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The anti-inflammation effect of human alpha-1 antitrypsin (hAAT)

ABSTRACT: The anti-inflammation effect of human alpha-1 antitrypsin (hAAT)

PROVIDER: PRJNA762471 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15852804.fastq.gz	Fastqsanger.gz
	SRR15852806.fastq.gz	Fastqsanger.gz
	SRR15852807.fastq.gz	Fastqsanger.gz
	SRR15852808.fastq.gz	Fastqsanger.gz
	SRR15852809.fastq.gz	Fastqsanger.gz

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The anti-inflammation effect of human alpha-1 antitrypsin (hAAT)

Project description:We tested the anti-inflammation effect of hAAT in transgenic Drosophila and human senescence in vitro model using RNA-seq. The results showed hAAT can extend the life-span and delay the aging-related motor activity decline in transgenic Drosophila via specifically suppressing the expression of inflammatory microbial peptides genes. Consistent with the findings observed in Drosophila, hAAT can specifically inhibit NF-kappaB mediated senescence-associated secretory phenotype genes expression.

2021-09-14 | GSE183948 | GEO

Comprehensive characterization of hepatic inflammatory changes in a mouse model of alpha-1 antitrypsin deficiency

Project description:In this study, we sought to thoroughly characterize the liver pathophysiology of a human transgenic mouse model for alpha-1 antitrypsin deficiency (AATD) with a strong manifestation of AATD-mediated liver disease. Male and female transgenic mice for normal variant human alpha-1 antitrypsin (Pi*M) and mutant human alpha-1 antitrypsin (Pi*Z) at 3 and 6 months of age with a C57BL/6J background were subjected to study. The progression of hepatic accumulation of mutant alpha-1 antitrypsin (ZAAT), hepatocyte injury, steatosis, liver inflammation and fibrotic features of this mouse model were monitored by performing an in vivo study.

2023-03-19 | GSE206619 | GEO

The Genomic Research in Alpha-1 Antitrypsin Deficiency and Sarcoidosis Study (GRADS) Alpha-1 study [A1AT]

Project description:Whole genome mRNA and microRNA profiling of bronchoalveolar lavage (BAL) and peripheral blood mononuclear cell (PBMC) in Alpha-1 Antitrypsin Deficiency patients with PiZZ or PiMZ alpha-1 antitrypsin genotypes

2020-11-03 | GSE109515 | GEO

Alpha-1-antitrypsin binds to the glucocorticoid receptor with anti-inflammatory and anti-mycobacterial significance in macrophages

Project description:Alpha-1-antitrypsin (AAT), a serine protease inhibitor produced mainly by the liver, is the third most abundant protein in plasma. Individuals who possess homozygous Z-AAT genotype have severe AAT deficiency and are at risk for early-onset emphysema, bronchiectasis, cirrhosis, panniculitis, and vasculitis. While a canonical receptor for AAT has not been identified, AAT can be internalized into the cytoplasm and is known to affect gene regulation. Since AAT has significant anti-inflammatory properties affecting many cell types including macrophages, we examined whether AAT binds the cytoplasmic glucocorticoid receptor (GR) in macrophages. We report the novel finding that AAT binds to GR in macrophages using several approaches, including co-immunoprecipitation, mass spectrometry, microscale thermophoresis, and in silico molecular modeling. We further demonstrate that AAT induction of angiopoietin-like 4 protein and AAT inhibition of lipopolysaccharide-induced nuclear factor-kappa B activation and interleukin-8 production are mediated, in part, through AAT–GR interaction. Furthermore, this interaction contributes to a host-protective role against Mycobacterium tuberculosis in macrophages. The interaction of AAT and GR described in this study identifies a mechanism for the anti-inflammatory and host-protective properties of AAT.

2022-08-24 | PXD030989 | Pride

Normal Alpha-1-Antitrypsin variants display in serum allele-specific protein levels

Project description:native mass spectrometry profiles of alpha-1-antitrypsin purified from individual donors. The cohort includes both healthy and diseased donors.

2022-12-20 | MSV000090934 | MassIVE

Effect anti-TNF-alpha treatment on CD4+ T cell activation

Project description:Effect anti-TNF-alpha treatment on CD4+ T cell activation

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Pulmonary gain-of-function toxicity in alpha-1 antitrypsin deficiency

Project description:Pulmonary gain-of-function toxicity in alpha-1 antitrypsin deficiency

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The Genomic Research in Alpha-1 Antitrypsin Deficiency and Sarcoidosis Study (GRADS) Alpha-1 study [A1AT]

Project description:The Genomic Research in Alpha-1 Antitrypsin Deficiency and Sarcoidosis Study (GRADS) Alpha-1 study [A1AT]

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Effect anti-TNF-alpha treatment on CD4+ T cell activation

Project description:The experiment was designed to test how autocrine TNF-alpha impacts human CD4+ T cell activation. Naïve CD4+ T cells from healthy human blood donors were either left unactivated or activated with anti-CD3/anti-CD28 in presence of an isotype control antibody or anti-TNF-alpha antibody. RNA was extracter at 48 hours. Analysis revealed that anti-TNF-alpha treatment prevented upregulation of activation-induced T cell metabolic, signaling and effector molecules.

2024-07-25 | GSE238247 | GEO

Modeling of Alpha-1 Antitrypsin Deficiency with Syngeneic Human iPSC-Hepatocytes Reveals Metabolic Dysfunction and Cellular Heterogeneity in PiMZ and PiZZ Hepatic Cells (scRNA-Seq)

Project description:Individuals homozygous for the "Z" mutation in alpha-1 antitrypsin deficiency are known to be at increased risk for liver disease. It has also become clear that some degree of risk is similarly conferred by the heterozygous state. A lack of model systems that recapitulate heterozygosity in human hepatocytes has limited the ability to study the impact of a single Z alpha-1 antitrypsin (ZAAT) allele on hepatocyte biology. Here, we describe the derivation of syngeneic induced pluripotent stem cells (iPSCs) engineered to determine the effects of ZAAT heterozygosity in iPSC-hepatocytes (iHeps). We find that heterozygous MZ iHeps exhibit an intermediate disease phenotype and share with ZZ iHeps alterations in AAT protein processing and downstream perturbations including altered endoplasmic reticulum (ER) and mitochondrial morphology, reduced mitochondrial respiration, and branch-specific activation of the unfolded protein response in cell subpopulations. Our model of MZ heterozygosity thus provides evidence that a single Z allele is sufficient to disrupt hepatocyte homeostatic function.

2022-12-06 | GSE198234 | GEO

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