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Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88 [scRNA-Seq]

ABSTRACT: Examination of the single cell trasncriptional profile of bone marrow sorted LSK 10 days post Poly(I:C) challenge

ORGANISM(S): Mus musculus

PROVIDER: GSE112541 | GEO | 2019/08/12

REPOSITORIES: GEO

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Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88 [Bulk RNA-Seq]

Project description:examination of the transcriptional profile of LSK and neutrophils (L6G+)

2019-08-12 | GSE112538 | GEO

Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88

Project description:Innate immune cells, and myeloid lineage cells in particular, constitute the first line ofdefense for the containment of invading pathogens. To meet the augmented demand of myeloidcells in response to systemic infections, inflammatory signals trigger a rapid transcriptional response inhematopoietic stem and progenitor cells (HSPCs), promoting their proliferation and preferential differentiation towards the granulocytic lineage

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Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-08-12 | GSE112542 | GEO

Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88

Project description:Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88

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Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88 [scRNA-Seq]

Project description:Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88 [scRNA-Seq]

| PRJNA448160 | ENA

Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88 [Bulk RNA-Seq]

Project description:Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88 [Bulk RNA-Seq]

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SPOP negatively regulates Toll-like receptor-induced inflammation by disrupting MyD88 self-association.

Project description:Toll-like receptor (TLR) signaling pathways need to be tightly controlled to avoid excessive inflammation and unwanted damage to the host. Myeloid differentiation primary response gene 88 (MyD88) is a critical adaptor of TLR signaling. Here, we identified the speckle-type POZ protein (SPOP) as a MyD88-associated protein. SPOP was recruited to MyD88 following TLR4 activation. TLR4 activation also caused the translocation of SPOP from the nucleus to the cytoplasm. SPOP depletion promoted the aggregation of MyD88 and recruitment of the downstream signaling kinases IRAK4, IRAK1 and IRAK2. Consistently, overexpression of SPOP inhibited the TLR4-mediated activation of NF-κB and production of inflammatory cytokines, whereas SPOP depletion had the opposite effects. Furthermore, knockdown of SPOP increased MyD88 aggregation and inflammatory cytokine production upon TLR2, TLR7 and TLR9 activation. Our findings reveal a mechanism by which MyD88 is regulated and highlight a role for SPOP in limiting inflammatory responses.

| S-EPMC8245473 | biostudies-literature

The E3 ubiquitin ligase SPOP controls resolution of systemic inflammation by triggering MYD88 degradation.

Project description:The response to systemic infection and injury requires the rapid adaptation of hematopoietic stem cells (HSCs), which proliferate and divert their differentiation toward the myeloid lineage. Significant interest has emerged in understanding the signals that trigger the emergency hematopoietic program. However, the mechanisms that halt this response of HSCs, which is critical to restore homeostasis, remain unknown. Here we reveal that the E3 ubiquitin ligase Speckle-type BTB-POZ protein (SPOP) restrains the inflammatory activation of HSCs. In the absence of Spop, systemic inflammation proceeded in an unresolved manner, and the sustained response in the HSCs resulted in a lethal phenotype reminiscent of hyper-inflammatory syndrome or sepsis. Our proteomic studies decipher that SPOP restricted inflammation by ubiquitinating the innate signal transducer myeloid differentiation primary response protein 88 (MYD88). These findings unearth an HSC-intrinsic post-translational mechanism that is essential for reestablishing homeostasis after emergency hematopoiesis.

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Trauma Induces Emergency Hematopoiesis through IL-1/MyD88-Dependent Production of G-CSF.

Project description:The inflammatory response to infection or injury dramatically increases the hematopoietic demand on the bone marrow to replace effector leukocytes consumed in the inflammatory response. In the setting of infection, pathogen-associated molecular patterns induce emergency hematopoiesis, activating hematopoietic stem and progenitor cells to proliferate and produce progeny for accelerated myelopoiesis. Sterile tissue injury due to trauma also increases leukocyte demand; however, the effect of sterile tissue injury on hematopoiesis is not well described. We find that tissue injury alone induces emergency hematopoiesis in mice subjected to polytrauma. This process is driven by IL-1/MyD88-dependent production of G-CSF. G-CSF induces the expansion of hematopoietic progenitors, including hematopoietic stem cells and multipotent progenitors, and increases the frequency of myeloid-skewed progenitors. To our knowledge, these data provide the first comprehensive description of injury-induced emergency hematopoiesis and identify an IL-1/MyD88/G-CSF-dependent pathway as the key regulator of emergency hematopoiesis after injury.

| S-EPMC6504560 | biostudies-literature

Bone marrow adipocytes fuel emergency hematopoiesis

Project description:Hematopoiesis advances cardiovascular disease by generating inflammatory leukocytes that attack the arteries, heart and brain. While it is well documented that the bone marrow niche regulates hematopoietic stem cell proliferation and hence the systemic leukocyte pool, it is less clear how cardiovascular disease affects the vasculature forming this niche. Here we show that arterial hypertension, atherosclerosis and myocardial infarction alter the anatomy and function of bone marrow vasculature. Hypertension and atherosclerosis instigated vascular fibrosis, leakage and endothelial dysfunction in the bone marrow. Myocardial infarction induced vascular leakage and bone marrow angiogenesis via Vegf signaling. Endothelial cell-specific deletion of the Vegf receptor 2 limited emergency hematopoiesis after myocardial infarction, indicating that new vasculature supports higher blood cell production. RNA-sequencing of bone marrow endothelial cells revealed inflammatory gene expression in mice with cardiovascular disease. Endothelial cell-specific deletion of interleukin 6 or versican, which were highly expressed in mice with atherosclerosis or myocardial infarction, respectively, reduced hematopoiesis and systemic myeloid cells. Taken together, cardiovascular disease affects the vascular bone marrow niche, thus influencing hematopoietic stem cell behavior and expanding innate immune cell supply to atherosclerotic plaque and ischemic myocardium. Interrupting this feed back loop may constrain cardiovascular inflammation.

2023-11-04 | GSE169267 | GEO

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