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Adrenal medulla (AM) from controls and SDHD-ESR mice

ABSTRACT: Several mechanisms have been proposed to account for Sdh-mutation-induced tumorigenesis, the most accepted of which is based on the constitutive expression of the hypoxia-inducible factor 1alpha (Hif1alpha) at normal oxygen tension, a theory referred to as pseudo-hypoxic drive. Other molecular processes, such as oxidative stress, apoptosis or chromatin remodeling have been also proposed to play a causative role. Nevertheless, the actual contribution of each of these mechanisms has not been definitively established. Moreover, the biological factors that determine the tissue-specificity of these tumors have not been identified. In this work, we made use of the inducible SDHD-ESR mouse, a conditional mutant in the SdhD gene, which encodes the small subunit of MCII, and that acts as a tumor suppressor gene in humans. We performed microarray analysis of adrenal medulla (AM) in order to identify other early gene expression changes elicited by SdhD deletion.

ORGANISM(S): Mus musculus

PROVIDER: GSE52195 | GEO | 2013/11/15

SECONDARY ACCESSION(S): PRJNA227142

REPOSITORIES: GEO

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Adrenal medulla (AM) from controls and SDHD-ESR mice

Project description:Several mechanisms have been proposed to account for Sdh-mutation-induced tumorigenesis, the most accepted of which is based on the constitutive expression of the hypoxia-inducible factor 1alpha (Hif1alpha) at normal oxygen tension, a theory referred to as pseudo-hypoxic drive. Other molecular processes, such as oxidative stress, apoptosis or chromatin remodeling have been also proposed to play a causative role. Nevertheless, the actual contribution of each of these mechanisms has not been definitively established. Moreover, the biological factors that determine the tissue-specificity of these tumors have not been identified. In this work, we made use of the inducible SDHD-ESR mouse, a conditional mutant in the SdhD gene, which encodes the small subunit of MCII, and that acts as a tumor suppressor gene in humans. We performed microarray analysis of adrenal medulla (AM) in order to identify other early gene expression changes elicited by SdhD deletion. 8 samples from heterozygous (+/-) and 8 samples from null mutants (SDHD-ESR), paired by two and hybrydized against a pool of 8 samples from homozygous wt (+/+) animals.

2013-11-15 | E-GEOD-52195 | biostudies-arrayexpress

Kidney from controls and SDHD-ESR mice

Project description:Several mechanisms have been proposed to account for Sdh-mutation-induced tumorigenesis, the most accepted of which is based on the constitutive expression of the hypoxia-inducible factor 1alpha (Hif1alpha) at normal oxygen tension, a theory referred to as pseudo-hypoxic drive. Other molecular processes, such as oxidative stress, apoptosis or chromatin remodeling have been also proposed to play a causative role. Nevertheless, the actual contribution of each of these mechanisms has not been definitively established. Moreover, the biological factors that determine the tissue-specificity of these tumors have not been identified. In this work, we made use of the inducible SDHD-ESR mouse, a conditional mutant in the SdhD gene, which encodes the small subunit of MCII, and that acts as a tumor suppressor gene in humans. We performed microarray analysis of kidney in order to identify other early gene expression changes elicited by SdhD deletion. 8 samples from heterozygous (+/-) and 8 samples from null mutants (SDHD-ESR), paired by two and hybrydized against a pool of 8 samples from homozygous wt (+/+) animals.

2013-11-15 | E-GEOD-52196 | biostudies-arrayexpress

Kidney from controls and SDHD-ESR mice

Project description:Several mechanisms have been proposed to account for Sdh-mutation-induced tumorigenesis, the most accepted of which is based on the constitutive expression of the hypoxia-inducible factor 1alpha (Hif1alpha) at normal oxygen tension, a theory referred to as pseudo-hypoxic drive. Other molecular processes, such as oxidative stress, apoptosis or chromatin remodeling have been also proposed to play a causative role. Nevertheless, the actual contribution of each of these mechanisms has not been definitively established. Moreover, the biological factors that determine the tissue-specificity of these tumors have not been identified. In this work, we made use of the inducible SDHD-ESR mouse, a conditional mutant in the SdhD gene, which encodes the small subunit of MCII, and that acts as a tumor suppressor gene in humans. We performed microarray analysis of kidney in order to identify other early gene expression changes elicited by SdhD deletion.

2013-11-15 | GSE52196 | GEO

Project description:The similarity in gene-expression profiles suggest that PGL2, like SDHD, is involved in the functionality of the SDH complex, and that tumor formation in these three subgroups involves the same pathways as in SDH linked paragangliomas. We were not able to clarify the identity of PGL2 on 11q13. The lack of differential gene-expression of chromosome 11 genes might indicate that chromosome 11 loss, as demonstrated in SDHD-linked paragangliomas, is an important feature in the formation of a paraganglioma regardless of the genetic background. Keywords: disease state analysis

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Project description:Analysis of knockdown of SDHD with or without knockdown of CDKN1C or SLC22A18 at gene expression level. The hypothesis tested in this study was to determine whether the gene expression signature following SDHD knockdown together with SLC22A18 or CDKN1C more closely resembles the signature found in tumors than the signature resulting from SDHD knockdown alone.

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Project description:Kidney from controls and SDHD-ESR mice

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Expression Profiling of pheochromocytomas of various genetic origins

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