Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transgenic mice with myeloid-specific overexpression of human S100A12

ABSTRACT: S100A12, a newly discovered member of the S100 family of calcium regulatory proteins, is located within the same gene cluster on chromosome 1q21 as other S100A family members. In humans, S100A12 is mainly secreted by neutrophils and monocytes, but can also be expressed by tissue cells, such as mucosal epithelial cells and keratinocytes. Rodents do not express S100A12.

ORGANISM(S): Mus <genus>

SUBMITTER: Yaling Han

PROVIDER: PXD060232 | iProX | Sat Jan 25 00:00:00 GMT 2025

REPOSITORIES: iProX

ACCESS DATA

Json Xml

Publications

S100A12 triggers NETosis to aggravate myocardial infarction injury via the Annexin A5-calcium axis.

Zhang Xi X Song Haixu H Liu Dan D Cai Yi Y Liu Ziqi Z Zhang Xiaolin X Zhao Xiaojie X Zhang Yan Y Jing Quanmin Q Yan Chenghui C Han Yaling Y

Nature communications 20250218 1

Neutrophil extracellular traps (NETs) play a critical role in acute myocardial infarction (AMI) and the externalization of S100 family members. Here, we show the effects of S100A12 on NETs formation and myocardial injury following AMI. S100A12 expression increases rapidly in neutrophils and peaks on day 1 after AMI, promoting NETs production and exacerbating myocardial injury. DNase I, an inhibitor of NETs, reduces apoptosis of cardiomyocytes induced by S100A12. Mechanistically, the interaction ...[more]

PMID: 39966386

Similar Datasets

NFIC overexpression perturbs normal haematopoeisis by promoting myeloid differentiaon

Project description:Nuclear factor I-C belongs to a family of CTF binding transcription factor which is known for its role cellular differentiation. In our recent study we identified increased expression of NFIC in. AML samples as compared to normal haematpoitic stem and progenitor cells (HSPCs). We also found that overexpression of NFIC in cord blood derived HSPCs perturbed normal haematopoiesis by increasing monocyte production. Therefore in this analysis we aimed to identify the effect of NFIC overexpression in normal HSPCs at single cell level using single cell RNA (scRNA) sequencing. Cluster analysis based on the cellular and functional identities, identified eight clusters according to their terminal differentiation as monocytes, erythrocytes, dendritic cells (DC), megakaryocytes, neutrophils, megakaryocyte-erythroid progenitor cells, basophil/mast progenitor cells and eosinophils. We found that NFIC overexpressing CD34+ HSPCs had increased percentage of monocytes as compared to control. To understand the molecular basis of this, we focussed our analysis on monocytes to determine changes in mRNA expression following NFIC overexpression. We identified 164 and 88 significantly up-regulated and down-regulated genes, respectively (p<0.05, FDR<0.05) in NFIC overexpressing monocytes as compared to control. Pathway analysis identified enrichment in genes involved in mTOR signalling, cancer cell death and survival, energy metabolism pathways and oxidative phosphorylation. Therefore our scRNA suggested that NFIC play a role in monocytic growth development and its overexpression may lead to monocytic bias in normal haematopoiesis.

2023-01-04 | GSE200456 | GEO

Oncogenic and microenvironmental signals drive cell type-specific apoptosis resistance in juvenile myelomonocytic leukemia

Project description:Juvenile myelomonocytic leukemia (JMML) is caused by constitutively activated RAS signalling and is characterized by increased proliferation and predominant myelomonocytic differentiation of hematopoietic cells. Using Mx-Cre;PTPN11D61Y mice, which reflect human JMML, we show that RAS pathway activation affects apoptosis signalling through cell type-dependent regulation of BCL-2 family members. Apoptosis resistance observed in monocytes and granulocytes was mediated by overexpression of the anti-apoptotic and down-regulation of the pro-apoptotic members of the BCL-2 family. Two anti-apoptotic proteins, BCL-XL and MCL-1, were directly regulated by the oncogenic RAS signalling but in addition were influenced by microenvironmental signals. While BCL-XL and BCL-2 were required for the survival of monocytes, MCL-1 was essential for neutrophils. Interestingly, stem and progenitor cells expressing the oncogenic PTPN11 mutant did not display any increased apoptosis resistance. BCL-XL inhibition was the most effective in killing myeloid cells in vitro but was not sufficient to completely resolve myeloproliferation in vivo.

2025-05-07 | PXD055845 | Pride

Overexpression of Ndr2 disturbs hippocampal circuitry and function

Project description:The Ndr (nuclear Dbf2-related) family members are highly conserved serine/threonine protein kinases, which function in many cellular processes extending from cytokinesis to neurite outgrowth. In humans, the NDR2 gene is located in a microduplication hotspot on chromosome 12p that is associated with intellectual disabilities in several individuals. To address a putative contribution of Ndr2 overexpression to such cognitive dysfunctions we generated conditional transgenic mice overexpressing Ndr2 in postmigratory forebrain neurons. Proteomic analysis identifies several interaction partners of transgenic Ndr2 relevant to MF maturation. including the leucin-rich repeat kinase 2 (Lrrk2).

2021-07-16 | PXD026867 | Pride

The ATP-hydrolyzing ectoenzyme E-NTPD8 attenuates colonic inflammation through regulation of P2X4 receptor-dependent metabolism in myeloid cells [F1347]

Project description:Extracellular adenosine triphosphate (ATP) released by mucosal immune cells and by microbiota in the intestinal lumen elicits diverse immune responses that mediate the intestinal homeostasis via P2 purinergic receptors, while overactivation of the ATP signaling leads to disruption of mucosal immune system linked to pathogenesis of intestinal inflammation. In the small intestine, hydrolysis of luminal ATP by E-NTPD7 in epithelial cells is essential for control of the number of Th17 cells. However, the molecular mechanism underlying regulation of microbiota-derived ATP in the colon is poorly understood. Here, we show that E-NTPD8 is highly expressed in large intestinal epithelial cells and hydrolyzes microbiota-derived luminal ATP. Compared to wild-type mice, Entpd8-/- mice develop more severe DSS-induced colitis. In this context, either depletion of neutrophils and monocytes by injecting with anti-Gr-1 antibody or introduction of P2rx4 deficiency into hematopoietic cells ameliorates colitis in Entpd8-/- mice. Increased level of luminal ATP in the colon of Entpd8-/- mice promotes glycolysis in neutrophils and monocytes through P2X4 receptor-dependent Ca2+ influx, which links to prolonged survival and elevated ROS production in these cells. Together, these results indicate that E-NTPD8 limits intestinal inflammation by controlling metabolic alteration toward glycolysis via P2X4 receptor in myeloid cells.

2021-09-23 | GSE160380 | GEO

The ATP-hydrolyzing ectoenzyme E-NTPD8 attenuates colonic inflammation through regulation of P2X4 receptor-dependent metabolism in myeloid cells [F0536]

2021-09-23 | GSE160379 | GEO

The ATP-hydrolyzing ectoenzyme E-NTPD8 attenuates colonic inflammation through regulation of P2X4 receptor-dependent metabolism in myeloid cells [F1413]

2021-09-23 | GSE160381 | GEO

GNF mouse atlas_macrophages

Project description:Monocytes and macrophages express an extensive repertoire of G Protein-Coupled Receptors (GPCRs) that regulate inflammation and immunity. In this study we performed a systematic microarray analysis of GPCR expression in primary mouse tissues to identify family members that are either enriched in macrophages compared to a panel of other cell types, or are regulated by an inflammatory stimulus, the bacterial product lipopolysaccharide (LPS). Keywords: macrophage Macrophage, osteoblast, osteoclast, and mast cell samples were profiled on our GNF1M array.

2008-05-05 | E-GEOD-11339 | biostudies-arrayexpress

GNF mouse atlas_macrophages

2008-05-05 | GSE11339 | GEO

TRIM33 deficiency in mature myeloid cells impairs resolution of colonic inflammation

Project description:Mature myeloid cells play a crucial role in the pathogenesis of Crohn disease (CD) but the molecular players that regulate their functions in CD are not fully characterized. Here we show that Trim33 mRNA level is decreased in CD patient’s blood monocytes and characterize TRIM33 functions in monocytes during dextran sulfate sodium (DSS) induced colitis. Mice deleted for trim33 only in mature myeloid cells (Trim33-/- mice) display an impaired resolution of colonic inflammation. This deficiency is associated with an increased number of blood and colon neutrophils and monocytes and a decreased number of colonic macrophages. In accordance, Trim33-/- monocytes are less competent that wild type monocytes for recruitment and differentiation into macrophages at the inflammatory site. Furthermore, during resolution of DSS-induced colitis, Trim33-/- colonic macrophages display an impaired M1/M2 switch and express a low level of membrane bound TNFα known to regulate resolution of inflammation. Altogether, these results show an important role of TRIM33 in monocytes/macrophages during the resolution of DSS-induced colonic inflammation and pinpoint TRIM33 as a novel Crohn disease biomarker and as a potential therapeutic target.

2019-07-26 | GSE124778 | GEO

Transcription profiling of mouse tissues - GNF Mouse GeneAtlas V3

Project description:Monocytes and macrophages express an extensive repertoire of G Protein-Coupled Receptors (GPCRs) that regulate inflammation and immunity. In this study we performed a systematic microarray analysis of GPCR expression in primary mouse tissues to identify family members that are either enriched in macrophages compared to a panel of other cell types, or are regulated by an inflammatory stimulus, the bacterial product lipopolysaccharide (LPS). Experiment Overall Design: Multiple tissues were taken from naÃ¯ve male C57BL6 mice for hybridization to MOE430_2 arrays

2008-06-11 | E-GEOD-10246 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data