Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Genotyping by SNP array of individuals from the general population of Finland and from the population sub-isolate late-settlement area

ABSTRACT: The dataset includes SNP genotypes and CNP signals for 40 individuals from the capital region of Finland representing general population (IDs as FIN_#) and 41 individuals from the population sub-isolate Late-settlement area (IDs as LSFIN_#).

ORGANISM(S): Homo sapiens

SUBMITTER: Ida Surakka

PROVIDER: E-MTAB-382 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Founder population-specific HapMap panel increases power in GWA studies through improved imputation accuracy and CNV tagging.

Surakka Ida I Kristiansson Kati K Anttila Verneri V Inouye Michael M Barnes Chris C Moutsianas Loukas L Salomaa Veikko V Daly Mark M Palotie Aarno A Peltonen Leena L Ripatti Samuli S

Genome research 20100901 10

The combining of genome-wide association (GWA) data across populations represents a major challenge for massive global meta-analyses. Genotype imputation using densely genotyped reference samples facilitates the combination of data across different genotyping platforms. HapMap data is typically used as a reference for single nucleotide polymorphism (SNP) imputation and tagging copy number polymorphisms (CNPs). However, the advantage of having population-specific reference panels for founder popu ...[more]

PMID: 20810666

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Project description:C-type natriuretic peptide (CNP) has been recently identified as an important anabolic regulator of endochondral bone growth, but the molecular mechanism mediating these effects are not completely understood. Here we demonstrate that CNP activates the p38 MAP kinase pathway in chondrocytes and that pharmacological inhibition of p38 blocks the anabolic effects of CNP in a tibia organ culture system. We further show that CNP stimulates endochondral bone growth largely through expansion of the hypertrophic zone of the growth plate, while delaying mineralization. Both effects are reversed by p38 inhibition. We performed Affymetrix microarray analyses to identify CNP target genes in the organ culture system. These studies confirmed that hypertrophic chondrocytes are the main targets of CNP signaling in the growth plate, potentially because cGMP-dependent kinases I and II, important transducers of CNP signaling and are expressed at much higher levels in these cells than in other areas of the tibia. One of the genes most strongly induced by CNP was the Ptgs2 gene, encoding Cox2. Real-time PCR confirmed that Cox2 expression was induced by CNP in hypertrophic chondrocytes, but surprisingly in a p38-independent manner. Moreover, Cox2 inhibition â in contrast to p38 inhibition - did not block the anabolic effects of CNP. In summary, our data identify novel target genes of CNP and demonstrate that the p38 pathway is a novel, essential mediator of CNP effects on endochondral ossification, with potential implications for numerous skeletal diseases. Experiment Overall Design: Tibiae from E15.5 day old embryonic mice were isolated and cultured in minimal media in the presence of vehicle, BSA/HCl (1mM), or C-type natriuretic peptide, CNP (10-6M). On the sixth day of treatment cultured tibias were micro-dissected into the resting/proliferating, hypertrophic, and mineralized areas. Distinct zones from approximately 24 bones were pooled together, from which RNA was isolated using the Qiagen RNeasy Lipid Extraction Kit. Once the quality of total RNA from three independent trials was determined using the Agilent 2100 bioanalyzer, microarray analyses were performed at the London Regional Genomics Centre using MOE430_2.0 Affymetrix arrays. Results were analyzed using GeneSpring 7.2 software.

Dataset Information

Genotyping by SNP array of individuals from the general population of Finland and from the population sub-isolate late-settlement area

Publications

Founder population-specific HapMap panel increases power in GWA studies through improved imputation accuracy and CNV tagging.

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