RGD Reference Report - Alterations in protein regulators of neurodevelopment in the cerebrospinal fluid of infants with post-hemorrhagic hydrocephalus of prematurity. - Rat Genome Database

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Alterations in protein regulators of neurodevelopment in the cerebrospinal fluid of infants with post-hemorrhagic hydrocephalus of prematurity.

Authors: Morales, DM  Townsend, RR  Malone, JP  Ewersmann, CA  Macy, EM  Inder, TE  Limbrick DD, JR 
Citation: Morales DM, etal., Mol Cell Proteomics. 2011 Dec 20.
RGD ID: 6483013
Pubmed: PMID:22186713   (View Abstract at PubMed)
PMCID: PMC3433889   (View Article at PubMed Central)
DOI: DOI:10.1074/mcp.M111.011973   (Journal Full-text)

Neurological outcomes of preterm infants with post-hemorrhagic hydrocephalus are among the worst in newborn medicine. There remains no consensus regarding the diagnosis or treatment of post-hemorrhagic hydrocephalus, and the pathological pathways leading to the adverse neurological sequelae are poorly understood. In the current study, we developed an innovative approach to simultaneously identify potential diagnostic markers of post-hemorrhagic hydrocephalus and investigate novel pathways of post-hemorrhagic hydrocephalus-related neurological disability. Tandem multi-affinity fractionation for specific removal of plasma proteins from the hemorrhagic cerebrospinal fluid samples was combined with high resolution label-free quantitative proteomics. Analysis of cerebrospinal fluid obtained from infants with post-hemorrhagic hydrocephalus demonstrated marked differences in the levels of 438 proteins when compared to cerebrospinal fluid from age-matched control infants. Amyloid precursor protein, neural cell adhesion molecule-L1, neural cell adhesion molecule-1, brevican and other proteins with important roles in neurodevelopment showed profound elevations in post-hemorrhagic hydrocephalus cerebrospinal fluid compared with control. Initiation of neurosurgical treatment of post-hemorrhagic hydrocephalus resulted in resolution of these elevations. The results from this foundational study demonstrate the significant promise of tandem multi-affinity fractionation-proteomics in the identification and quantitation of protein mediators of neurodevelopment and neurological injury. More specifically, our results suggest that cerebrospinal fluid levels of proteins such as amyloid precursor protein or neural cell adhesion molecule-L1 should be investigated as potential diagnostic markers of post-hemorrhagic hydrocephalus. Notably, dysregulation of the levels these and other proteins may directly affect ongoing neurodevelopmental processes in these preterm infants, providing an entirely new hypothesis for the developmental disability associated with post-hemorrhagic hydrocephalus.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
BCANHumanPosthemorrhagic Hydrocephalus treatmentIEP  RGD 
BcanRatPosthemorrhagic Hydrocephalus treatmentISOBCAN (Homo sapiens) RGD 
BcanMousePosthemorrhagic Hydrocephalus treatmentISOBCAN (Homo sapiens) RGD 
L1CAMHumanPosthemorrhagic Hydrocephalus  IEP protein:increased expression:cerebrospinal fluid (human)RGD 
L1camMousePosthemorrhagic Hydrocephalus  ISOL1CAM (Homo sapiens)protein:increased expression:cerebrospinal fluid (human)RGD 
L1camRatPosthemorrhagic Hydrocephalus  ISOL1CAM (Homo sapiens)protein:increased expression:cerebrospinal fluid (human)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Bcan  (brevican)
L1cam  (L1 cell adhesion molecule)

Genes (Mus musculus)
Bcan  (brevican)
L1cam  (L1 cell adhesion molecule)

Genes (Homo sapiens)
BCAN  (brevican)
L1CAM  (L1 cell adhesion molecule)


Additional Information