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 knockout (P4KO) and P4KO rescued with PMCA4a primary vascular smooth muscle cells

ABSTRACT: Husain lab cell proliferation in vitro experimental data showed that electroporating PMCA4a 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 P4KO and P4KO+PMCA4a VSMC at the late G1/S stage in serum synchronized cell populations (n=4 populations for each genotype). Serum synchronized late G1/S stage cell populations (P4KO and P4KO+PMCA4a) were employed to extract total RNA which was used for microarray analysis.

ORGANISM(S): Mus musculus

SUBMITTER: Mansoor Husain

PROVIDER: E-GEOD-46744 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Vascular calcification is a complex process and has been associated with aging, diabetes, chronic kidney disease (CKD). Although there have been several studies studying the role of miRNAs (miRs) in bone osteogenesis, little is known about the role of miRs in vascular calcification and their role in the pathogenesis of vascular abnormalities. Matrix vesicles (MV) are known to play an important role in initiating vascular smooth muscle cell (VSMC) calcification. In the present study, we performed miRNA microarray analysis to identify the dysregulated miRs between MV and VSMC derived from CKD rats to understand the role of post-transcriptional regulatory networks governed by these miRNAs in vascular calcification and to uncover the differential miRNA content of MV. The percentage of miRNA to total RNA was increased in MV compared to VSMC. Comparison of expression profiles of miRNA by microarray demonstrated 33 miRs to be differentially expressed with the majority (~ 57%) of them down-regulated. Target genes controlled by differentially expressed miRNAs were identified utilizing two different complementary computational approaches Miranda and Targetscan to understand the functions and pathways that may be affected due to the production of MV from calcifying VSMC thereby contributing to the regulation of genes by miRs. We found several processes including vascular smooth muscle contraction, response to hypoxia and regulation of muscle cell differentiation to be enriched. Signaling pathways identified included MAP-kinase and wnt signaling that have previously been shown to be important in vascular calcification. In conclusion, our results demonstrate that miRs are concentrated in MV from calcifying VSMC, and that important functions and pathways are affected by the miRs dysregulation between calcifying VSMC and the MV they produce. This suggests that miRs may play a very important regulatory role in vascular calcification in CKD by controlling an extensive network of post-transcriptional targets. Compare miRNA from matrix vesicles to miRNA from vascular smooth muscle cells that gave rise to the matrix vesicles from 3 sets of MV and VSMC derived from 3 normal and 3 CKD rats

Dataset Information

Genome wide analysis of genes expressed in late G1/S phase of the cell cycle in PMCA4 knockout (P4KO) and P4KO rescued with PMCA4a primary vascular smooth muscle cells

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