Differential levels of CHMP2B, LLPH, and SLC25A51 proteins in secondary renal amyloidosis.
Expert Rev Proteomics
; 18(1): 65-73, 2021 01.
Article
em En
| MEDLINE
| ID: mdl-33583303
ABSTRACT
OBJECTIVES:
Renal amyloidosis (RA) is a rare disease, typically manifested with proteinuria, nephrotic syndrome, and ultimately leads to renal failure. The present study aims to profile the proteomes of renal amyloidosis patient's serum and healthy controls, along with relative quantification to find out robust markers for RA.METHODS:
In this study, 12 RA patients and their corresponding age and gender-matched healthy controls were recruited from the Nephrology department of Max Super Specialty Hospital, New Delhi. We employed gel-based proteomic approach coupled with MALDI-TOF MS to compare protein expression patterns in RA patients and controls. Furthermore, validation of differential proteins (selected) was done using bio-layer interferometry.RESULTS:
Eleven proteins showed remarkably altered expression levels. Moreover, expression modulation of three proteins (LLPH, SLC25A51, and CHMP2B) was validated which corroborated with two-dimensional gel electrophoresis (2-DE) results showing significant upregulation (p < 0.05) in RA patients followed by ROC analysis which demonstrated the diagnostic potential of these proteins. A protein-protein master network was generated implicating the above identified proteins along with their interactors, fishing out the routes leading to amyloidosis.CONCLUSION:
This study indicates that the identified serum proteomic signatures could improve early diagnosis and lead to possible therapeutic targets in RA.Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteínas Nucleares
/
Proteínas de Ligação a RNA
/
Proteínas de Transporte da Membrana Mitocondrial
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Proteômica
/
Complexos Endossomais de Distribuição Requeridos para Transporte
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Amiloidose
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Nefropatias
Tipo de estudo:
Screening_studies
Limite:
Female
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Humans
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Male
Idioma:
En
Ano de publicação:
2021
Tipo de documento:
Article