells detaches from the dish and thus leaves a clear hole in a cell monolayer. Plaque assay works only for HeLa-adapted HRV-A and -B serotypes that can make visible plaques on the cell monolayer. Currently the end point dilution assay and plaque assay have not been developed for the newly discovered HRV-C.

Kao, C. Y., Chen, Y., Zhao, Y. H., & Reen, W. u. (2003). ORFeome-based search of airway epithelial cell-specific novel human β-defensin genes. American Journal of Respiratory Cell and Molecular Biology, 29(1), 71-80.

PMID: 12600824;Abstract:

β-Defensin is one of the major host defense shields produced by various tissues and organs against microbial infection. To date, four human β-defensins (DEFBs) gene products that share a consensus six-cysteine motif have been discovered. The hidden Markov model (HMM) profile was constructed from the common features of those known β-defensin peptides to search for additional novel DEFB genes. A genome-wide search of the profile against ORFeome-based peptide databases (e.g., Ensembl project) led to the identification of six new DEFB members that also shared the conserved six-cysteine motif. Phylogenetic analysis supported a close relationship of these six new members with existing DEFB genes. Polymerase Chain Reaction studies of human tissue cDNA panels confirmed the expression of all six novel DEFB genes in various tissues. Two of them, DEFB106 and DEFB109, were expressed in the lung. A pilot study with cRNA probes for in situ hybridization and a synthetic propeptide for the functional characterization demonstrated the tissue-/ cell-specific expression and the strong antimicrobial activity of DEFB106. These results support the utility of ORFeome-based HMM search in gene discovery for members of a specific gene family. The novel DEFB genes identified in this study may significantly contribute to overall antimicrobial host defenses.

Dongfang, Y. u., Walters, D. M., Zhu, L., Lee, P., & Chen, Y. (2011). Vanadium pentoxide (V2O5) induced mucin production by airway epithelium. American Journal of Physiology - Lung Cellular and Molecular Physiology, 301(1), 31-39.

PMID: 21531775;PMCID: PMC3129903;Abstract:

Exposure to environmental pollutants has been linked to various airway diseases and disease exacerbations. Almost all chronic airway diseases uch as chronic obstructive pulmonary disease and asthma are aused by complicated interactions between gene and environment. ne of the major hallmarks of those diseases is airway mucus verproduction (MO). Excessive mucus causes airway obstruction and significantly increases morbidity and mortality. Metals are major components of environmental particulate matters (PM). Among them, vanadium has been suggested to play an important role in PM-induced mucin production. Vanadium pentoxide (V2O5) is the most common commercial source of vanadium, and it has been associated with occupational chronic bronchitis and asthma, both of which are MO diseases. However, the underlying mechanism is not entirely clear. In this study, we used both in vitro and in vivo models to demonstrate the robust inductions of mucin production by V2O5. Furthermore, the follow-up mechanistic study revealed a novel v-raf-1 murine leukemia viral oncogene homolog 1-IKK-NF-κB pathway that mediated V2O5- induced mucin production. Most interestingly, the reactive oxygen species and the classical mucin-inducing epidermal growth factor receptor (EGFR)-MAPK pathway appeared not to be involved in this process. Thus the V2O5-induced mucin production may represent a novel EGFR-MAPK-independent and environmental toxicant-associated MO model. Complete elucidation of the signaling pathway in this model will not only facilitate the development of the treatment for V2O5-associated occupational diseases but also advance our understanding on the EGFR-independent mucin production in other chronic airway diseases. © 2011 the American Physiological Society.

Chen, Y., Zhao, Y. H., & Reen, W. u. (2001). In silico cloning of mouse Muc5b gene and upregulation of its expression in mouse asthma model. American Journal of Respiratory and Critical Care Medicine, 164(6), 1059-1066.

PMID: 11587997;Abstract:

Using a BLAST-searching approach, we identified a mouse expressed sequence tag (EST) clone (AA038672) showing great similarity to the 3′ end of the human MUC5B gene. The clone was named "3pmmuc5b-1" after complete nucleotide sequencing (Genbank Accession, AF369933). A subsequent search of the mouse genome database with the 3pmmuc5b-1 sequence identified two overlapping genomic clones (AC020817 and AC020794) that contained the sequence of both 3pmmuc5b-1 and the mouse Muc5ac gene. Like their human homologs, the genomic order of the mouse Muc genes is 5′-Muc5ac-Muc5b-3′. These results suggest that the newly identified EST clone, 3pmmuc5b-1, is part of the 3′ portion of the mouse Muc5b gene. In situ hybridization demonstrated that this putative mouse Muc5b message was expressed in a restricted manner in the sublingual gland region of the tongue and the submucosal gland region of the mouse trachea in a normal animal. However, the gene expression was greatly enhanced in airway surface epithelium and the submucosal gland region in ovalbumin-induced asthmatic mice. These results were consistent with previous studies of human airway tissues. We therefore conclude that this newly cloned mouse Muc5b gene could be used as a marker for studying aberrant mucin gene expression in mouse models of various airway diseases.