Project description:Using a PTSD mouse model, we investigated the longitudinal transcriptomic changes in heart tissues after the exposure to stress through intimidation We designed our time-course study (Study II) with three experimental conditions where we varied the length of time that subservient mice were exposed to aggressor mice with the same length of rest time after the exposure (1day). The conditions included were 1day-exposure (T1R1), 2day-exposure (T2R1) and 3day-exposure (T3R1).
Project description:Using a PTSD mouse model, we investigated the longitudinal transcriptomic changes in heart tissues after the exposure to stress through intimidation We designed our initial study (Study I) with four experimental conditions where we varied the length of time that subservient mice were exposed to aggressor mice and the length of rest time after the exposure. The conditions included were short exposure-short rest (T5R1-T indicates the number of days of trauma exposure; R indicates the number of days of rest after exposure), short exposure-long rest (T5R10), long exposure-short rest (T10R1) and long exposure-long rest (T10R42)
Project description:Using a PTSD mouse model, we investigated the longitudinal transcriptomic changes in heart tissues after the exposure to stress through intimidation We designed our time-course study (Study II) with three experimental conditions where we varied the length of time that subservient mice were exposed to aggressor mice with the same length of rest time after the exposure (1day). The conditions included were 1day-exposure (T1R1), 2day-exposure (T2R1) and 3day-exposure (T3R1). We designed our initial study (Study I) with four experimental conditions where we varied the length of time that subservient mice were exposed to aggressor mice and the length of rest time after the exposure. The conditions included were short exposure-short rest (T5R1-T indicates the number of days of trauma exposure; R indicates the number of days of rest after exposure), short exposure-long rest (T5R10), long exposure-short rest (T10R1) and long exposure-long rest (T10R42)
Project description:Using a PTSD mouse model, we investigated the longitudinal transcriptomic changes in heart tissues after the exposure to stress through intimidation We designed our initial study (Study I) with four experimental conditions where we varied the length of time that subservient mice were exposed to aggressor mice and the length of rest time after the exposure. The conditions included were short exposure-short rest (T5R1-T indicates the number of days of trauma exposure; R indicates the number of days of rest after exposure), short exposure-long rest (T5R10), long exposure-short rest (T10R1) and long exposure-long rest (T10R42)
Project description:We identified a number of affected pathways through transcriptome analysis on the skin biopsy samples of the FPPK patients. Our findings suggest that TRPV3 dysfunction may increase apoptotic activity, inhibit keratinocyte differentiation and disturb the intricate balance between proliferation and differentiation state of keratinocytes in the skin. From a 37-year-old Chinese male (II-7) and his 12-year-old son (III-7), biopsies from unaffected and affected skin tissues were obtained and their transcriptome profiles were analyzed in order to identify molecular changes related with the pathology of FPPK.
Project description:We identified a number of affected pathways through transcriptome analysis on the skin biopsy samples of the FPPK patients. Our findings suggest that TRPV3 dysfunction may increase apoptotic activity, inhibit keratinocyte differentiation and disturb the intricate balance between proliferation and differentiation state of keratinocytes in the skin. To understand the effect of TRPV3 mutation, transcriptome of HaCaT cell lines transfected with mutant TRPV3 were profiled in time-course manner (16, 24 and 40hr).
Project description:We identified a number of affected pathways through transcriptome analysis on the skin biopsy samples of the FPPK patients. Our findings suggest that TRPV3 dysfunction may increase apoptotic activity, inhibit keratinocyte differentiation and disturb the intricate balance between proliferation and differentiation state of keratinocytes in the skin. To understand the effect of TRPV3 mutation, transcriptome of 293T cell lines transfected with mutant TRPV3 were profiled in time-course manner (16, 24 and 40hr).
Project description:We have used a social defeat (SD) mouse model of post-traumatic stress disorder (PTSD) that is based on a brief exposure of a mouse to the aggressor mice for either 5 d or 10 d stress periods. Mice simulating aspects of posttraumatic stress disorder exhibit behavioral changes, body weight gain, increased body temperature, and inflammatory and fibrotic histopathologies and transcriptomic changes of heart tissue. Liver tissue of these mice was subjected to mRNA analysis. Transcriptomic analysis of liver indicated chronic toxicities and metabolic alterations in aggressor-exposed mice that possibly contributed to the persistent metabolic disturbance Two-condition experiment, C57BL6/J mice Biological replicates: 4-6 control replicates, 5-6 stressed replicates.
Project description:Because iron toxicity and deficiency are equally life threatening, maintaining intracellular iron levels within a narrow optimal range is critical for nearly all known organisms. However, regulatory mechanisms that establish homeostasis are not well understood in organisms that dwell in environments at the extremes of pH, temperature, and salinity. Under conditions of limited iron, the extremophile Halobacterium salinarum, a salt-loving archaeon, mounts a specific response to scavenge iron for growth. We have identified and characterized the role of two transcription factors (TFs), Idr1 and Idr2, in regulating this important response. An integrated systems analysis of TF knockout gene expression profiles and genome-wide binding locations in the presence and absence of iron has revealed that these TFs operate collaboratively to maintain iron homeostasis. In the presence of iron, Idr1 and Idr2 bind near each other at 24 loci in the genome, where they are both required to repress some genes. In contrast, Idr1 and Idr2 are both necessary to activate other genes in a putative a feed forward loop. Even at loci bound independently, the two TFs target different genes with similar functions in iron homeostasis. We discuss conserved and unique features of the Idr1-Idr2 system in the context of similar systems in organisms from other domains of life. Data in this GEO archive are linked to the publication: Schmid AK, Pan M, Sharma K, Baliga NS.2011. Two transcription factors are necessary for iron homeostasis in a salt-dwelling archaeon.Nucleic Acids Res.39(7):2519-33. Cultures containing either the gene encoding the Idr1 or Idr2 transcription factors with c-terminal fusions to the myc epitope were grown to mid-logarithmic phase in the presence or absence of 100 uM FeSO4. Cultures were subjected to ChIP-chip as described in Facciotti, MT, Reiss, DJ, Pan, M, Kaur, A, Vuthoori, M, Bonneau, R, Shannon, P, Srivastava, A, Donohoe, SM, Hood, LE and Baliga, NS. General transcription factor specified global gene regulation in archaea. Proc Natl Acad Sci U S A. 2007;104: 4630-4635. Each Sample is based on two arrrays (one with dye-swap).