RGD Reference Report - Expression of immunological molecules by cardiomyocytes and inflammatory and interstitial cells in rat autoimmune myocarditis. - Rat Genome Database

Send us a Message



Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

Expression of immunological molecules by cardiomyocytes and inflammatory and interstitial cells in rat autoimmune myocarditis.

Authors: Yoshida, T  Hanawa, H  Toba, K  Watanabe, H  Watanabe, R  Yoshida, K  Abe, S  Kato, K  Kodama, M  Aizawa, Y 
Citation: Yoshida T, etal., Cardiovasc Res. 2005 Nov 1;68(2):278-88. Epub 2005 Jul 12.
RGD ID: 4891990
Pubmed: PMID:16018993   (View Abstract at PubMed)
DOI: DOI:10.1016/j.cardiores.2005.06.006   (Journal Full-text)

BACKGROUND: In a heart with myocarditis, there are cardiomyocytes, inflammatory cells, and non-inflammatory interstitial cells. Immunological molecules are thought to influence not only inflammatory cells but also cardiac function and remodeling. Whatever their origin, the cells they target and the intercellular crosstalk they mediate remain unclear. Here, we examined native gene expression of immunological molecules in normal and rat experimental autoimmune myocarditis (EAM) 18 and 90 days after immunization, using real time RT-PCR in cardiomyocytes, CD11b(+) cells, alphabetaT cells and non-cardiomyocytic non-inflammatory (NCNI) cells. METHODS AND RESULTS: Cells were isolated by collagenase perfusion on a Langendorff apparatus and purified by passing through a stainless-steel sieve followed by magnetic bead column separation using appropriate monoclonal antibodies. Most immunological molecules were expressed in inflammatory cells. However, some were expressed in NCNI cells or cardiomyocytes. Interestingly, most of interleukin (IL)-10, monocyte chemoattractant protein (MCP)-1, or tumor necrosis factor (TNF)-alpha receptor were found in NCNI cells and most of fractalkine were found in NCNI cells and cardiomyocytes. Moreover, TNF-alpha significantly upregulated fractalkine and MCP-1 mRNA in cultivated cells from EAM hearts. CONCLUSION: In the rat experimental myocarditis heart, inflammatory cells express many immunological molecules. Some of them are thought to influence NCNI cells or cardiomyocytes directly via receptors on these cell types. It is further suggested that fractalkine, IL-10, and MCP-1 expressed in NCNI cells or cardiomyocytes regulate inflammatory cells.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
CX3CL1Humanmyocarditis  ISOCx3cl1 (Rattus norvegicus)mRNA:increased expression:cardiac muscle cellRGD 
Cx3cl1Ratmyocarditis  IEP mRNA:increased expression:cardiac muscle cellRGD 
Cx3cl1Mousemyocarditis  ISOCx3cl1 (Rattus norvegicus)mRNA:increased expression:cardiac muscle cellRGD 

Objects Annotated

Genes (Rattus norvegicus)
Cx3cl1  (C-X3-C motif chemokine ligand 1)

Genes (Mus musculus)
Cx3cl1  (C-X3-C motif chemokine ligand 1)

Genes (Homo sapiens)
CX3CL1  (C-X3-C motif chemokine ligand 1)


Additional Information