{"database":"biostudies-arrayexpress","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown","Transcriptomics","Genomics","Proteomics"],"submitter":["Yuko Oda"],"study_type":["transcription profiling by array"],"organism":["Mus musculus"],"species":["Mus musculus"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/E-GEOD-50670"],"description":["Transcriptional coactivator Mediator complex facilitates transcription of various transcription factors. Previously, we have generated Med1 conditional null mice, where a critical subunit of Mediator, Med1, is removed from keratinocytes. Here we present evidence that ablation of Med1 accelerated epidermal regeneration after injury. As bulge keratinocyte stem cells are important contributors to regenerate epidermis, we first analyzed properties of stem cells in Med1 null mice. BrdU long retaining analysis revealed that deletion of Med1 still maintained quiescence of bulge keratinocyte stem cells, despite of general hyperplasia observed in Med1 deficient keratinocytes. Gene expression analysis demonstrated that a series of niche matrix proteins decreased in Med1 deficient keratinocytes. In contrast, the expression of stem cell marker Sox9 was not altered, suggesting stem cells are present but activated because of abnormal niche surrounding stem cells. In addition, Med1 deletion suppressed injury induced inflammatory reaction, which indirectly regulates epidermal regeneration.  We also indicated that TGFβ1 significantly decreased in both bulge and epidermal keratinocytes upon Med1 deletion. Our study demonstrates that coactivator Med1 has a critical role to maintain bulge stem cells and epidermal regeneration presumably through regulation in TGFβ signaling. n=3 WT and KO (each sample contain RNA isolated from wounded or nonwounded skins excised from 3 mice)"],"repository":["biostudies-arrayexpress"],"sample_protocol":["Sample Treatment - Med1 KO mice and their littermate control mice received two full-thickness wounds with a 6-mm biopsy punch on the telogen skin. Med1 KO mice showed both telogen and pigmented anagen skin because of hair cycling defects, In contrast, control skin was in telogen in whole area at 8 wk of age. We made wounds on telogen skin. The telogen wounded skin was excised by using 8-mm biopsy punch after 24 hr of wound preparation. Non-wounded telogen skin was also excised from the same mouse as a control.","Growth Protocol - Coactivator MED1 is removed from keratin 14 (K14) expressing keratinocytes by using Crelox stragety","Nucleic Acid Extraction - Total RNA was isolated from wounded or non wounded skin by using combination of RNAzol and RNAeasy RNA purification kit (Qiagen).","Labeling - Standard Illumina hybridization protocol cDNA labeled by Biotin and detected by Cy3-streptoavidin","Hybridization - Standard Illumina hybridization protocol done by UCLA neuroscience genomics core","Scaning - Standard Illumina hybridication protocol done by UCLA neuroscience genomics core"],"figure_sub":["MIAME Score","Organization","Assays and Data","Processed Data","MAGE-TAB Files","Array Designs"],"pubmed_authors":["Daniel Bikle","Frankie Fong","Thai Nguyen","Yuko Oda","Lizhi Hu"],"data_protocol":["Data Transformation - data were normalized by using quantile method in Genome studio V2011.1 ID_REF =  VALUE = quantile normalized using Genome Studio p-value ="],"additional_accession":[]},"is_claimable":false,"name":"Ablation of coactivator Med1 regulates bulge keratinocyte stem cells and accelerates epidermal regeneration after injury [skin wound]","description":"Transcriptional coactivator Mediator complex facilitates transcription of various transcription factors. Previously, we have generated Med1 conditional null mice, where a critical subunit of Mediator, Med1, is removed from keratinocytes. Here we present evidence that ablation of Med1 accelerated epidermal regeneration after injury. As bulge keratinocyte stem cells are important contributors to regenerate epidermis, we first analyzed properties of stem cells in Med1 null mice. BrdU long retaining analysis revealed that deletion of Med1 still maintained quiescence of bulge keratinocyte stem cells, despite of general hyperplasia observed in Med1 deficient keratinocytes. Gene expression analysis demonstrated that a series of niche matrix proteins decreased in Med1 deficient keratinocytes. In contrast, the expression of stem cell marker Sox9 was not altered, suggesting stem cells are present but activated because of abnormal niche surrounding stem cells. In addition, Med1 deletion suppressed injury induced inflammatory reaction, which indirectly regulates epidermal regeneration.  We also indicated that TGFβ1 significantly decreased in both bulge and epidermal keratinocytes upon Med1 deletion. Our study demonstrates that coactivator Med1 has a critical role to maintain bulge stem cells and epidermal regeneration presumably through regulation in TGFβ signaling. n=3 WT and KO (each sample contain RNA isolated from wounded or nonwounded skins excised from 3 mice)","dates":{"release":"2014-01-01T00:00:00Z","modification":"2023-09-02T18:40:49.395Z","creation":"2022-02-23T17:27:18.56Z"},"accession":"E-GEOD-50670","cross_references":{"GEO":["GSE50670"],"EFO":["EFO_0002768"]}}