Unknown,Transcriptomics,Genomics,Proteomics

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Genome wide analysis of genes expressed in late G1/S phase of the cell cycle in PMCA4 wild type (P4WT), PMCA4 knockout(P4KO), P4KO rescued with PMCA4b and P4KO rescued with Vector primary vascular smooth muscle cells

ABSTRACT: Husain lab cell proliferation in vitro experimental data showed that electroporating PMCA4b cDNA into P4KO cells rescued the G1 arrest phenotype in P4KO primary vascular smooth muscle cells (VSMC). This microarray documents the different gene expression profiles of P4WT, P4KO, P4KO+PMCA4b and P4KO+Vector VSMC at the late G1/S stage in serum synchronized cell populations (n=4 or 5 populations for each genotype). Serum synchronized late G1/S stage cell populations (P4WT, P4KO, P4KO+PMCA4b and P4KO+Vector) were employed to extract total RNA which was used for microarray analysis.

ORGANISM(S): Mus musculus

SUBMITTER: Mansoor Husain

PROVIDER: E-GEOD-38319 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Fibrosis is defined as an abnormal matrix remodeling and loss of tissue homeostasis due to excessive synthesis and accumulation of extracellular matrix proteins in tissues. At present, there is no effective therapy for organ fibrosis. Previous studies demonstrated that aged plasminogen activator inhibitor-1(PAI-1) knockout mice develop spontaneously cardiac-selective fibrosis without affecting any other organs including kidney. Therefore, the PAI-1 knockout model of cardiac fibrosis provides an excellent opportunity to find the igniter(s) of cardiac fibrosis and its status in unaffected organs. We hypothesized that differential expressions of profibrotic and antifibrotic genes in PAI-1 knockout hearts and unaffected organs lead to cardiac selective fibrosis. In order to address this prediction, we have used a genome-wide gene expression profiling of transcripts derived from aged PAI-1 knockout hearts and kidneys. The variations of global gene expression profiling were compared within four groups: wildtype heart vs. knockout heart; wildtype kidney vs. knockout kidney; knockout heart vs. knockout kidney and wildtype heart vs. wildtype kidney. Analysis of illumina-based microarray data revealed that several genes involved in different biological processes such as immune system processing, response to stress, cytokine signaling, cell proliferation, adhesion, migration, matrix organization and transcriptional regulation were affected in hearts and kidneys by the absence of PAI-1, a potent inhibitor of urokinase- and tissue-type plasminogen activator. Importantly, the expressions of a number of genes, involved in profibrotic pathways were upregulated or downregulated in PAI-1 knockout hearts compared to wildtype hearts and PAI-1 knockout kidneys. To our knowledge, this is the first comprehensive report on the influence of PAI-1 on global gene expression profiling in the heart and kidney and its implication in several biological processes including fibrogenesis. Total RNA was extracted from hearts and kidneys derived from three PAI-1 knockout (12- month old) and three wild-type mice (12-month old) using RNeasy Fibrous Tissue Mini Kit (Qiagen, Valencia, CA) following the manufacturer’s instructions. The quality of RNA (RNA Integrity, RIN) in all 12 samples (3 wildtype hearts; 3 PAI-1 KO hearts; 3 wildtype kidneys; and 3 PAI-1 KO kidneys) was checked using the bioanalyzer. We have used a genome-wide gene expression profiling of transcripts derived from aged PAI-1 knockout hearts and kidneys. The variations of global gene expression profiling were compared within four groups: wildtype heart vs. knockout heart; wildtype kidney vs. knockout kidney; knockout heart vs. knockout kidney and wildtype heart vs. wildtype kidney.

Dataset Information

Genome wide analysis of genes expressed in late G1/S phase of the cell cycle in PMCA4 wild type (P4WT), PMCA4 knockout(P4KO), P4KO rescued with PMCA4b and P4KO rescued with Vector primary vascular smooth muscle cells

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