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Institute for Translational Medicine and Science

Home / Faculty / Joseph Jude, B.V.Sc., Ph.D.

Joseph Jude, B.V.Sc., Ph.D.

Joseph Jude, B.V.Sc., Ph.D.

Assistant Research Professor, Department of Pharmacology & Toxicology, Ernest Mario School of Pharmacy

Assistant Professor, Department of Pharmacology, Robert Wood Johnson Medical School

Rutgers Institute for Translational Medicine and Science
Child Health Institute of New Jersey
Rutgers, The State University of New Jersey
89 French Street
New Brunswick, NJ 08901

(732) 235-8057
Fax: (732) 235-7178
joseph.antonyjude@rutgers.edu

Education

Ph.D., University of Minnesota, St. Paul, MN
B.V.Sc., University of Peradeniya, Sri Lanka

Postdoctoral Fellowship

University of Pennsylvania, Philadelphia, PA
University of Minnesota, St Paul, MN

Airway smooth muscle (ASM) cells contribute to asthma pathology through their synthetic and mechanical (contractile) functions. Dr. Jude is interested in the molecular and cellular signaling mechanisms of ASM cells in airway disorders such as asthma. His current research focus is on the mechanisms of airway hypersensitivity exacerbation by environmental pollutants like ozone. Ozone and other environmental pollutants are associated exacerbation of clinical signs in asthmatic patients.

Research Synopsis

  1. Obesity alters airway smooth muscle phenotype
    Obesity is associated with both allergic and non-allergic asthma. Our recent findings show that airway smooth muscle cells isolated from obese human donors have are hyper-reactive to contractile agonists. We have done a phospho-proteomics/proteomics screening to understand the proteomic signature of obese-donor derived ASM cells. Newer protein targets are being pursued to determine how obesity is linked to enhanced ASM cells shortening.
  1. Sensitizers act on airway smooth muscle and epithelial cells to modulate alarmin secretions and functions
    Allergic and non-allergic asthma are exacerbated by environmental toxicants. Many of these toxicants are either occupational or ambient by origin. Our studies showed that exposure to ambient toxicant (formaldehyde in tobacco smoke) or occupational toxicant (DNCB) alter ASM cell function. Alarmins are a group of mediators secreted generally by airway structural cells in response to toxicant/pathogen exposure. Current experiments focus on how alarmins induced by specific toxicants (i.e: DNCB) regulate excitation-contraction coupling in ASM cells. We also focus on how these alarmins render the ASM cells insensitive to bronchodilators, a critical part of asthma therapy.
  1. Free fatty acid receptors regulate excitation-contraction coupling in airway smooth muscle cells
    Free fatty acid levels are elevated in obese subjects. Receptors for some of these free fatty acids are expressed and functional in ASM cells. We are testing a hypothesis that free fatty acid receptors (FFAR) modulate excitation-contraction coupling in ASM cells.
  1. Cyclic AMP (cAMP) pump expression and function in airway smooth muscle cells
    Cyclic AMP (cAMP) is an intracellular second messenger. It is elevated upon activation of beta2 adrenergic receptor (b2AR) on ASM cells. Bronchodilators, such as albuterol, act on b2AR to relax ASM. Recent reports showed that a cAMP pump, called ABCC1/4 (MRP1/4) is expressed in ASM cells. Pumping of cAMP by these proteins may reduce intra-cellular cAMP, therefore attenuate b2AR-induced ASM relaxation. Current experiments focus on expression levels of these proteins in ASM cells in non-asthma and asthma human donors.
  1. ANO1/TMEM16A: A chloride channel with potential role in cellular Ca2+ dynamics in airway smooth muscle cells
    Membrane depolarization is one way of regulating voltage-sensitive Ca2+ channels in excitable cells, such as smooth muscle cells. Anoctamin 1 (ANO1) is a Ca2+-activated-Chloride channel expressed in ASM cells. Studies showed that inhibiting ANO1 with drugs, such as benzbromarone, attenuates contraction in human small airways. The current studies focus on regulation of ANO1 expression by various cytokines and the functional effects in ASM cells as the result of modified expression.

 References:

  1. Obesity increases airway smooth muscle responses to contractile agonists. Orfanos S, Jude J, Deeney BT, Cao G, Rastogi D, van Zee M, Pushkarsky I, Munoz HE, Damoiseaux R, Di Carlo D, Panettieri R Jr. Am J Physiol Lung Cell Mol Physiol. 2018. 315(5):L673L681.
  2. Salicylic acid amplifies Carbachol-induced bronchoconstriction in human precision-cut lung slices. Jude J, Botelho D, Karmacharya N, Cao GY, Jester W, Panettieri RA Jr. Respir Res. 2019 Apr 11;20(1):72.
  3. Novel identification of the free fatty acid receptor FFAR1 that promotes contraction in airway smooth muscle. Mizuta K, Zhang Y, Mizuta F, Hoshijima H, Shiga T, Masaki E, Emala CW Sr. Am J Physiol Lung Cell Mol Physiol. 2015 Nov 1;309(9):L970-82.
  4. A role for multidrug resistance protein 4 (MRP4; ABCC4) in human dendritic cell migration. van de Ven R, Scheffer GL, Reurs AW, Lindenberg JJ, Oerlemans R, Jansen G, Gillet JP, Glasgow JN, Pereboev A, Curiel DT, Scheper RJ, de Gruijl TD. Blood. 2008 Sep 15;112(6):2353-9.
  5. Activation of Ca(2+) -activated Cl(-) channel ANO1 by localized Ca(2+) signals. Jin X, Shah S, Du X, Zhang H, Gamper N.J Physiol. 2016 Jan 1;594(1):19-30. doi: 10.1113/jphysiol.2014.275107.

 

Selected Publications

  1. Adventitial stromal cells and myofibroblasts recruit pro- and anti-inflammatory immune cells in allergic airway inflammation. Xu E, Cao G, Yang Z, Zhang Y, Si Y, Singh K, Jude J, An SS, Koziol-White CJ, Panettieri RA Jr, Yang Q.Allergy. 2023 Nov;78(11):2994-2997. doi: 10.1111/all.15766. Epub 2023 May 20.PMID: 37171245
  2. Glucocorticoid regulation of CD38 expression in human airway smooth muscle cells: role of dual specificity phosphatase 1. Kang BN, Jude JA, Panettieri RA Jr, Walseth TF, Kannan MS.Am J Physiol Lung Cell Mol Physiol. 2008 Jul;295(1):L186-93. doi: 10.1152/ajplung.00352.2007. Epub 2008 Apr 25.PMID: 18441094
  3. Differential induction of CD38 expression by TNF-{alpha} in asthmatic airway smooth muscle cells. Jude JA, Solway J, Panettieri RA Jr, Walseth TF, Kannan MS.Am J Physiol Lung Cell Mol Physiol. 2010 Dec;299(6):L879-90. doi: 10.1152/ajplung.00021.2010. Epub 2010 Aug 6.PMID: 20693316
  4. TNF-α regulation of CD38 expression in human airway smooth muscle: role of MAP kinases and NF-κB. Jude JA, Panettieri RA Jr, Walseth TF, Kannan MS.Adv Exp Med Biol. 2011;691:449-59. doi: 10.1007/978-1-4419-6612-4_46.PMID: 21153349
  5. Regulation of CD38 expression in human airway smooth muscle cells: role of class I phosphatidylinositol 3 kinases. Jude JA, Tirumurugaan KG, Kang BN, Panettieri RA, Walseth TF, Kannan MS.Am J Respir Cell Mol Biol. 2012 Oct;47(4):427-35. doi: 10.1165/rcmb.2012-0025OC. Epub 2012 May 3.PMID: 22556157
  6. miR-140-3p regulation of TNF-α-induced CD38 expression in human airway smooth muscle cells. Jude JA, Dileepan M, Subramanian S, Solway J, Panettieri RA Jr, Walseth TF, Kannan MS.Am J Physiol Lung Cell Mol Physiol. 2012 Sep;303(5):L460-8. doi: 10.1152/ajplung.00041.2012. Epub 2012 Jul 6.PMID: 22773691
  7. Altered CD38/Cyclic ADP-Ribose Signaling Contributes to the Asthmatic Phenotype. Jude JA, Dileepan M, Panettieri RA Jr, Walseth TF, Kannan MS.J Allergy (Cairo). 2012;2012:289468. doi: 10.1155/2012/289468. Epub 2012 Nov 20.PMID: 23213344
  8. MicroRNA-708 regulates CD38 expression through signaling pathways JNK MAP kinase and PTEN/AKT in human airway smooth muscle cells. Dileepan M, Jude JA, Rao SP, Walseth TF, Panettieri RA, Subramanian S, Kannan MS.Respir Res. 2014 Aug 31;15(1):107. doi: 10.1186/s12931-014-0107-0.PMID: 25175907
  9. Epithelium-generated neuropeptide Y induces smooth muscle contraction to promote airway hyperresponsiveness. Li S, Koziol-White C, Jude J, Jiang M, Zhao H, Cao G, Yoo E, Jester W, Morley MP, Zhou S, Wang Y, Lu MM, Panettieri RA Jr, Morrisey EE.J Clin Invest. 2016 May 2;126(5):1978-82. doi: 10.1172/JCI81389. Epub 2016 Apr 18.PMID: 27088802
  10. Formaldehyde Induces Rho-Associated Kinase Activity to Evoke Airway Hyperresponsiveness. Jude J, Koziol-White C, Scala J, Yoo E, Jester W, Maute C, Dalton P, Panettieri R Jr.Am J Respir Cell Mol Biol. 2016 Oct;55(4):542-553. doi: 10.1165/rcmb.2015-0254OC.PMID: 27149505
  11. Serum amyloid A: an ozone-induced circulating factor with potentially important functions in the lung-brain axis. Erickson MA, Jude J, Zhao H, Rhea EM, Salameh TS, Jester W, Pu S, Harrowitz J, Nguyen N, Banks WA, Panettieri RA Jr, Jordan-Sciutto KL.FASEB J. 2017 Sep;31(9):3950-3965. doi: 10.1096/fj.201600857RRR. Epub 2017 May 22.PMID: 28533327
  12. House Dust Mite-Induced Allergic Airway Disease Is Independent of IgE and FcεRIα. McKnight CG, Jude JA, Zhu Z, Panettieri RA Jr, Finkelman FD.Am J Respir Cell Mol Biol. 2017 Dec;57(6):674-682. doi: 10.1165/rcmb.2016-0356OC.PMID: 28700253