APC
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ABSTRACT:
PROVIDER: PRJEB36850 | ENA |
REPOSITORIES: ENA
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Project description:Aeolian soil erosion, exacerbated by anthropogenic perturbations, has become one of the most alarming processes of land degradation and desertification. By contrast, dust deposition might confer a potential fertilization effect. To examine how they affect topsoil microbial community, we conducted a study GeoChip techniques in a semiarid grassland of Inner Mongolia, China. We found that microbial communities were significantly (P<0.039) altered and most of microbial functional genes associated with carbon, nitrogen, phosphorus and potassium cycling were decreased or remained unaltered in relative abundance by both erosion and deposition, which might be attributed to acceleration of organic matter mineralization by the breakdown of aggregates during dust transport and deposition. As a result, there were strong correlations between microbial carbon and nitrogen cycling genes. amyA genes encoding alpha-amylases were significantly (P=0.01) increased by soil deposition, reflecting changes of carbon profiles. Consistently, plant abundance, total nitrogen and total organic carbon were correlated with functional gene composition, revealing the importance of environmental nutrients to soil microbial function potentials. Collectively, our results identified microbial indicator species and functional genes of aeolian soil transfer, and demonstrated that functional genes had higher susceptibility to environmental nutrients than taxonomy. Given the ecological importance of aeolian soil transfer, knowledge gained here are crucial for assessing microbe-mediated nutrient cyclings and human health hazard. The experimental sites comprised of three treatments of control, soil erosion and deposition, with 5 replicates of each treatment.
2015-03-28 | E-GEOD-67347 | biostudies-arrayexpress
Project description:Aeolian soil erosion, exacerbated by anthropogenic perturbations, has become one of the most alarming processes of land degradation and desertification. By contrast, dust deposition might confer a potential fertilization effect. To examine how they affect topsoil microbial community, we conducted a study GeoChip techniques in a semiarid grassland of Inner Mongolia, China. We found that microbial communities were significantly (P<0.039) altered and most of microbial functional genes associated with carbon, nitrogen, phosphorus and potassium cycling were decreased or remained unaltered in relative abundance by both erosion and deposition, which might be attributed to acceleration of organic matter mineralization by the breakdown of aggregates during dust transport and deposition. As a result, there were strong correlations between microbial carbon and nitrogen cycling genes. amyA genes encoding alpha-amylases were significantly (P=0.01) increased by soil deposition, reflecting changes of carbon profiles. Consistently, plant abundance, total nitrogen and total organic carbon were correlated with functional gene composition, revealing the importance of environmental nutrients to soil microbial function potentials. Collectively, our results identified microbial indicator species and functional genes of aeolian soil transfer, and demonstrated that functional genes had higher susceptibility to environmental nutrients than taxonomy. Given the ecological importance of aeolian soil transfer, knowledge gained here are crucial for assessing microbe-mediated nutrient cyclings and human health hazard.
2015-03-28 | GSE67347 | GEO
Project description:Vertical distribution of airborne bacterial communities over Asian dust (Kosa) area during a dust event
| PRJDB3139 | ENA
Project description:Background-The endothelial protein C receptor (EPCR) plays an important role within the protein C (PC) pathway in regulating coagulation and inflammation. Recently, we described a novel mechanism of EPCR release from the surface of primary physiological cells. Induced by exogenous activated protein C (APC), EPCR is released in microparticulate form. Its bound APC retains proteolytic anticoagulant activity and we now hypothesise that this microparticulate EPCR-APC complex can also cleave endothelial protease activated receptor 1 (PAR1) to modulate inflammation and cytoprotection. Methods & Results-The gene profiling effect on human endothelial cells by 40nM APC, in free or microparticulate form, was assessed. Transcript profile results showed upregulation of anti-apoptotic and inflammatory genes by APC in either form, which were confirmed by RT-PCR. These translated into increased GM-CSF and interleukin 8 secretion and cytoprotection against staurosporine-induced apoptosis. PC or PAR1 antagonism reversed these results to demonstrate that induced effects by microparticles were APC specific and PAR1-dependent. Further analysis of human plasma from septic patients, by confocal microscopy and ELISA, showed evidence of circulating microparticle-associated EPCR during recombinant APC treatment. Functional coagulation and cellular studies demonstrate that these express APC-specific effects on anticoagulation with PAR1-mediated gene induction and anti-apoptotic function. Conclusions-APC induction of microparticle-associated EPCR release can occur in vivo. These microparticles could potentially disseminate the function of the EPCR-APC complex to PAR1 on different cells and vascular sites. Keywords: free apc versus mp-apc
2010-02-28 | GSE5660 | GEO
Project description:Background-The endothelial protein C receptor (EPCR) plays an important role within the protein C (PC) pathway in regulating coagulation and inflammation. Recently, we described a novel mechanism of EPCR release from the surface of primary physiological cells. Induced by exogenous activated protein C (APC), EPCR is released in microparticulate form. Its bound APC retains proteolytic anticoagulant activity and we now hypothesise that this microparticulate EPCR-APC complex can also cleave endothelial protease activated receptor 1 (PAR1) to modulate inflammation and cytoprotection. Methods & Results-The gene profiling effect on human endothelial cells by 40nM APC, in free or microparticulate form, was assessed. Transcript profile results showed upregulation of anti-apoptotic and inflammatory genes by APC in either form, which were confirmed by RT-PCR. These translated into increased GM-CSF and interleukin 8 secretion and cytoprotection against staurosporine-induced apoptosis. PC or PAR1 antagonism reversed these results to demonstrate that induced effects by microparticles were APC specific and PAR1-dependent. Further analysis of human plasma from septic patients, by confocal microscopy and ELISA, showed evidence of circulating microparticle-associated EPCR during recombinant APC treatment. Functional coagulation and cellular studies demonstrate that these express APC-specific effects on anticoagulation with PAR1-mediated gene induction and anti-apoptotic function. Conclusions-APC induction of microparticle-associated EPCR release can occur in vivo. These microparticles could potentially disseminate the function of the EPCR-APC complex to PAR1 on different cells and vascular sites. Keywords: free apc versus mp-apc MP were isolated from huvec after estimulation with apc; the apc content of the mp was estimated by chromogenic substrate and a standard curve. 40nM apc on mp was used for estimulation of huvec for 4 hours for study of gene expression. APC relevance was studied by blocking experiments with antibody and par1 involvement was studied by including a par1 antagonist. All experiments were done in triplicate. A basline control was obtained by looking at the profile of non-estimulated cells under the same conditions.
2010-06-24 | E-GEOD-5660 | biostudies-arrayexpress
Project description:Background-The endothelial protein C receptor (EPCR) plays an important role within the protein C (PC) pathway in regulating coagulation and inflammation. Recently, we described a novel mechanism of EPCR release from the surface of primary physiological cells. Induced by exogenous activated protein C (APC), EPCR is released in microparticulate form. Its bound APC retains proteolytic anticoagulant activity and we now hypothesise that this microparticulate EPCR-APC complex can also cleave endothelial protease activated receptor 1 (PAR1) to modulate inflammation and cytoprotection. Methods & Results-The gene profiling effect on human endothelial cells by 40nM APC, in free or microparticulate form, was assessed. Transcript profile results showed upregulation of anti-apoptotic and inflammatory genes by APC in either form, which were confirmed by RT-PCR. These translated into increased GM-CSF and interleukin 8 secretion and cytoprotection against staurosporine-induced apoptosis. PC or PAR1 antagonism reversed these results to demonstrate that induced effects by microparticles were APC specific and PAR1-dependent. Further analysis of human plasma from septic patients, by confocal microscopy and ELISA, showed evidence of circulating microparticle-associated EPCR during recombinant APC treatment. Functional coagulation and cellular studies demonstrate that these express APC-specific effects on anticoagulation with PAR1-mediated gene induction and anti-apoptotic function. Conclusions-APC induction of microparticle-associated EPCR release can occur in vivo. These microparticles could potentially disseminate the function of the EPCR-APC complex to PAR1 on different cells and vascular sites. Keywords: pre versus rhAPC-treatment mp in vivo MP were isolated from sepsis patients pre and during-rhAPC treatment. MP were counted by FACS using CD13 positivity and same number of mp was used in pre and during treatment comparisons. HUVEC were incubated with the in vivo mps according to mp number or apc content, and controls for both were done using non-treated patients or free-apc. The role of apc and par1 was analysed by including apc blocking antibody or par1 antaginist peptide respectively.
2010-06-24 | E-GEOD-5661 | biostudies-arrayexpress
Project description:Transcriptional profiling of mouse intestinal crypt epithelial cells comparing Apc+/Î716 mice with Apc+/Î716 Id2-/- mice. One-condition experiment, Apc+/Î716 mice vs. Apc+/Î716 Id2-/- mice, Biological replicates: 1 pooled intestinal crypt epithelium from 3 Apc+/Î716 mice, 1 pooled intestinal crypt epithelium from 3 Apc+/Î716 Id2-/- mice. One replicate per array.
2016-03-01 | E-GEOD-66480 | biostudies-arrayexpress
Project description:Background-The endothelial protein C receptor (EPCR) plays an important role within the protein C (PC) pathway in regulating coagulation and inflammation. Recently, we described a novel mechanism of EPCR release from the surface of primary physiological cells. Induced by exogenous activated protein C (APC), EPCR is released in microparticulate form. Its bound APC retains proteolytic anticoagulant activity and we now hypothesise that this microparticulate EPCR-APC complex can also cleave endothelial protease activated receptor 1 (PAR1) to modulate inflammation and cytoprotection. Methods & Results-The gene profiling effect on human endothelial cells by 40nM APC, in free or microparticulate form, was assessed. Transcript profile results showed upregulation of anti-apoptotic and inflammatory genes by APC in either form, which were confirmed by RT-PCR. These translated into increased GM-CSF and interleukin 8 secretion and cytoprotection against staurosporine-induced apoptosis. PC or PAR1 antagonism reversed these results to demonstrate that induced effects by microparticles were APC specific and PAR1-dependent. Further analysis of human plasma from septic patients, by confocal microscopy and ELISA, showed evidence of circulating microparticle-associated EPCR during recombinant APC treatment. Functional coagulation and cellular studies demonstrate that these express APC-specific effects on anticoagulation with PAR1-mediated gene induction and anti-apoptotic function. Conclusions-APC induction of microparticle-associated EPCR release can occur in vivo. These microparticles could potentially disseminate the function of the EPCR-APC complex to PAR1 on different cells and vascular sites. Keywords: pre versus rhAPC-treatment mp in vivo
2010-02-28 | GSE5661 | GEO
Project description:Transmission of SARS-CoV-2 is driven by contact, fomite, and airborne transmission. The relative contribution of different transmission routes remains subject to debate. Here, we show Syrian hamsters are susceptible to SARS-CoV-2 infection through intranasal, aerosol and fomite exposure. Different routes of exposure present with distinct disease manifestations. Intranasal and aerosol inoculation causes severe respiratory pathology, higher virus loads and increased weight loss. In contrast, fomite exposure leads to milder disease manifestation characterized by an anti-inflammatory immune state and delayed shedding pattern. Whereas the overall magnitude of respiratory virus shedding is not linked to disease severity, the onset of shedding is. Early shedding is linked to an increase in disease severity. Airborne transmission is more efficient than fomite transmission and dependent on the direction of the airflow. Carefully characterized SARS-CoV-2 transmission models will be crucial to assess potential changes in transmission and pathogenic potential in the light of the ongoing SARS-CoV-2 evolution
2021-08-04 | GSE177027 | GEO