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GM-CSF-activated STAT5A but not STAT5B regulates macrophage functions and inflammation in atherosclerosis

ABSTRACT: GM-CSF-activated STAT5A but not STAT5B regulates macrophage functions and inflammation in atherosclerosis

PROVIDER: PRJNA901347 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22272453.fastq.gz	Fastqsanger.gz
	SRR22272454.fastq.gz	Fastqsanger.gz
	SRR22272455.fastq.gz	Fastqsanger.gz
	SRR22272456.fastq.gz	Fastqsanger.gz
	SRR22272457.fastq.gz	Fastqsanger.gz

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GM-CSF-activated STAT5A but not STAT5B regulates macrophage functions and inflammation in atherosclerosis

Project description:Inhibition of STAT5 was recently reported to reduce mouse atherosclerosis. However, the regulatory role of STAT5 isoforms STAT5A and STAT5B in human disease and more specifically in macrophages remains unknown. Here, we demonstrate reciprocal expression regulation of STAT5A and B in human atherosclerotic lesions. The former was highly upregulated in ruptured over stable plaque and correlated with macrophage presence, a finding that was corroborated by the high chromosomal accessibility of STAT5A but not B gene in plaque macrophages. Phosphorylated STAT5 correlated with macrophages confirming its activation status. As macrophage STAT5 is activated by GM-CSF, we studied the effects of its silencing in GM-CSF differentiated human macrophages. STAT5A knockdown blunted NF-kB pathway, phagocytosis, cholesterol metabolism, and apoptosis terms. These changes at transcriptional level could be confirmed at functional level, with significant increases in apoptosis and phagocytosis and decreases in lipid uptake and IL-6, IL8, and TNFa cytokine secretion after STAT5A knockdown. Finally, inhibition of general and isoform A specific STAT5 inhibitor significantly reduced the secretion of TNFa, IL-8 and IL-10 in ex vivo tissue slices of advanced human atherosclerotic plaques. In summary, we identify STAT5A as important determinant of macrophage functions and inflammation in the context of atherosclerosis and show its promise as therapeutic target for human atherosclerotic plaque inflammation.

2023-10-02 | GSE217893 | GEO

GM-CSF-mediated granulopoiesis is regulated by the transcription factor STAT5A/B

Project description:GM-CSF controls the development of granulocytes but little is known about the contribution of the downstream mediating transcription factor STAT5A/B. To elucidate this pathway, we generated mice lacking the Stat5a and 5b genes in blood cells. Peripheral neutrophils were decreased and administration of 5-FU and GM-CSF failed to induce granulopoiesis in Stat5a/b-mutant mice. GMPs were isolated and cultured with GM-CSF. Both the number and size of STAT5A/B-null colonies were reduced and GM-CSF-induced survival of mature STAT5A/B-null neutrophils was impaired. Time-lapse cinematography and single cell tracking of GMPs revealed that STAT5A/B-null cells were characterized by a longer generation time and an increased cell death. Gene expression profiling experiments suggested that STAT5A/B directs GM-CSF signaling through the regulation of cell survival genes.

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Transcription profiling of mouse wild type and Stat5a or 5b knock-out blood cells treated with GM-CSF to induce granulopoiesis

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Prolactin-inducible Stat5a-mediated and Stat5b-mediated gene profiles

Project description:Stat5a and Stat5b proteins are highly homologous with greater than 90% amino acid identity and share binding to the palindromic Stat5 consensus sequence, TTCNNNGAA, but individual roles of each transcription factor in breast cancer have not been thoroughly evaluated. To determine the degree of similarity between transcripts modulated by Stat5a and Stat5b proteins in human breast cancer, we utilized genome-wide transcript profiling to identify genes regulated specifically by Stat5a or Stat5b in response to prolactin. Stat5a or Stat5b was transiently overexpressed using adenoviral gene delivery in MCF7 breast cancer cells followed 16 hr serum starvation and a brief 4 hr exposure to 10nM human prolactin to identify immediate-early transcripts modulated by each transcription factor. Basal activation of Stat5a or Stat5b was not present in cells not stimulated with prolactin. mRNA from each condition was harvested and validated using the Agilent bioanalyzer. cDNA was generated and genome-wide transcript profiling was performed in triplicate using the Affymetrix HuGene 1.0 ST array.

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RNA-seq data from wildtype, STAT5A-knockout and STAT5B-knockout BCR/ABLp185+ transformed mouse bone marrow cell lines

Project description:RNA-Seq of immortalized Stat5a-/-, Stat5b-/-, and wildtype BCR/ABLp185+ cell lines was used to identify STAT5A and STAT5B specific target genes.

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Project description:Bone marrow cells were isolated, primed with M-CSF (M-BMDM) or GM-CSF (GM-BMDM) and cultured for 7 days. The proteomic difference between GM-BMDM and M-BMDM were analyzed to describe the phenotye and function of two types of macrophages.

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Microarray Experiments for mice lacking or with the Stat5a and 5b genes in blood cells that were treated w/o CMP

2010-02-21 | E-GEOD-14698 | biostudies-arrayexpress