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Pregled bibliografske jedinice broj: 989423

Proteome alterations in response to aristolochic acids in experimental animal model.


Rucevic M1, Rosenquist T, Breen L, Cao L, Clifton J, Hixson D, Josic D.
Proteome alterations in response to aristolochic acids in experimental animal model. // Journal of Proteomics, 76 (2012), 79-90 (međunarodna recenzija, članak, znanstveni)


CROSBI ID: 989423 Za ispravke kontaktirajte CROSBI podršku putem web obrasca

Naslov
Proteome alterations in response to aristolochic acids in experimental animal model.

Autori
Rucevic M1, Rosenquist T, Breen L, Cao L, Clifton J, Hixson D, Josic D.

Izvornik
Journal of Proteomics (1874-3919) 76 (2012); 79-90

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, članak, znanstveni

Ključne riječi
Aristolochic acidsEndemic nephropathyPlasma, urinary and tissue proteomicsBiomarkersCytoskeletonVimentin

Sažetak
Strong indications have been presented that dietary poisoning with aristolochic acids (AA) is responsible for Endemic Nephropathy (EN) and AA associated cancer of the upper urinary tract (UUTC). Our recent investigation showed drastic urinary proteome changes in AA treated mice. This study was designed to identify proteome changes associated with AA nephrotoxicity in experimental animal model. The DBA and C57BL mice, which differ in AA sensitivity, were exposed to AA for 4 days. The strategy for urinary, plasma and kidney tissue proteome study of AA exposed and control mice integrated gel-based and in-solution tryptic digestion combined with LC-ESI-MS/MS. To maximize proteome coverage, plasma fractionation scheme was developed and MS compatible sequential tissue extraction procedure was established. Proteomic analyses of urinary, plasma and kidney tissue tryptic digests resulted in identification of several cytoskeletal proteins, as well as proteins involved in kidney development and inflammatory response, that are differentially expressed in both AA exposed and control mice. These proteins are consistent with renal pathogenesis of endotoxicity and cancer. This proteomic strategy could be effectively translated for unbiased discovery of potential biomarkers for EN and associated UUTC in humans. At the same time, these results highlight the significance of AA exposure with EN. This article is part of a Special Issue entitled: Integrated omics.

Izvorni jezik
Engleski

Znanstvena područja
Biotehnologija u biomedicini (prirodno područje, biomedicina i zdravstvo, biotehničko područje)



POVEZANOST RADA



Citiraj ovu publikaciju:

Rucevic M1, Rosenquist T, Breen L, Cao L, Clifton J, Hixson D, Josic D.
Proteome alterations in response to aristolochic acids in experimental animal model. // Journal of Proteomics, 76 (2012), 79-90 (međunarodna recenzija, članak, znanstveni)
Rucevic M1, Rosenquist T, Breen L, Cao L, Clifton J, Hixson D, Josic D. (2012) Proteome alterations in response to aristolochic acids in experimental animal model.. Journal of Proteomics, 76, 79-90.
@article{article, year = {2012}, pages = {79-90}, keywords = {Aristolochic acidsEndemic nephropathyPlasma, urinary and tissue proteomicsBiomarkersCytoskeletonVimentin}, journal = {Journal of Proteomics}, volume = {76}, issn = {1874-3919}, title = {Proteome alterations in response to aristolochic acids in experimental animal model.}, keyword = {Aristolochic acidsEndemic nephropathyPlasma, urinary and tissue proteomicsBiomarkersCytoskeletonVimentin} }
@article{article, year = {2012}, pages = {79-90}, keywords = {Aristolochic acidsEndemic nephropathyPlasma, urinary and tissue proteomicsBiomarkersCytoskeletonVimentin}, journal = {Journal of Proteomics}, volume = {76}, issn = {1874-3919}, title = {Proteome alterations in response to aristolochic acids in experimental animal model.}, keyword = {Aristolochic acidsEndemic nephropathyPlasma, urinary and tissue proteomicsBiomarkersCytoskeletonVimentin} }

Časopis indeksira:


  • Current Contents Connect (CCC)
  • Web of Science Core Collection (WoSCC)
    • Science Citation Index Expanded (SCI-EXP)
    • SCI-EXP, SSCI i/ili A&HCI
  • Scopus
  • MEDLINE





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