Ontology highlight
ABSTRACT:
PROVIDER: PRJNA555452 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Oscillibacter valericigenes overview
| PRJNA42897 | ENA
Project description:Oscillibacter valericigenes Sjm18-20 Genome sequencing
| PRJNA41823 | ENA
Project description:Microbiota contributes to induction of type 2 diabetes by high-fat/high-sugar (HFHS), but which organs/pathways are impacted by microbiota remains unknown. Using multi-organ network and transkingdom analyses, we found that microbiota-dependent. impairment of OXPHOS /mitochondria in white adipose tissue (WAT) plays a primary role in regulating systemic glucose metabolism. The follow-up analysis established that Mmp12+ macrophages link microbiota-dependent inflammation and OXPHOS damage in WAT. Moreover, the molecular signature of Mmp12+ macrophages in WAT was associated with insulin resistance in obese patients. Next, we tested functional effects of MMP12 and found that Mmp12 genetic deficiency or MMP12 inhibition improved glucose metabolism in conventional, but not in germfree mice. MMP12 treatment induced insulin resistance in adipocytes. TLR2-ligands present in Oscillibacter valericigenes bacteria, which are expanded by HFHS, induce Mmp12 in WAT macrophages in a MYD88-ATF3-dependent manner. Thus, HFHS induces Mmp12+ macrophages and MMP12, representing a microbiota-dependent bridge between inflammation and mitochondrial damage in WAT and causing insulin resistance. doi: https://doi.org/10.1084/jem.20220017
2022-05-24 | GSE203516 | GEO
Project description:Paper abstract: Microbiota contribute to the induction of type 2 diabetes by high-fat/high-sugar (HFHS) diet, but which organs/pathways are impacted by microbiota remain unknown. Using multiorgan network and transkingdom analyses, we found that microbiotadependent impairment of OXPHOS/mitochondria in white adipose tissue (WAT) plays a primary role in regulating systemic glucose metabolism. The follow-up analysis established that Mmp12+ macrophages link microbiota-dependent inflammation and OXPHOS damage in WAT. Moreover, the molecular signature of Mmp12+ macrophages in WAT was associated with insulin resistance in obese patients. Next, we tested the functional effects of MMP12 and found that Mmp12 genetic deficiency or MMP12 inhibition improved glucose metabolism in conventional, but not in germ-free mice. MMP12 treatment induced insulin resistance in adipocytes. TLR2-ligands present in Oscillibacter valericigenes bacteria, which are expanded by HFHS, induce Mmp12 in WAT macrophages in a MYD88-ATF3–dependent manner. Thus, HFHS induces Mmp12+ macrophages and MMP12, representing a microbiota-dependent bridge between inflammation and mitochondrial damage in WAT and causing insulin resistance.
2022-10-13 | GSE215226 | GEO
Project description:Microbiota contributes to induction of type 2 diabetes by high-fat/high-sugar (HFHS), but which organs/pathways are impacted by microbiota remains unknown. Using multi-organ network and transkingdom analyses, we found that microbiota-dependent. impairment of OXPHOS /mitochondria in white adipose tissue (WAT) plays a primary role in regulating systemic glucose metabolism. The follow-up analysis established that Mmp12+ macrophages link microbiota-dependent inflammation and OXPHOS damage in WAT. Moreover, the molecular signature of Mmp12+ macrophages in WAT was associated with insulin resistance in obese patients. Next, we tested functional effects of MMP12 and found that Mmp12 genetic deficiency or MMP12 inhibition improved glucose metabolism in conventional, but not in germfree mice. MMP12 treatment induced insulin resistance in adipocytes. TLR2-ligands present in Oscillibacter valericigenes bacteria, which are expanded by HFHS, induce Mmp12 in WAT macrophages in a MYD88-ATF3-dependent manner. Thus, HFHS induces Mmp12+ macrophages and MMP12, representing a microbiota-dependent bridge between inflammation and mitochondrial damage in WAT and causing insulin resistance. doi: https://doi.org/10.1084/jem.20220017
2022-05-27 | GSE203488 | GEO
Project description:Microbiota contributes to induction of type 2 diabetes by high-fat/high-sugar (HFHS), but which organs/pathways are impacted by microbiota remains unknown. Using multi-organ network and transkingdom analyses, we found that microbiota-dependent. impairment of OXPHOS /mitochondria in white adipose tissue (WAT) plays a primary role in regulating systemic glucose metabolism. The follow-up analysis established that Mmp12+ macrophages link microbiota-dependent inflammation and OXPHOS damage in WAT. Moreover, the molecular signature of Mmp12+ macrophages in WAT was associated with insulin resistance in obese patients. Next, we tested functional effects of MMP12 and found that Mmp12 genetic deficiency or MMP12 inhibition improved glucose metabolism in conventional, but not in germfree mice. MMP12 treatment induced insulin resistance in adipocytes. TLR2-ligands present in Oscillibacter valericigenes bacteria, which are expanded by HFHS, induce Mmp12 in WAT macrophages in a MYD88-ATF3-dependent manner. Thus, HFHS induces Mmp12+ macrophages and MMP12, representing a microbiota-dependent bridge between inflammation and mitochondrial damage in WAT and causing insulin resistance. doi: https://doi.org/10.1084/jem.20220017
2022-05-27 | GSE203489 | GEO
Project description:Blastema formation is a hallmark of limb regeneration that requires proliferation and migration of progenitors derived from many tissues to the amputation plane. To better understand the genetic programs that initiate limb regeneration, we reasoned that blastemal progenitors would be among early proliferating cells in the stump following amputation. Here we separately profiled dividing and non-dividing stump tissues, as well as the wound epidermis, during early axolotl limb regeneration to examine transcriptional programs of blastemal progenitors. We provide a description of the changes in gene expression specific to early dividing cells at the site of amputation, inclusive of progenitors for the regenerating limb. This work collectively demonstrates differential suppression/activation of core developmental signaling pathways in subsets of the early regenerating limb and further suggests that interleukin-8 (il-8) signaling is important for regeneration.
2019-01-01 | GSE111213 | GEO
Project description:Aeromonas hydrophila caused patient death.
| PRJNA484846 | ENA
Project description:Although the majority of genomic binding sites for the insulator protein CTCF are constitutively occupied, a subset show variable occupancy. Such variable sites provide an opportunity to assess context-specific CTCF functions in gene regulation. Here we have identified a variably occupied CTCF site in the Ultrabithorax (Ubx) gene in Drosophila. This site is occupied in tissues where Ubx is active (third thoracic imaginal leg disc) but is not bound in tissues where the Ubx gene is repressed (first thoracic imaginal leg disc).
2014-10-11 | GSE62234 | GEO
Project description:Improved diagnostics are necessary to differentiate between multipe potential etiologies of acute illness in a hospitalized patient. The peripheral blood host gene expression response can act as a supplementary diagnostic tool and better inform the full host immune response to a pathogen. We performed RNA sequencing on peripheral blood from 48 hospitalized patients with confirmed candidemia as well as patients with other acute viral, bacterial, and non-infectious illnesses and derived pathogen class-specific gene expression classifiers.
2021-06-08 | GSE176260 | GEO