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Effect of HDL enriched with Serum Amyloid A1 (HDL+SAA1) on Gene Expression by Classical CD14+/CD16- Human Peripheral Blood Monocytes from Asthmatics

ABSTRACT: IL-6 and PTGS2 were the most highly expressed mRNA transcripts in Classical CD14+/CD16- Monocytes from Asthmatic Subjects in response to treatment with HDL+SAA1

ORGANISM(S): Homo sapiens

PROVIDER: GSE134591 | GEO | 2020/07/31

REPOSITORIES: GEO

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Effect of HDL enriched with Serum Amyloid A1 (HDL+SAA1) on Gene Expression by Classical CD14+/CD16- Human Peripheral Blood Monocytes from Asthmatics

Project description:Effect of HDL enriched with Serum Amyloid A1 (HDL+SAA1) on Gene Expression by Classical CD14+/CD16- Human Peripheral Blood Monocytes from Asthmatics

| PRJNA555747 | ENA

Effect of serum amyloid A1 (SAA1) on gene expression in primary murine macrophages

Project description:Macrophages are important regulators of the immune system and are critically involved in the pathophysiology of many diseases. Serum amlyoidosis is a protein misfolding disease which can follow chronic inflammatory conditions. Deposition of fibrils formed from serum amyloid A1 (SAA1) protein occurs systemically and can lead to severe or even fatal outcomes. Macrophages play a critical role in the misfolding and deposition of SAA1-derived fibrils and the role of macrophages in this context has been studied extensively. It is known that SAA1 can bind to some surface receptors on macrophages and it is taken up by the macrophages and metabolized in the lysosomes. On the other hand, the effect of SAA1 on macrophage physiology has been much less investigated so far. Therefore, we aim to investigate the effect of SAA1 on macrophage gene expression by gene microarray analysis. To this end, primary peritoneal macrophages from NMRI mice were treated with endotoxin-free recombinantly expressed full-length mSAA1 for 6 and 24 h and gene expression was analyzed.

2021-07-20 | GSE155278 | GEO

Serum Amyloid A1 (SAA1) Revisited: Restricted Leukocyte-Activating Properties of Homogeneous SAA1.

Project description:Infection, sterile injury, and chronic inflammation trigger the acute phase response in order to re-establish homeostasis. This response includes production of positive acute phase proteins in the liver, such as members of the serum amyloid A (SAA) family. In humans the major acute phase SAAs comprise a group of closely related variants of SAA1 and SAA2. SAA1 was proven to be chemotactic for several leukocyte subtypes through activation of the G protein-coupled receptor FPRL1/FPR2. Several other biological activities of SAA1, such as cytokine induction, reported to be mediated via TLRs, have been debated recently. Especially commercial SAA1, recombinantly produced in Escherichia coli, was found to be contaminated with bacterial products confounding biological assays performed with this rSAA1. We purified rSAA1 by RP-HPLC to homogeneity, removing contaminants such as lipopolysaccharides, lipoproteins and formylated peptides, and re-assessed several biological activities attributed to SAA1 (chemotaxis, cytokine induction, MMP-9 release, ROS generation, and macrophage differentiation). The homogeneous rSAA1 (hrSAA1) lacked most cell-activating properties, but its leukocyte-recruiting capacity in vivo and it's in vitro synergy with other leukocyte attractants remained preserved. Furthermore, hrSAA1 maintained the ability to promote monocyte survival. This indicates that pure hrSAA1 retains its potential to activate FPR2, whereas TLR-mediated effects seem to be related to traces of bacterial TLR ligands in the E. coli-produced human rSAA1.

| S-EPMC7240019 | biostudies-literature

sRNA sequencing of HDL from human donors

Project description:miRNAs and other small RNAs have been found associated with high-density lipoproteins (HDL). The aim of this study was to investigate the miRNA signature on human HDL from 10 donors.

2019-01-03 | GSE124559 | GEO

Effect of serum amyloid A1 (SAA1) on gene expression in primary murine macrophages

Project description:Effect of serum amyloid A1 (SAA1) on gene expression in primary murine macrophages

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Expression data from human coronary artery endothelial cells treated with HDL components

Project description:We quantified differential gene (mRNA) expression in human coronary artery cells treated with native HDL, reconstituted HDL, lipid-free apolipoprotein A-I, small unilamellar vesicles, or PBS control. These data were used to determine which genes are regulated by native HDL compared to components of HDL and categorize data based on shared sets of genes and distinct sets of genes regulated by each component.

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HDL suppresses the type I interferon response

Project description:Background: High density lipoprotein (HDL) protects the artery wall by removing cholesterol from lipid-laden macrophages. However, recent evidence suggests that it might also inhibit atherogenesis by combating inflammation. Methods and Results: To identify potential anti-inflammatory mechanisms, we challenged macrophages with lipopolysaccharide (LPS), an inflammatory microbial ligand for Toll-like receptor 4 (TLR4). HDL inhibited the expression of 33% (301 of 911) of the genes normally induced by LPS, microarray analysis revealed. One of its major targets was the type I interferon response pathway, a family of potent viral immunoregulators controlled by TLR4 and the TRAM/TRIF signaling pathway. Unexpectedly, HDL’s ability to inhibit gene expression was independent of cellular cholesterol stores. Moreover, it was unaffected by downregulation of two ATP-binding cassette transporters, ABCA1 and ABCG1, that promote cholesterol efflux. To examine the pathway’s potential in vivo relevance, we used mice deficient in apolipoprotein (apo) A-I, HDL’s major protein. After infection with Salmonella (a Gram-negative bacterium that expresses LPS), apoA-I–deficient mice had 6-fold higher plasma levels of interferon-beta-a key regulator of the type I interferon response than did wild-type mice. Conclusions: HDL inhibits a subset of LPS-stimulated macrophage genes that regulate the type I interferon response, and its action is independent of sterol metabolism. These findings raise the possibility that regulation of macrophage genes by HDL might link innate immunity and cardioprotection. 12 arrays, 3 experimental groups, mMncN (no treatment), mMncL (LPS treated, exposed for 4 h to serum-free medium or serum-free medium supplemented with 100 ng/mL of LPS), and mMwtL (HDL treated, Macrophages were treated for 4 h with serum-free medium or serum-free medium supplemented with 50 mg/mL of HDL, washed twice with PBS).

2010-10-01 | E-GEOD-19340 | biostudies-arrayexpress

sRNA sequencing of miRNAs exported to HDL from primary human islets

Project description:miRNAs are exported to high density lipoproteins (HDL). This study aimed to understand what miRNAs are exported from primary islets to HDL in vitro.

2019-01-16 | GSE125136 | GEO

MicroRNA expression data from human coronary artery endothelial cells treated with HDL components

Project description:We quantified differential microRNA (miRNA) expression in human coronary artery cells treated with native HDL, reconstituted HDL, lipid-free apolipoprotein A-I, small unilamellar vesicles, or PBS control. These data were used to determine whichmiRNAs are regulated by native HDL compared to components of HDL and categorize data based on shared sets of miRNAs and distinct sets of miRNAs regulated by each component.

2014-02-27 | GSE53315 | GEO

Effect of fetal HDL on gene expression in human placental endothelial cells

Project description:The aim of this study was to identify HDL and apoE-regulated genes in human placental endothelial cells (HPEC), which are exposed to fetal HDL. HPECs extracted from 5 human placentas were cultivated and treated for 16 h with 15ug/ml fetal HDL, 15ug/ml reconstituted HDL (rHDL), or endothelial basal medium (EBM) as vehicle control. Gene expression analysis from these 3 conditions (5 biological replicates) using 15 Applied Biosystems Human Whole Genome Survey V2.0 Microarrays was perfomed and significantly differentially expressed genes between two different groups (HDL vs control or rHDL vs control) were identified.

2011-09-01 | E-MEXP-3299 | biostudies-arrayexpress

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