Gene expression in Krt16 null paw lesions relative to WT paw skin
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ABSTRACT:
PROVIDER: PRJNA481940 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The type I intermediate filament keratin 16 (Krt16 gene; K16 protein) is constitutively expressed in ectoderm-derived appendages and volar palmar/plantar epidermis, and is otherwise inducibly expressed in non-volar epidermis when skin epithelia are under stress. Mutations at the (human) KRT16 locus can cause pachyonychia congenita (PC) and focal non-epidermolytic palmoplantar keratoderma (PPK), which each entail painful calluses on palmar and/or plantar skin. Krt16 null mice develop footpad lesions that mimic several aspects of PC-associated PPK and FNEPPK, including hypoactive Keap1-Nrf2 signaling and elevated expression of skin barrier homeostasis genes and Danger Associated Molecular Patterns (DAMPs). This provides a unique opportunity to understand the intricacies of PPK and devise effective therapies (see Lessard and Coulombe, J. Invest. Dermatol. 2012; Lessard et al. PNAS (USA) 2013; Kerns et al. J. Clin. Invest. 2016; Kerns et al., J. Invest. Dermatol. 2018; Zieman and Coulombe Exp. Dermatol. 2018). Here, we report on insight gained from a genome-wide analysis of gene expression in PPK-like lesions of Krt16 null mice. In this dataset, we include expression data obtained from Krt16 null paw skin lesions and WT littermate controls (C57Bl/6 strain background) at two months of age.
2019-07-19 | GSE117375 | GEO
Project description:We have employed whole genome microarray expression profiling to identify genes with the potential to distinguish young and aged interfollicular epidermis. Gene expression of paw whole skin samples from 4 young (6 week-old) and 4 aged (102 week-old) C57BL6 mice was analyzed.
2017-07-11 | E-MTAB-4916 | biostudies-arrayexpress
Project description:Nowadays one of the main challenges is moving towards an eco-sustainable agriculture, able to preserve the food production through a reduced use of pesticides. The current global food sustenance by intensive agriculture mainly based on economic crop monocultures drastically reduces the biodiversity increasing the yield losses due to biotic and abiotic stress. To try to ensure yield stability also enhancing the plant resistance responses to promote an eco-sustainable management of plant diseases, a technology based on plasma activated water (PAW), characterized by the production of reactive oxygen and nitrogen species, was tested. Differential expression levels of selected genes involved in the plant defence pathways and the microRNAs composition in PAW treated- micropropagated periwinkle shoots and grapevines were analyzed. The results indicate that PAW treatment enhances plant defence responses at both, transcriptional and post-transcriptional level, leading to an increased synthesis in periwinkle of vinblastine and vindoline, anti-oxidant compounds employed in the pharmaceutical industry and in grapevine of resveratrol that is an important compound for human health.
2020-11-12 | GSE146177 | GEO
Project description:compare basic metabolism between wildtype and tPA null mice in brain tissue
2014-11-11 | ST000160 | MetabolomicsWorkbench
Project description:Recessive dystrophic epidermolysis bullosa (RDEB) is a genetic disorder caused by loss of function of the Col7a1 gene that encodes collagen VII, a critical structural protein that anchors the epidermis to the dermis. Manifestations of this disease include chronic wounding, blistering, immune dysfunction, and eventually squamous cell carcinoma. Symptoms are likely due to the disruption and dysregulation of the dermal microenvironment. Mice with RDEB symptoms, due to Col7a1 knockout, have been developed to study the disease's development and pathological manifestations in an in vivo model. Single cell RNA sequencing was performed on a single cell suspension of the paw skin of 2 week old RDEB mice, along with their wild-type littermates, to create a transcriptomic view of their dermal microenvironment. We analyzed the sequencing data at different resolutions. One focusing on the overall tissue level as well as closer analysis of specific cell types (fibroblasts, keratinocytes, immune cells, and vascular cells).
2023-03-02 | GSE222250 | GEO
Project description:The multi-ligand Receptor for AGE (RAGE) contributes to atherosclerosis in apolipoprotein (ApoE) null mice in both the non-diabetic and diabetic states. Previous studies using soluble RAGE, the extracellular ligand-binding domain of RAGE, or homozygous RAGE null mice showed that blockade or deletion of RAGE resulted in marked reduction in atherosclerotic lesion area and complexity compared to control animals. In parallel, significant down-regulation of inflammatory mediators and matrix metalloproteinases was evident in ApoE null mice aortas devoid of RAGE compared to those of ApoE null RAGE-expressing mice. Although these findings suggested that RAGE triggered pro-atherogenic mechanisms via regulation of inflammatory gene expression, these studies did not reveal the broader pathways by which RAGE contributed to atherosclerosis in ApoE null mice. Therefore, we performed Affymetrix gene expression arrays on aortas of non-diabetic and diabetic ApoE null mice expressing RAGE or devoid of RAGE at nine weeks of age, as this reflected a time point at which frank atherosclerotic lesions were not yet present, but, that we would be able to identify the genes likely involved in diabetes- and RAGE-dependent atherogenesis. The comparisons were as follows: 1. diabetic ApoE null relative to non-diabetic ApoE null; 2. non-diabetic ApoE null / RAGE null relative to non-diabetic ApoE null; 3. diabetic ApoE null / RAGE null relative to non-diabetic ApoE null / RAGE null; and 4. diabetic ApoE null / RAGE null relative to diabetic ApoE null aorta. Our data reveal that there is very little overlap of the genes which are differentially expressed both in the onset of diabetes in ApoE null mice, and in the effect of RAGE deletion in diabetic ApoE null mice. We next performed a Pathway-Express analysis to determine the pathways that were most associated with the onset of diabetes in ApoE null mice and the effect of RAGE gene deletion in diabetic ApoE null mice. Rigorous statistical analysis was undertaken and revealed that the transforming growth factor-β pathway (tgf-β) and focal adhesion pathways might be expected to play a significant role in both the mechanism by which diabetes facilitates the formation of atherosclerotic plaques in ApoE null mice, and the mechanism by which deletion of RAGE ameliorates this effect. We focused on three genes of the tgf-β family which were found to be up-regulated in diabetic vs. non-diabetic ApoE null aorta, and which were reduced by deletion of RAGE. These included: thrombospondin1 (Thbs1), transforming growth factor-β2 (tgf-β2) and rho-associated kinase (ROCK1). Real-time quantitative polymerase chain reaction and Western blotting experiments were performed, as well as ROCK1 activity assays in mouse aorta, and validated the findings of the Affymetrix gene array. Further, confocal microscopy revealed that a principal cell type in the ApoE null aorta expressing these factors was the vascular smooth muscle cell. Our data suggest the novel finding that the observed reduction of accelerated atherosclerosis in diabetic ApoE null / RAGE null vs. diabetic ApoE null mice occurs, all or in part, through the ROCK1 branch of the TGF-β pathway. We have inferred a detailed mechanism for this process. Taken together, these data suggest that suppression of ROCK1 activity in the atherosclerosis-vulnerable vessel wall, especially in diabetes, but in non-diabetes as well, may underlie the beneficial effects of RAGE antagonism and genetic deletion in murine models. These findings highlight logical and novel targets for therapeutic intervention in cardiovascular disease and diabetes.
2010-03-01 | GSE15729 | GEO
Project description:The multi-ligand Receptor for AGE (RAGE) contributes to atherosclerosis in apolipoprotein (ApoE) null mice in both the non-diabetic and diabetic states. Previous studies using soluble RAGE, the extracellular ligand-binding domain of RAGE, or homozygous RAGE null mice showed that blockade or deletion of RAGE resulted in marked reduction in atherosclerotic lesion area and complexity compared to control animals. In parallel, significant down-regulation of inflammatory mediators and matrix metalloproteinases was evident in ApoE null mice aortas devoid of RAGE compared to those of ApoE null RAGE-expressing mice. Although these findings suggested that RAGE triggered pro-atherogenic mechanisms via regulation of inflammatory gene expression, these studies did not reveal the broader pathways by which RAGE contributed to atherosclerosis in ApoE null mice. Therefore, we performed Affymetrix gene expression arrays on aortas of non-diabetic and diabetic ApoE null mice expressing RAGE or devoid of RAGE at nine weeks of age, as this reflected a time point at which frank atherosclerotic lesions were not yet present, but, that we would be able to identify the genes likely involved in diabetes- and RAGE-dependent atherogenesis. The comparisons were as follows: 1. diabetic ApoE null relative to non-diabetic ApoE null; 2. non-diabetic ApoE null / RAGE null relative to non-diabetic ApoE null; 3. diabetic ApoE null / RAGE null relative to non-diabetic ApoE null / RAGE null; and 4. diabetic ApoE null / RAGE null relative to diabetic ApoE null aorta. Our data reveal that there is very little overlap of the genes which are differentially expressed both in the onset of diabetes in ApoE null mice, and in the effect of RAGE deletion in diabetic ApoE null mice. We next performed a Pathway-Express analysis to determine the pathways that were most associated with the onset of diabetes in ApoE null mice and the effect of RAGE gene deletion in diabetic ApoE null mice. Rigorous statistical analysis was undertaken and revealed that the transforming growth factor-beta pathway (tgf-beta) and focal adhesion pathways might be expected to play a significant role in both the mechanism by which diabetes facilitates the formation of atherosclerotic plaques in ApoE null mice, and the mechanism by which deletion of RAGE ameliorates this effect. We focused on three genes of the tgf-betafamily which were found to be up-regulated in diabetic vs. non-diabetic ApoE null aorta, and which were reduced by deletion of RAGE. These included: thrombospondin1 (Thbs1), transforming growth factor-beta (tgf-beta) and rho-associated kinase (ROCK1). Real-time quantitative polymerase chain reaction and Western blotting experiments were performed, as well as ROCK1 activity assays in mouse aorta, and validated the findings of the Affymetrix gene array. Further, confocal microscopy revealed that a principal cell type in the ApoE null aorta expressing these factors was the vascular smooth muscle cell. Our data suggest the novel finding that the observed reduction of accelerated atherosclerosis in diabetic ApoE null / RAGE null vs. diabetic ApoE null mice occurs, all or in part, through the ROCK1 branch of the TGF-betapathway. We have inferred a detailed mechanism for this process. Taken together, these data suggest that suppression of ROCK1 activity in the atherosclerosis-vulnerable vessel wall, especially in diabetes, but in non-diabetes as well, may underlie the beneficial effects of RAGE antagonism and genetic deletion in murine models. These findings highlight logical and novel targets for therapeutic intervention in cardiovascular disease and diabetes. 1. diabetic ApoE null relative to non-diabetic ApoE null; 2. non-diabetic ApoE null / RAGE null relative to non-diabetic ApoE null; 3. diabetic ApoE null / RAGE null relative to non-diabetic ApoE null / RAGE null; and 4. diabetic ApoE null / RAGE null relative to diabetic ApoE null aorta. There were 4 mice in each group initially. However there are only 3 non-diabetic ApoE null / RAGE null mice in the final experimental sample in group 3 due to a failure to generate cRNA from that sample. All samples were normalized to remove chip-dependent regularities using the RMA method. Chips and controls at each combination of genotype and disease sate were normalized together. The statistical significance of differential expression was calculated using the empirical Bayesian LIMMA (LInear Model for MicroArrays) method A cut-off B>0 was used for the statistical significance of gene expression.
2010-03-07 | E-GEOD-15729 | biostudies-arrayexpress
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2024-01-30 | E-MTAB-13734 | biostudies-arrayexpress
Project description:PAW-plasma activated water-triggers plant defence responses
| PRJNA609664 | ENA