RGD Reference Report - Neuroinflammation after neonatal hypoxia-ischemia is associated with alterations in the purinergic system: adenosine deaminase 1 isoenzyme is the most predominant after insult. - Rat Genome Database

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Neuroinflammation after neonatal hypoxia-ischemia is associated with alterations in the purinergic system: adenosine deaminase 1 isoenzyme is the most predominant after insult.

Authors: Pimentel, Victor Camera  Moretto, Maria Beatriz  Oliveira, Mariana Colino  Zanini, Daniela  Sebastião, Ana Maria  Schetinger, Maria Rosa Chitolina 
Citation: Pimentel VC, etal., Mol Cell Biochem. 2015 May;403(1-2):169-77. doi: 10.1007/s11010-015-2347-9. Epub 2015 Feb 27.
RGD ID: 152995398
Pubmed: PMID:25720338   (View Abstract at PubMed)
DOI: DOI:10.1007/s11010-015-2347-9   (Journal Full-text)

Hypoxic-ischemic (HI) injury perinatal brain is a major contributor to morbidity and mortality to infants and children. Adenosine may play a role in the pathophysiology of HI, since it modulates the inflammatory process and the release of several neurotransmitters. Thus, the aim of this study was to identify the isoforms of adenosine deaminase (ADA) responsible for the enzymatic activity as well as the adenosine kinase (ADK) and A1 adenosine receptor (A1R) expression in the cerebral cortex eight days after HI. Myeloperoxidase (MPO) and N-acetyl-glucosaminidase (NAG) were assessed as inflammation markers. ADA activity was analyzed, in the presence or absence of a specific ADA1 inhibitor, erythro-9-(2-hydroxy-3-nonyl) adenine. The ADA1 activity (92.6%) was significantly higher than ADA2 (7.4%) activity in the cerebral cortex eight days after HI. A1Rs and ADK protein expression showed decreased 8 days after insult. Interestingly, the ADA1, MPO, and NAG activities were correlated positively. In view of this, we conclude that the inhibitor of ADA1, in in vitro conditions, was effective in decreasing the ADA activity, and that mainly ADA1 isoform is responsible for the increase in the ADA activity 8 days after HI insult. Therefore, HI neonatal was able to alter the ADK and A1R expression. Thus, due to the importance of adenosine signaling in the regulation of inflammatory and immune process and the crucial role of ADA in the postischemic homeostase of adenosine as well as during inflammatory process, we suggest that ADA1 inhibitors may play an important role in the regulation of events that follow the HI insult, favoring the increase in the adenosine in the sites of tissue injury. Together, these results highlight a role of the purinergic signaling cascade in the pathophysiology of HI neonatal.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Brain Hypoxia-Ischemia  ISOAda (Rattus norvegicus)152995398; 152995398protein:increased activity:brain:RGD 
Brain Hypoxia-Ischemia  ISOAdk (Rattus norvegicus)152995398; 152995398protein:decreased expression:brain:RGD 
Brain Hypoxia-Ischemia  ISOAdora1 (Rattus norvegicus)152995398; 152995398protein:decreased expression:brain:RGD 
Brain Hypoxia-Ischemia  IEP 152995398; 152995398; 152995398protein:increased activity:brain:RGD 
Brain Hypoxia-Ischemia  IEP 152995398; 152995398protein:decreased expression:brain:RGD 
Brain Hypoxia-Ischemia  ISOMpo (Rattus norvegicus)152995398; 152995398protein:increased activity:brain:RGD 
Brain Hypoxia-Ischemia  ISONaglu (Rattus norvegicus)152995398; 152995398protein:increased activity:brain:RGD 

Objects Annotated

Genes (Rattus norvegicus)
Ada  (adenosine deaminase)
Adk  (adenosine kinase)
Adora1  (adenosine A1 receptor)
Mpo  (myeloperoxidase)
Naglu  (N-acetyl-alpha-glucosaminidase)

Genes (Mus musculus)
Ada  (adenosine deaminase)
Adk  (adenosine kinase)
Adora1  (adenosine A1 receptor)
Mpo  (myeloperoxidase)
Naglu  (alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB))

Genes (Homo sapiens)
ADA  (adenosine deaminase)
ADK  (adenosine kinase)
ADORA1  (adenosine A1 receptor)
MPO  (myeloperoxidase)
NAGLU  (N-acetyl-alpha-glucosaminidase)


Additional Information