RGD Reference Report - Cell adhesion molecule mediation of myocardial inflammatory responses associated with ventricular pacing. - Rat Genome Database

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Cell adhesion molecule mediation of myocardial inflammatory responses associated with ventricular pacing.

Authors: Yamazaki, Katrina Go  Ihm, Sang-Hyun  Thomas, Robert L  Roth, David  Villarreal, Francisco 
Citation: Yamazaki KG, etal., Am J Physiol Heart Circ Physiol. 2012 Apr 1;302(7):H1387-93. doi: 10.1152/ajpheart.00496.2011. Epub 2012 Jan 20.
RGD ID: 13702908
Pubmed: PMID:22268115   (View Abstract at PubMed)
PMCID: PMC3330786   (View Article at PubMed Central)
DOI: DOI:10.1152/ajpheart.00496.2011   (Journal Full-text)

Poorly synchronized activation of the ventricles can lead to impairment of normal cardiac structure/function. We reported previously that short term (4 h) left ventricular (LV) pacing-induced ventricular dyskinesis led to an inflammatory response localized to the epicardium. Results from this study demonstrated that neutrophils may play a major role in this inflammatory process. Neutrophil recruitment to a site of injury is a process that is highly dependent on an upregulation of cell adhesion molecules (CAM). The dependence of ventricular dysynchrony-induced inflammatory responses on CAM upregulation has not been explored. To gain further insight, we used a mouse model of LV pacing to evaluate the role of CAM in mediating the inflammatory response associated with ventricular dyskinesis. We first examined the effects of LV pacing in wild-type mice. Results demonstrate that 40 min of LV pacing increases ICAM-1 immunostaining as well as myeloperoxidase activity and tissue oxidative stress by twofold in early-activated myocardium. Matrix metalloproteinase-9 activity also increased in the same region by ~3.5-fold. To determine the role of CAM, mice null for ICAM-1 or p-selectin were subjected to 40 min LV pacing. Results demonstrate that the inflammatory response seen in the wild-type mice was significantly mitigated in the ICAM-1 and p-selectin null mice. In conclusion, results demonstrate that CAM expression plays a critical role in the triggering of LV pacing-induced inflammation, thus providing evidence of a vascular mechanism underlying this response. The mechanisms that trigger an upregulation of myocardial CAM expression and, therefore, inflammation await further investigation since they suggest a specific involvement of vascular events.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
myocarditis  ISOIcam1 (Mus musculus)13702908; 13702908 RGD 
myocarditis  IMP 13702908; 13702908 RGD 
myocarditis  ISOSele (Mus musculus)13702908; 13702908 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Icam1  (intercellular adhesion molecule 1)
Sele  (selectin E)

Genes (Mus musculus)
Icam1  (intercellular adhesion molecule 1)
Sele  (selectin, endothelial cell)

Genes (Homo sapiens)
ICAM1  (intercellular adhesion molecule 1)
SELE  (selectin E)


Additional Information