Fibrinogen-induced differentiation of WT adult neural stem cells into astrocytes
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Dietmar Pfeifer
PROVIDER: E-MTAB-3013 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:This SuperSeries is composed of the following subset Series: GSE18023: Mice with FIA develop anti-native and anti-in vitro citrullinated fibrinogen antibodies GSE18024: FIA plasma induces arthritis in naïve mice GSE18025: Fibrinogen-reactive T cells transfer disease to naïve mice Refer to individual Series
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Project description:Determination of the mechanism by which fibrinogen, a central blood coagulation protein drives immunological responses targeted to the CNS. Results identify the factors involved in the regulation and provide mechanistic basis. We subjected fibrinogen-injected corpus callosum to microarray to determine the genes involved in innate and adaptive immune responses by fibrinogen deposited in the CNS after blood-brain barrier disruption. Corpus callosum tissues were isolated from mice received stereotactic injection of fibrinogen or ACSF at 12 hr. Tissues were subjected for RNA extraction and hybridization on Affymatrix microarrays. Two ACSF and two fibrinogen samples were generated.
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Project description:Synovial antigen arrays were probed with 1:150 dilutions of plasma derived from SJL mice immunized with fibrinogen emulsified in CFA or with CFA alone. Autoantibody binding was detected with a Cy3-conjugated goat-anti-mouse IgG/M secondary antibody. SAM was applied to identify antigens with statistically significant differences in array reactivity between FIA and CFA control plasma (q < 0.01) obtained from mice before boosting. The SAM hits were subjected to hierarchical cluster analysis and are displayed as a heatmap. Synovial array profiling of FIA plasma demonstrated autoreactive B-cell responses against peptides representing native fibrinogen, and B-cell epitope spreading resulting in additional targeting of citrullinated fibrinogen in the samples obtained before boosting. Custom-spotted protein slides were probed with plasma samples from individual mice. Four slides were probed with plasma derived from mice immunized with CFA and six slides were probed with plasma derived from mice immunized with fibrinogen emulsified in CFA.
2010-05-05 | E-GEOD-18023 | biostudies-arrayexpress
Project description:Splenocytes harvested from mice with FIA were cultured in vitro and stimulated with 0.01 mg/ml fibrinogen for 3 days. Enriched T cells were transferred into 6-week-old naïve SJL mice, which developed visible signs of arthritis within 2 weeks. Synovial array profiling of plasma from the arthritic recipient mice demonstrated autoreactive B cell responses against peptides representing native fibrinogen, and further spreading of the responses to target collagen type V, cartilage gp39, and citrullinated vimentin. Custom-spotted protein slides were with plasma samples from individual mice. Four slides were probed with plasma derived from naïve mice and five slides were probed with plasma derived from mice injected with FIA T cells.
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Project description:Impaired secretion of an essential blood coagulation factor fibrinogen leads to hepatic fibrinogen storage disease (HFSD), characterized by the presence of fibrinogen-positive inclusion bodies and hypofibrinogenemia. However, the molecular mechanisms underlying the biogenesis of fibrinogen in the endoplasmic reticulum (ER) remains unexplored. Here we uncovered a key role of SEL1L-HRD1 complex of ER-associated degradation (ERAD) in the formation of aberrant inclusion bodies, and the biogenesis of nascent fibrinogen protein complex in hepatocytes. Serendipitously, acute or chronic deficiency of SEL1L-HRD1 ERAD, but not UPR sensor IRE1α, in the hepatocytes led to the formation of hepatocellular inclusion bodies. Proteomics studies followed by biochemical assays revealed fibrinogen, not albumin or α1-antitrypsin, as a major component of the inclusion bodies. Degradation of misfolded endogenous fibrinogen Aα, Bβ, and γ chains by SEL1L-HRD1 ERAD was required for the formation of a functional fibrinogen complex in the ER. Providing clinical relevance of these findings, SEL1L-HRD1 ERAD indeed degraded and thereby attenuated the pathogenicity of a disease-causing fibrinogen γ mutant. Together, this study demonstrates an essential role of SEL1L-HRD1 ERAD in fibrinogen biogenesis and provides novel insights into the pathogenesis of protein-misfolding diseases.
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Project description:Fibrinogen is highly susceptible to oxidation compared to other plasma proteins. Fibrinogen oxidation damages its structure and affects the protein function. Fibrinogen was isolated from citrated human plasma by the modified cold ethanol precipitation technique. Oxidation of fibrinogen by ozone: a solution of 2.0 mg of fibrinogen in 1 ml of 0.05 M Tris/0.15 M NaCl buffer (pH 7.4) was introduced into a quartz reactor filled with ozone–oxygen mixture. The full exhaustion of ozone in each experiment was confirmed by spectrophotometry by the absorption band at 254 nm. The amount of ozone was varied in the range of 50–100 μM per 1 μM of fibrinogen. Ozone-induced oxidative modifications of the fibrinogen Aα, Bβ, and γ polypeptide chains upon addition of various amounts of the oxidizer have been studied by mass-spectrometry.
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Project description:Disulfide bonds link pairs of cysteine amino acids and their formation is assumed to be complete in the mature, functional protein. We tested this assumption by quantifying the redox state of disulfide bonds in the thrombosis protein, fibrinogen. There is an extraordinary disulfide lability in fibrinogen, with 13 bonds in the protein ranging from 10 to 50% reduced in human donors, indicating that fibrinogen exists in hundreds of different disulfide-bonded states. The significance of this finding for fibrinogen conversion to fibrin was investigated. Fibrin polymer formation triggers formation of disulfides in fibrin molecules, which is required for a robust fibrin matrix that withstands the mechanical forces of flowing blood and resists premature fibrinolysis. The covalent states of fibrinogen are changed by fluid shear forces ex vivo and in vivo, indicating that the different states are dynamic. These findings demonstrate that proteins can exist and function as a multitude of covalent forms.
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Project description:Murine WT and Id3-/- adult neural stem cells were plated as dissociated cells and treated for 3 hours with rhBMP-2 under differentiation conditions to mimic traumatic brain injury in vitro
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Project description:Determination of the mechanism by which fibrinogen, a central blood coagulation protein drives immunological responses targeted to the CNS. Results identify the factors involved in the regulation and provide mechanistic basis. We subjected fibrinogen-injected corpus callosum to microarray to determine the genes involved in innate and adaptive immune responses by fibrinogen deposited in the CNS after blood-brain barrier disruption.
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Project description:characterization of fibrinogen expression in the kidney, excretion in the urine following kidney damage and evaluating the therapeutic potential of fibrinogen in acute kidney injury.
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