Articles

Jennifer H. Shaw, Associate Professor mediators of oxidative stress (hydrogen sulfide & hydrogen peroxide), infectious disease   Ph.D., 2000, University of Montana Phone: 405-744-9679 Email: Jennifer.h.shaw@okstate.edu Lab website: http://jenniferhshaw.wix.com/the-shaw-lab

Specific Interests

Our lab seeks to understand molecular mechanisms of survival; one project involves an extremophile fish system while the other utilizes a murine infection model. 1) We are studying how extremophile fishes maintain cellular respiration amidst lethal levels of hydrogen sulfide. We are discovering modifications to gene expression, mitochondrial function & detoxification capacity in tolerant populations (in collaboration with Drs. Tobler & Kelley). 2) We are studying an alternate host cell exit mechanism employed by C. trachomatis (“extrusion”) in a murine model to better understand how this microbe survives in the host, manipulates the host immune response & drives pathogenesis (in collaboration with Dr. Lutter).

Selected Publications

• Shaw JH, Behar AR, Snider TA, Allen NA, Lutter EI. Comparison of Murine Cervicovaginal Infection by Chlamydial Strains: Identification of Extrusions Shed In vivo. Frontiers in Cellular & Infection Microbiology. 7:18 (2017).
• Passow C, Henpita C, Shaw JH, Quakenbush CR, Warren WC, Arias-Rodriguez L, Kelley JL, Tobler M. The Roles of Plasticity and Evolutionary Change in Shaping Gene Expression Variation in Natural Populations of Extremophile Fish. Molecular Ecology. doi: 10.111/mec.14360 (2017).
• Tobler M, Passow CN, Greenway RS, Kelley JL, Shaw JH. The evolutionary ecology of animals inhabiting hydrogen sulfide rich environments. Annual Review in Ecology, Evolution and Systematics. 47:239-62. doi: 10.1146/annurev-ecolsys-121415-032418 (2016).
• Tobler M, Henpita C, Bassett B, Kelley J, Shaw JH. H2S exposure elicits differential expression of candidate genes in fish adapted to sulfidic and non-sulfidic environments. Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology (2014) doi: 10.1016/j.cbpa.2014.04.012.
• Xiang L, Varshney R, Rashdan N, Shaw JH, Lloyd PG. Placenta growth factor and vascular endothelial growth factor-A have differential, cell-type specific patterns of expression in vascular cells. Microcirculation (2014) doi: 10.1111/micc.12113.
• Shaw JH, Lloyd PG. Post-transcriptional regulation of placenta growth factor mRNA by hydrogen peroxide.  Microvascular Research 84 (2012) 155-160.
• Shaw JH, Xiang L, Shah A, and Lloyd PG. Placental growth factor expression is regulated by hydrogen peroxide in vascular smooth muscle cells. American Journal of Physiology 2011 Feb; 300(2):C349-55.
• Shaw J, Grund V, Durling L, Crane D, Caldwell HD. Infect Immun. 2002 Mar: 70(3): 1097-105. Dendritic cells pulsed with a recombinant chlamydial major outer membrane protein antigen elicit a CD4(+) type 2 rather than type 1 immune response that is not protective.
• Shaw JH, Grund VR, Durling L, Caldwell HD. Infect Immuno. 2001 Jul: 69(7):4667-72. Expression of genes encoding Th1 cell-activating cytokines and lymphoid homing chemokines by chlamydia-pulsed dendritic cells correlates with protective immunizing efficacy.