Browsing by Author "McIver, Lauren J."
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- Comparative Global Gene Expression Profiles of Wild-Type Yersinia pestis CO92 and Its Braun Lipoprotein Mutant at Flea and Human Body TemperaturesGalindo, Cristi L.; Sha, Jian; Moen, Scott T.; Agar, Stacy L.; Kirtley, Michelle L.; Foltz, Sheri M.; McIver, Lauren J.; Kozlova, E. V.; Garner, Harold R.; Chopra, Ashok K. (Hindawi, 2010-05-19)Braun/murein lipoprotein (Lpp) is involved in inflammatory responses and septic shock. We previously characterized a lpp mutant of Yersinia pestis CO92 and found that this mutant was defective in surviving in macrophages and was attenuated in a mouse inhalation model of plague when compared to the highly virulent wild-type (WT) bacterium. We performed global transcriptional profiling of WT Y. pestis and its lpp mutant using microarrays. The organisms were cultured at 26 and 37 degrees Celsius to simulate the flea vector and mammalian host environments, respectively. Our data revealed vastly different effects of lpp mutation on the transcriptomes of Y. pestis grown at 37 versus . While the absence of Lpp resulted mainly in the downregulation of metabolic genes at , the Y. pestislpp mutant cultured at exhibited profound alterations in stress response and virulence genes, compared to WT bacteria. We investigated one of the stress-related genes (htrA) downregulated in the lpp mutant relative to WT Y. pestis. Indeed, complementation of the lpp mutant with the htrA gene restored intracellular survival of the Y. pestislpp mutant. Our results support a role for Lpp in Y. pestis adaptation to the host environment, possibly via transcriptional activation of htrA.
- 'Cut from the same cloth': Shared microsatellite variants among cancers link to ectodermal tissues-neural tube and crest cellsKarunasena, Enusha; McIver, Lauren J.; Bavarva, Jasmin H.; Wu, Xiaowei; Zhu, Hongxiao; Garner, Harold R. (Impact Journals, 2015-09-08)
- Somatic intronic microsatellite loci differentiate glioblastoma from lower-grade gliomasKarunasena, Enusha; McIver, Lauren J.; Rood, Brian R.; Wu, Xiaowei; Zhu, Hongxiao; Bavarva, Jasmin H.; Garner, Harold R. (Impact Journals, 2014-08-15)
- Transcriptional profile of isoproterenol-induced cardiomyopathy and comparison to exercise-induced cardiac hypertrophy and human cardiac failureGalindo, Cristi L.; Skinner, Michael A.; Errami, Mounir; Olson, L Danielle; Watson, David A.; Li, Jing; McCormick, John F.; McIver, Lauren J.; Kumar, Neil M.; Pham, Thinh Q.; Garner, Harold R. (2009-12-09)Background Isoproterenol-induced cardiac hypertrophy in mice has been used in a number of studies to model human cardiac disease. In this study, we compared the transcriptional response of the heart in this model to other animal models of heart failure, as well as to the transcriptional response of human hearts suffering heart failure. Results We performed microarray analyses on RNA from mice with isoproterenol-induced cardiac hypertrophy and mice with exercise-induced physiological hypertrophy and identified 865 and 2,534 genes that were significantly altered in pathological and physiological cardiac hypertrophy models, respectively. We compared our results to 18 different microarray data sets (318 individual arrays) representing various other animal models and four human cardiac diseases and identified a canonical set of 64 genes that are generally altered in failing hearts. We also produced a pairwise similarity matrix to illustrate relatedness of animal models with human heart disease and identified ischemia as the human condition that most resembles isoproterenol treatment. Conclusion The overall patterns of gene expression are consistent with observed structural and molecular differences between normal and maladaptive cardiac hypertrophy and support a role for the immune system (or immune cell infiltration) in the pathology of stress-induced hypertrophy. Cross-study comparisons such as the results presented here provide targets for further research of cardiac disease that might generally apply to maladaptive cardiac stresses and are also a means of identifying which animal models best recapitulate human disease at the transcriptional level.