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Decreased estrogen level in ovariectomized mice causes an increase in oxidative stress in osteal macrophages leading to development of cellular senescence

ABSTRACT: Osteal macrophages were isolated from ovariectomized and control mice 4 weeks after surgery. Oeritoneal macrophages collected from ovariectomized mice exhibited gene signature of NADPH oxidase activation which is known as key modulator in aging and cell senescence.

ORGANISM(S): Mus musculus

PROVIDER: GSE275459 | GEO | 2024/11/26

REPOSITORIES: GEO

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Decreased estrogen level in ovariectomized mice causes an increase in oxidative stress in osteal macrophages leading to development of cellular senescence [scRNA-seq]

Project description:Osteal macrophages were isolated from ovariectomized and control mice 4 weeks after surgery. Oeritoneal macrophages collected from ovariectomized mice exhibited gene signature of NADPH oxidase activation which is known as key modulator in aging and cell senescence.

2024-11-26 | GSE275976 | GEO

Decreased estrogen level in ovariectomized mice causes an increase in oxidative stress in osteal macrophages leading to development of cellular senescence

Project description:Decreased estrogen level in ovariectomized mice causes an increase in oxidative stress in osteal macrophages leading to development of cellular senescence

| PRJNA1150972 | ENA

Decreased estrogen level in ovariectomized mice causes an increase in oxidative stress in osteal macrophages leading to development of cellular senescence [scRNA-seq]

Project description:Decreased estrogen level in ovariectomized mice causes an increase in oxidative stress in osteal macrophages leading to development of cellular senescence [scRNA-seq]

| PRJNA1154008 | ENA

Mycobacterium tuberculosis is protected from NADPH oxidase and LC3-associated phagocytosis by the LCP protein CpsA

Project description:Mycobacterium tuberculosis’success as a pathogen comes from itsability to evade degradation by macrophages. Normally macro-phages clear microorganisms that activate pathogen-recognitionreceptors (PRRs) through a lysosomal-trafficking pathway called“LC3-associated phagocytosis”(LAP). AlthoughM.tuberculosisac-tivates numerous PRRs, for reasons that are poorly understoodLAP does not substantially contribute toM.tuberculosiscontrol.LAP depends upon reactive oxygen species (ROS) generated byNADPH oxidase, butM.tuberculosisfails to generate a robustoxidative response. Here, we show that CpsA, a LytR-CpsA-Psr(LCP) domain-containing protein, is required forM.tuberculosisto evade killing by NADPH oxidase and LAP. Unlike phagosomescontaining wild-type bacilli, phagosomes containing theΔcpsAmutant recruited NADPH oxidase, produced ROS, associated withLC3, and matured into antibacterial lysosomes. Moreover, CpsAwas sufficient to impair NADPH oxidase recruitment to fungal par-ticles that are normally cleared by LAP. Intracellular survival of theΔcpsAmutant was largely restored in macrophages missing LAPcomponents (Nox2,Rubicon,Beclin,Atg5,Atg7,orAtg16L1) butnot in macrophages defective in a related, canonical autophagypathway (Atg14,Ulk1,orcGAS). TheΔcpsAmutant was highlyimpaired in vivo, and its growth was partially restored in micedeficient in NADPH oxidase,Atg5,orAtg7, demonstrating thatCpsA makes a significant contribution to the resistance ofM.tu-berculosisto NADPH oxidase and LC3 trafficking in vivo. Overall,our findings reveal an essential role of CpsA in innate immuneevasion and suggest that LCP proteins have functions beyond theirpreviously known role in cell-wall metabolism.

2019-12-13 | GSE141931 | GEO

Transcriptome profiling of oxidase knockout mice response to gingival inflammation using RNA-seq

Project description:Genetic defects in neutrophil function or trafficking are highly associated with oral inflammation and periodontitis. The leukocyte NADPH oxidase enzymes complex is a multi-subunit enzyme that has been described to play important immunomodulatory roles in limiting the inflammatory responses of neutrophils and macrophages. Here, we determined the impact of loss of NADPH oxidase dependent reactive oxygen species (ROS) generation in gingival inflammatory responses using a model of ligature induced murine periodontitis.

2024-04-23 | GSE184556 | GEO

Genome-wide analysis of renal gene expression during hyperoxaluria development

2012-12-20 | GSE36446 | GEO

Transcription profiling of Salmonella typhimurium isolated from mice bone marrow derived macrophages with and without NADPH oxidase

Project description:NADPH dependent phagocytic oxidase, by producing hydroxyradicals such as hydrogen peroxide, is essential for host defense against Salmonella infection. We used gene array analysis to identify Salmonella enterica serovar Typhimurium genes regulated by NADPH dependent phagocytic oxidase intracellularly in comparison to those expressed in vitro by hydrogen peroxide.

2007-05-02 | E-MEXP-1089 | biostudies-arrayexpress

The development and growth related transcriptome landscape of ovariectomized goat muscle

Project description:In this study, ovariectomized and normal ewe longissimus thoracis were used to thoroughly explore the global transcriptome to reveal how the castrated ewes influence muscle development by Illumina2000 sequencing technology. As a result, 1,612 differently expressed unigenes were revealed between ovariectomized and normal ewe groups, which containing 718 up-regulated and 894 down-regulated genes in ovariectomized ewe muscle. Moreover, in the 1,612 unigenes, 903 genes were expressed commonly in the two groups, 288 and 421 genes were uniquely expressed in normal and ovariectomized ewe group, respectively. This study validated some differently expressed genes in samples by quantitative real-time PCR, and the results were consistent with the RNA-seq. Furthermore, this study revealed 24 and 11 differently expressed genes which associated with development and reproduction, respectively. These results were helpful for elucidating the molecular mechanism of muscle development of ovariectomized animal and the application of female castrated on fatting.

2016-07-10 | GSE84110 | GEO

Genome-wide analysis of renal gene expression during hyperoxaluria development

Project description:Previous studies have proposed that production of reactive oxygen species (ROS) is an important contributor to renal injury and inflammation following exposure to oxalate or calcium-oxalate crystals. The present study was conducted to determine, utilizing global transcriptome analyses, if the NADPH oxidase system is activated in kidneys of rats fed a diet leading to hyperoxaluria and crystal deposition. HLP was used to induce hyperoxaluria. Hyperoxaluria will lead to crystallization and up regulation of various NADPH oxidase subunits followed by increased expression of different specific genes. It is our hypothesis that crystallization induces inflammation of the kidneys via the activation of renin-angiotensin system (RAS) and production of reactive oxygen species (ROS) through NADPH oxidase complex. Apocynin was used to block hyperoxaluria and production of reactive oxygen species (ROS) with the inhibition of NADPH oxidase system as Apocynin inhibits membrane translocation of p47 subunit of NADPH oxidase. The present study was designed based on NADPH oxidase system and rats were divided into 4 groups (n= 6/group). Group 1 was fed regular rat chow diet, Group 2 received regular rat chow diet supplemented with 5% (Hydroxy-L-Proline) HLP, Group 3 received rat chow diet with 4 mmol Apocynin to drink, and Group 4 received regular rat chow diet with 5% HLP and 4 mmol Apocynin. After 28 days each rat was euthanized, their kidneys freshly explanted and dissected to obtain both cortex and medulla tissues. So the 4 groups were divided into cortex and medulla forming 8 groups. RNA was isolated from all the 8 specimens

2012-12-20 | E-GEOD-36446 | biostudies-arrayexpress

IFNg Regulates NAD+ Metabolism in Human Monocytes

Project description:IFNg is an essential and pleiotropic activator of monocytes, but little is known about the changes in cellular metabolism required for IFNg-induced activation. We sought to characterize and elucidate the mechanisms by which IFNg reprograms monocyte metabolism to support its immunologic activities. Monocytes from healthy controls and patients with gain-of-function mutations in STAT1 (STAT1 GOF), or loss-of-function mutations in mitochondrial complex I (Leigh syndrome) and NADPH oxidase (chronic granulomatous disease, CGD) were metabolically phenotyped. We found that IFNg increased oxygen consumption rates (OCR), indicative of reactive oxygen species generation by both mitochondria and NADPH oxidase. Transcriptional profiling of human monocyte derived macrophages revealed that this oxidative phenotype was driven by an IFNg-induced reprogramming of NAD+ metabolism, which is dependent on nicotinamide phosphoribosyltransferase (NAMPT)-mediated NAD+ salvage to generate NADH and NADPH for oxidation by mitochondrial complex I and NADPH oxidase, respectively. Monocytes from patients with STAT1 GOF demonstrated higher than normal OCR, while monocytes from Leigh syndrome and CGD patients demonstrated reduced OCR. Chemical inhibition of NAMPT completely abrogated the IFNg-induced oxygen consumption, comparable to levels observed in CGD patients. These data identify an IFNg-induced, NAMPT-dependent, NAD+ salvage pathway that is critical for IFNg activation of human monocytes.

2021-12-31 | GSE176562 | GEO

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