Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from BMP9-treated human dermal microvascular endothelial cells (HMVEC-D)

ABSTRACT: BMP9 signaling has been implicated in hereditary hemorrhagic telangiectasia and vascular remodeling, acting via the HHT target genes, endoglin and ALK1. This study sought to identify endothelial BMP9-regulated proteins that could affect the HHT phenotype. Gene ontology analysis of cDNA microarray data obtained following BMP9 treatment of primary human endothelial cells indicated regulation of chemokine, adhesion, and inflammation pathways. The sample set is comprised of three biological replicate control human dermal microvascular endothelial cells, and three treated (5 ng/ml human recombinant BMP9) biological replicate human dermal microvascular endothelial cells

ORGANISM(S): Homo sapiens

SUBMITTER: Calvin Vary

PROVIDER: E-GEOD-40960 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Microgravity alters the immune response to in vitro LPS assault engineered in spaceflight: A multi-omics study Microgravity can facilitate creation of a potent environment for opportunistic infection by augmenting virulence and suppressing the host defense. Presumably, extraterrestrial infection may trigger potentially novel bionetworks different from the terrestrial equivalent, which could only be probed by investigating the host-pathogen relationship with minimum terrestrial bias. Towards this objective, we strategically engineered a cell culture module equipped with a feedback controlled semi-automated platform to expose human endothelial cells to lipopolysaccharide (LPS). The assay was carried out in the STS-135 space shuttle, and a concurrent ground study constituted the baseline. Transcriptomic investigation revealed an immune blunting in microgravity; Lbp, MyD88 and MD-2 failed to encode proteins responsible for early LPS uptake. Longer exposure results implied that there was a delayed response, potentially ineffectual in preventing pathogens from opportunistically modulating the infection network. Lack of recruitment of growth factors and a debilitated apoptosome supported this potential explanation. Certain cytokines, such as IL-6 and IL-8, surged in response to LPS insult in microgravity. Contrasting expressions of B2M, TIMP-1 and VEGRs suggested impaired pro-survival adaptation and healing mechanisms. The susceptibility of oxidative stress and immune regulation to microgravity compelled further investigation of the respective microRNA modulators such as miR-200a and miR-146b. These miRNAs were expressed differently in response to LPS assaults in different gravitational limits. In conclusion, despite a serious drawback attributed to the small sample size, we delineated some of the important aspects of the extraterrestrial etiology; more comprehensive follow up studies are warranted. Present study though compromised by the small sample size was able to shade lights on several aspects of immunological responses to the endotoxic assault mediated by Î¼G. Implementing the host-pathogen interactions in the spaceflight and subsequently lysing the cells onboard presented the critical distinguishing features of the present study from the past reports. We identified the CCM of Tissue Genesis, Inc., HI as the suitable hardware system to carry out the experiment in the spaceflight. CCM is an automated, feedback controlled module that can concurrently support 24 bioreactors following protocols exclusively programmed for individual bioreactor. For this experiment we use samples EA41, EA 47, EA45, and EA155 that were exposed to LPS for 4 hours. Samples EA123, EA165, EA127, EA126 were exposed to LPS for 8Hrs. Samples EA33, EA 125, EA79 and EA 39 were controls in this experiment.

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Expression data from BMP9-treated human dermal microvascular endothelial cells (HMVEC-D)

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