Project description:To identify genetic alterations involved in the pathogenesis of PETs, we have analysed a total of 32 PET samples (29 tissue specimens and 3 cell lines) using high-resolution single nucleotide polymorphism (SNP) arrays. Keywords: comparative genomic hybridisation
Project description:allele call files from analysis of NCI60 cell line DNA on 100K SNP arrays. Keywords = NCI60, SNP array, cancer cell line Keywords: other
Project description:To study the gene expression profiles of brown (BAT) and white (WAT) adipose tissues in wild type and LR11-deficeint mice. The four RNA sources, WT scWAT, Lr11 -/- scWAT, WT BAT and Lr11 -/- BAT, were prepared from subcutaneous WAT and BAT from wild-type mice and Lr11 -/- mice, respectively (n=3 each).
Project description:Obesity and type 2 diabetes cause a loss in brown adipose tissue (BAT) activity in mice and human, but the molecular mechanisms that drive BAT cell remodeling remain largely. Using a multilayered approach, we comprehensively map a deep reorganization in the BAT cells. We uncovered a subset of macrophages as the lipid-associated macrophages (LAM), which were massively increased in genetic and dietary model of BAT expansion. LAM participate in this scenario by capturing extracellular vesicles carrying damaged lipids and mitochondria released from metabolically-stressed brown adipocytes. CD36 scavenger receptor drives LAM phenotype and through * in vitro* and *in vivo* models, we demonstrated that CD36-deficient LAM increased brown fat genes. LAM release Tgfb1 that reduces brown adipocytes identity through Aldh1a1 induction. This study provides the first description of cell dynamics in BAT of obese models identifying LAM as responder to tissue-level metabolic stress and key driver to loss of BAT cell identity.
Project description:Obesity and type 2 diabetes cause a loss in brown adipose tissue (BAT) activity in mice and human, but the molecular mechanisms that drive BAT cell remodeling remain largely. Using a multilayered approach, we comprehensively map a deep reorganization in the BAT cells. We uncovered a subset of macrophages as the lipid-associated macrophages (LAM), which were massively increased in genetic and dietary model of BAT expansion. LAM participate in this scenario by capturing extracellular vesicles carrying damaged lipids and mitochondria released from metabolically-stressed brown adipocytes. CD36 scavenger receptor drives LAM phenotype and through * in vitro* and *in vivo* models, we demonstrated that CD36-deficient LAM increased brown fat genes. LAM release Tgfb1 that reduces brown adipocytes identity through Aldh1a1 induction. This study provides the first description of cell dynamics in BAT of obese models identifying LAM as responder to tissue-level metabolic stress and key driver to loss of BAT cell identity.
