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An Epigenetic Memory of Inflammation Induces Context-Dependent Lineage Plasticity in the Pancreas with Divergent Phenotypic Outcomes

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE198564 | GEO | 2023/10/24

REPOSITORIES: GEO

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An Epigenetic Memory of Inflammation Induces Context-Dependent Lineage Plasticity in the Pancreas with Divergent Phenotypic Outcomes [memory + KrasG12D scRNA-seq]

Project description:An Epigenetic Memory of Inflammation Induces Context-Dependent Lineage Plasticity in the Pancreas with Divergent Phenotypic Outcomes [memory + KrasG12D scRNA-seq]

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An Epigenetic Memory of Inflammation Induces Context-Dependent Lineage Plasticity in the Pancreas with Divergent Phenotypic Outcomes [bulk ATAC-seq]

Project description:Inflammation is essential to the disruption of tissue homeostasis, and, in the pancreas, can destabilize the identity of terminally differentiated acinar cells. Herein we employ lineage-traced mouse models to delineate the chromatin dynamics that accompany the cycle of metaplasia and regeneration following pancreatitis, and unveil the presence of an epigenetic memory of inflammation in the pancreatic acinar cell compartment. We observe that despite histologic resolution of pancreatitis, acinar cells fail to return to their molecular baseline after several months, representing an incomplete cell fate decision. In vivo, this epigenetic memory controls lineage plasticity, with diminished metaplasia in response to a second inflammatory insult but increased tumorigenesis with an oncogenic Kras mutation. We demonstrate that both persistent chromatin and transcriptional changes constituting memory are recalled with oncogenic stress. Together, our findings define the dynamics and recall of an epigenetic memory of inflammation that impacts cell fate decisions in a context-dependent manner.

2023-10-24 | GSE198563 | GEO

An Epigenetic Memory of Inflammation Induces Context-Dependent Lineage Plasticity in the Pancreas with Divergent Phenotypic Outcomes [Acute Pancreatitis scRNA-seq]

Project description:An Epigenetic Memory of Inflammation Induces Context-Dependent Lineage Plasticity in the Pancreas with Divergent Phenotypic Outcomes [Acute Pancreatitis scRNA-seq]

2023-10-24 | GSE198183 | GEO

An Epigenetic Memory of Inflammation Induces Context-Dependent Lineage Plasticity in the Pancreas with Divergent Phenotypic Outcomes

Project description:An Epigenetic Memory of Inflammation Induces Context-Dependent Lineage Plasticity in the Pancreas with Divergent Phenotypic Outcomes

| PRJNA815980 | ENA

An Epigenetic Memory of Inflammation Induces Context-Dependent Lineage Plasticity in the Pancreas with Divergent Phenotypic Outcomes [memory + KrasG12D scRNA-seq]

Project description:An Epigenetic Memory of Inflammation Induces Context-Dependent Lineage Plasticity in the Pancreas with Divergent Phenotypic Outcomes [memory + KrasG12D scRNA-seq]

| PRJNA814078 | ENA

An Epigenetic Memory of Inflammation Induces Context-Dependent Lineage Plasticity in the Pancreas with Divergent Phenotypic Outcomes [bulk ATAC-seq]

Project description:An Epigenetic Memory of Inflammation Induces Context-Dependent Lineage Plasticity in the Pancreas with Divergent Phenotypic Outcomes [bulk ATAC-seq]

| PRJNA815985 | ENA

An Epigenetic Memory of Inflammation Induces Context-Dependent Lineage Plasticity in the Pancreas with Divergent Phenotypic Outcomes [Acute Pancreatitis scRNA-seq]

Project description:An Epigenetic Memory of Inflammation Induces Context-Dependent Lineage Plasticity in the Pancreas with Divergent Phenotypic Outcomes [Acute Pancreatitis scRNA-seq]

| PRJNA814079 | ENA

An epigenetic memory of inflammation controls context-dependent lineage plasticity in the pancreas [bulk RNA-seq]

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An epigenetic memory of inflammation controls context-dependent lineage plasticity in the pancreas [bulk RNA-seq]

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Direct Lineage Reprogramming: Harnessing Cell Plasticity between Liver and Pancreas.

Project description:Direct lineage reprogramming of abundant and accessible cells into therapeutically useful cell types holds tremendous potential in regenerative medicine. To date, a number of different cell types have been generated by lineage reprogramming methods, including cells from the neural, cardiac, hepatic, and pancreatic lineages. The success of this strategy relies on developmental biology and the knowledge of cell-fate-defining transcriptional networks. Hepatocytes represent a prime target for β cell conversion for numerous reasons, including close developmental origin, accessibility, and regenerative potential. We present here an overview of pancreatic and hepatic development, with a particular focus on the mechanisms underlying the divergence between the two cell lineages. Additionally, we discuss to what extent this lineage relationship can be exploited in efforts to reprogram one cell type into the other and whether such an approach may provide a suitable strategy for regenerative therapies of diabetes.

| S-EPMC7328458 | biostudies-literature

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