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Comparison of gene expression in mouse placentas with different combination of MT1-MMP and MT2-MMP alleles

ABSTRACT: MT1-MMP and MT2-MMP double deficiency in mice leads to development of a placental defect resulting in embryonic death after E10.5. The protein substrate for these two proteases in placenta is unknown, which poses an obstacle in uncovering of molecular mechanism behind the observed placental defect. In search for a potential substrate for these two proteases in placenta we have employed whole genome microarray expression profiling as a discovery platform to identify genes, expression of which might be affected by double MMP deficiency.

ORGANISM(S): Mus musculus

PROVIDER: GSE18604 | GEO | 2010/03/01

SECONDARY ACCESSION(S): PRJNA121429

REPOSITORIES: GEO

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Comparison of gene expression in mouse placentas with different combination of MT1-MMP and MT2-MMP alleles

Project description:MT1-MMP and MT2-MMP double deficiency in mice leads to development of a placental defect resulting in embryonic death after E10.5. The protein substrate for these two proteases in placenta is unknown, which poses an obstacle in uncovering of molecular mechanism behind the observed placental defect. In search for a potential substrate for these two proteases in placenta we have employed whole genome microarray expression profiling as a discovery platform to identify genes, expression of which might be affected by double MMP deficiency. Fetal parts of mouse placentas were isolated from E10.5 placentas of different genotypes for MT1- and MT2-MMP.

2010-03-09 | E-GEOD-18604 | biostudies-arrayexpress

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Project description:ADAMTS9 and ADAMTS20 are homologous secreted proteases implicated in ECM proteolysis and ciliogenesis, but few relevant substrates of these proteases are currently known. Quantitative N-terminomics comparison of RPE-1 cells lacking ADAMTS9 with parental RPE-1 cells identified transmembrane protease MT1-MMP (MMP14) as a novel ADAMTS9 substrate. The resulting enhanced cell-surface MT1-MMP activity in the gene-edited cells contributes to their adhesion defect, but not lack of cilia. A key physiological function of ADAMTS9/20 may be to dampen cell-surface MT1-MMP activity.

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Project description:Mammary gland branching morphogenesis is thought to depend on the mobilization of the membrane-anchored matrix metalloproteinases, MT1-MMP and MT2-MMP, that drive epithelial cell invasion by remodeling the extracellular matrix and triggering associated signaling cascades. However, the roles that these proteinases play during mammary gland development in vivo remains undefined. A mammary gland branching program that occurs during the first 10 days of early postnatal development was used to characterize the impact of global Mt1-mmp or Mt2-mmp targeting on mammary gland morphogenesis. Transcriptome profiling of ductal networks and associated stroma was used to investigate the functional roles of MT2-MMP in the early postnatal mammary gland in an unbiased fashion.

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Project description:Expression of the MT1-MMP gene induces a significant upregulation of of oncogenes and tumorignenic genes in 184B5-MT1 cells. Keywords: Genetic modification

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Genome-wide analysis of MCF-7 cells expressing or not MMP-14 (MT1-MMP) growing in monolayer cell culture conditions

Project description:In order to investigate the impact of MMP-14 (MT1-MMP) on the transcriptomes of a human breast adenocarcinoma cell line, we performed a microarray analysis from RNAs isolated from MCF-7 cells expressing either an empty vector (VEC) or human MMP-14 cDNA (MT1) in monolayer growth conditions. MCF-7 cells were stably transfected with either an empty vector (pcDNA3.1/Zeo) or human MMP-14 cDNA (pcDNA3.1-MMP-14/Zeo). Cells were grown for 48 hours in monolayer culture. Cells were then lysed in TRIzol and total RNA was isolated. For each experimental condition, total RNAs isolated from 3 independant biological replicates were pooled.

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Affymetrix microarrays of early postnatal Mt1-mmp-targeted and Mt2-mmp-targeted mammary glands

Project description:This SuperSeries is composed of the SubSeries listed below.

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