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PROTEIN PROFILING OF AIA RAT JOINTS IN RESPONSE TO ANTI-ARTHRITIC THERAPY

ABSTRACT: Troxerutin (TXR), a potent antioxidant compound shows anti-inflammatory activity and possesses hepatoprotective effect. In this study, we aimed to exploit its anti-arthritic properties using adjuvant induced arthritic model. Using relative quantitative proteomics approach, we also tried to understand the mode of action of TXR at mechanistic details and its possible usage in the treatment of arthritis. Results provide a set of candidate biomarkers for responses to TXR in the arthritis and suggest new modalities of anti-arthritic activities. A number proteins were identified from the joint homogenates of the experimental rats using isobaric tag for relative and quantitative proteomics (iTRAQ) method. The detailed study and validation of these proteins involved may be useful in finding out newer treatment modalities.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Rattus Norvegicus (ncbitaxon:10116)

SUBMITTER: Debasis Sahu

PROVIDER: MSV000080172 | MassIVE |

SECONDARY ACCESSION(S): PXD004982

REPOSITORIES: MassIVE

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Distinct Serum Proteome Profiles Associated with Collagen induced Arthritis, and Complete Freund’s Adjuvant-induced Inflammation in CD38-/- mice: the Discriminative Power of Protein Species or Proteoforms. Protein identification by Peptide Mass Fingerprinting (PMF)

Project description:Collagen-type-II-induced arthritis (CIA) is an autoimmune disease, which involves a complex host systemic response including inflammatory and autoimmune reactions. CIA in C57BL/6 mice resembles human rheumatoid arthritis (RA) in terms of its disease course, histological findings, and in its response to commonly used anti-arthritic drugs. In this study, the goal has been to identify proteins from serum that change in their abundance in CD38-KO versus WT mice which may reflect their distinct response to an antigen-challenge that induces the development of an autoimmune disease. CIA is milder in CD38-/- than in Wild-type (WT) mice. We analyzed the sera from CD38-/- versus WT mice either with arthritis (CIA+), with no arthritis (CIA-), or with inflammation (Complete Freund’s adjuvant (CFA)-treated mice). To decrease the dynamic concentration range of serum a combinatorial ligand library composed of hexapeptides was used (called ProteoMiner). ProteoMiner-equalized serum samples were then subjected to 2D-DiGE and MS-MALDI-TOF/TOF analyses to identify proteins that changed in their relative abundances. Multivariate analyses revealed that a multi-protein signature (n = 28) was able to discriminate CIA+ from CIA- mice, and WT from CD38-/- mice within each condition. Likewise, a distinct multi-protein signature (n = 16) was identified which differentiated CIA+ CD38-/- mice from CIA+ WT mice, and lastly, a third multi-protein signature (n = 18) indicated that CD38-/- and WT mice could be segregated in response to CFA treatment This approach allows the identification of multiple protein species, or proteoforms of a given protein in a single analysis, and therefore, to focus the interest in fully characterize just the protein species that differ in abundance.

2015-07-17 | PXD001799 | Pride

Distinct Serum Proteome Profiles Associated with Collageninduced Arthritis, and Complete Freund’s Adjuvant-induced Inflammation in CD38-/- mice: the Discriminative Power of Protein Species or Proteoforms

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Distinct Serum Proteome Profiles Associated with Collagen-induced Arthritis, and Complete Freund’s Adjuvant-induced Inflammation in CD38-/- mice: the Discriminative Power of Protein Species or Proteoforms. Spot 269_Spot 500

Project description:Collagen-type-II-induced arthritis (CIA) is an autoimmune disease, which involves a complex host systemic response including inflammatory and autoimmune reactions. CIA in C57BL/6 mice resembles human rheumatoid arthritis (RA) in terms of its disease course, histological findings, and in its response to commonly used anti-arthritic drugs. In this study, the goal has been to identify proteins from serum that change in their abundance in CD38-KO versus WT mice which may reflect their distinct response to an antigen-challenge that induces the development of an autoimmune disease.CIA is milder in CD38-/- than in Wild-type (WT) mice. We analyzed the sera from CD38-/- versus WT mice either with arthritis (CIA+), with no arthritis (CIA-), or with inflammation (Complete Freund’s adjuvant (CFA)-treated mice). To decrease the dynamic concentration range of serum a combinatorial ligand library composed of hexapeptides was used (called ProteoMiner). ProteoMiner-equalized serum samples were then subjected to 2D-DiGE and MS-MALDI-TOF/TOF analyses to identify proteins that changed in their relative abundances. Multivariate analyses revealed that a multi-protein signature (n = 28) was able to discriminate CIA+ from CIA- mice, and WT from CD38-/- mice within each condition. Likewise, a distinct multi-protein signature (n = 16) was identified which differentiated CIA+CD38-/- mice from CIA+ WT mice, and lastly, a third multi-protein signature (n = 18) indicated that CD38-/- and WT mice could be segregated in response to CFA treatment This approach allows the identification of multiple protein species, or proteoforms of a given protein in a single analysis, and therefore, to focus the interest in fully characterize just the protein species that differ in abundance.

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