Project description:Identification of gravisensitive gene expression in rat soleus muscle exposed to 7 and 14 days of Hindlimb suspension (HS) simulated microgravity. Microgravity causes muscle atrophy possibly due to muscle wasting overtake regeneration. Results provide insight into the molecular mechanisms regulating muscle atrophy. The expression of 787 (373 upregulated and 414 downregulated) and 923 (491 upregulated and 432 downregulated) genes out of 28000 was altered respectively at least 2-fold of 7 and 14 days TS, which represented 397 (233 upregulated and 164 downregulated) genes of common alteration. By using real-time PCR assays, we verified the microarray data using some of the expected genes. The tissue was collected from Sprague-Dawley rats (8 weeks of age) subjected to 7, 14days of TS. mRNA expression profile was determined in three groups: control (CN), TS for 7 days (TS-7), and TS for 14 days (TS-14).Three mRNA microarray chips were analyzed for mixture of four samples of each of the three groups.
Project description:Identification of gravisensitive miRNAs expression in rat soleus muscle exposed to 7 and 14 days of Hindlimb suspension (HS) simulated microgravity. Microgravity causes muscle atrophy possibly due to muscle wasting overtake regeneration. Results provide insight into the molecular mechanisms regulating muscle atrophy. The expression of 23 out of 174 miRNAs was found to change at least 2-fold of 7 and/or 14 days of TS. By using real-time PCR assays, we verified the microarray data using some of the expected genes. The tissue was collected from Sprague-Dawley rats (8 weeks of age) subjected to 7, 14days of TS. miRNA expression profile was determined in three groups: control (CN), TS for 7 days (TS-7), and TS for 14 days (TS-14).Three miRNA microarray chips were analyzed for mixture of four samples of each of the three groups.
Project description:The effect of cafeteria (CAF) diet in PBMC gene expression was analyzed in two inbred rat strains the Wistar Kyoto(WKY) and Lewis (LEW) rat PBMCs were isolated following a CAF or standard diet and subjected to whole genome expression analysis Rats from each strain were either fed with standard chow diet (n=5) or CAF (n=5). After 7 weeks of the indicated diet, rats were fasted for 9 hours, culled and PBMCs isolated from whole blood collected from the abdominal aorta
Project description:Heat acclimation (AC) allows its faster re-induction following its decline. Constitutively preserved euchromatin state in hsp70 promoter during acclimation decline/regain pushed forward the hypothesis that acclimation decline is a period of M-bM-^@M-^\dormant memoryM-bM-^@M-^] involving molecular program including epigenetic controlled transcriptional regulation leading to heat acclimation mediated cytoprotective memory. We used microarray to uncover hallmark pathways in the induction of heat-acclimation-mediated memory, focusing on markers of epigenetic processes. Rats subjected to heat acclimation, deacclimation, reacclimation and untreated controls were used. We showed here that (i) AC2d provides the molecular switch for acclimation (ii) AC30 heart demonstrates qualitative adaptations (iii) specific molecular program encompassing up/down regulated gene during DeAC, of which epigenetic markers such as class A histones, chromatin modifiers and microRNA suggest epigenetic transcriptional regulation linked to acclimation memory (iv) constitutive upregulation of MAPK P38 module and targets as well as jak/stat and AKT associated pathways during DeAC imply its major role in this process. Noteworthy are players such as poly-(ADP-ribose)polymerase-1 (PARP1) and linker histones (histones H1 cluster in this process).
Project description:Middle cerebral artery occlusion (MCAo) in rat represent the ischemic stroke in human. Rodents subjected to MCAo and treated with venom phospholipase A2 showed reduction in infarct volume after 24hours of stroke. We studied the global gene expression of the reduction in infarct volume using Affymetrix Gene Chips. We analysed all the genes that were up or down regulated in the study. Total RNA isolated from sham, MCAo and MCAo+nPLA rat brains, was pooled to minimize inter-individual variation and hybridized to each array of the RAE-230A or U34A GeneChipTM according to protocols described in the GeneChipTM expression analysis package (Affymetrix, CA).
Project description:Emerging evidence suggests that estrogen and prolactin (PRL) play a key role in prostate cancer development, yet their relationship and molecular actions in prostate is not well understood. To address this issue, we made the first direct comparison of estrogen and PRL actions in the Noble rat (NBL) prostate dysplasia model. Prostatic dysplasia in lateral prostate (DLP) has been induced by elevated circulating levels of estrogen and PRL in NBL with estrogen (E2)-filled implants, while physiological level of testosterone (T) was maintained with T-filled implants. The effect of estrogen and PRL was studied by using ICI and bromocriptine (Br) as their respective blockers, both can effectively inhibited dysplasia development under T+E2 induction. Transcript expression profile of the four treatment groups (Control, T+E2, T+E2+Br, and T+E2+ICI) has been characterized in this array.
Project description:Two out-bred rat selection lines were separated to produce different hypersensitivity phenotypes following nerve injury. These lines were termed High Pain and Low Pain (HP or LP). Each sub-strain was either subject to a Sham surgery or a Spinal Nerve Ligation (SNL) surgery to the L4 and L5 spinal nerves. Three days following surgery L4/L5 Dorsal Root Ganglia (DRG) were dissected from these animals. For the rat line separation protocol see: Devor M, Raber P (1990) Heritability of symptoms in an experimental model of neuropathic pain. Pain 42:51-67. 12 Hybridizations, 3 per condition; Sham HP DRG; 3 day SNL HP DRG; Sham LP DRG; 3 day SNL LP DRG.
Project description:A delay in the mammalian inflammatory response is a prominent feature of infection with Yersinia pestis, the agent of bubonic and pneumonic plague. Y. pestis factors have been identified that either do not stimulate a normal inflammatory response, or actively suppress it. Prominent among these are components of the Type III secretion system that is encoded on the Yersinia virulence plasmid (pYV). We used a rat model of bubonic plague to characterize the kinetics and extent of the mammalian transcriptomic response to infection with wild-type or pYV-negative Y. pestis in the draining lymph node. Remarkably, dissemination and multiplication of wild-type Y. pestis during the bubonic stage of disease did not induce any detectable gene expression response by host lymph node cells. This was followed, however, by an extensive transcriptomic response, including upregulation of several cytokine, chemokine, and other immune response genes, after systemic spread during septicemic plague. Matched lymph node samples used for histopathology and extracellular cytokine measurements, combined with the microarray data set, broadly outlined the mammalian immune response to Y. pestis and how it is influenced by pYV-encoded factors. The results indicate that both WT and pYV– Y. pestis induce primarily a Th17 response, and not a Th1 or Th2 response. In the absence of pYV, a sustained recruitment of polymorphonuclear leukocytes, the major Th17 effector cell, to the lymph node resulted in clearance of infection. Thus, the ability to counteract a Th17- driven PMN response in the lymph node appears to be a major function of the Y. pestis virulence plasmid. In contrast, classic markers of the proinflammatory response and macrophage activation, such as TNF-á and IFN-ã, were not induced at all by pYV– Y. pestis, and appeared only late in infection with WT Y. pestis. Rats treated with PBS and Yersinia pestis at various time points.
Project description:Analysis of E14 embryonic stem cells lacking Trip12 ubiquitin ligase activity. We used microarrays to detail the global gene expression profiles affected by Trip12 ubiquitin ligase activity in mouse embryonic stem cell. Total RNA was extracted from wild-type and Trip12 mutant mouse embryonic stem cells and hybridized on Affymetrix microarrays.