|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
12
|
|
pubmed:dateCreated |
2008-6-23
|
|
pubmed:abstractText |
Tissue damage following injury leads to inflammation and fibrosis. To understand the molecular mechanisms and the proteins involved in the fibrotic process, we used the well-established unilateral ureteric obstruction rat model and we analyzed the alterations at early and late time intervals using a classical proteomic approach. Data analysis demonstrates a correlation between calreticulin up-regulation and progression of fibrosis. Calreticulin is involved in Ca++ homeostasis but has not been previously implicated in animal models of fibrosis. Proteomic analysis consistently revealed up-regulation of calreticulin in both early and late time intervals. These findings were further confirmed by biochemical and morphological approaches. Next, animal models of lung fibrosis (bleomycin-induced) and heart fibrosis (desmin-null) were examined. In the lung model, calreticulin expression was up-regulated from early time intervals, whereas in the heart model no change in the expression of calreticulin was observed. In addition, TGF-beta, a well known major contributing factor in several fibrotic processes, was found to up-regulate calreticulin in cultured human proximal tubule epithelial cells. The above observations suggest that calreticulin might be involved in fibrotic processes; however the mechanism(s) underlying its possible involvement are yet unresolved.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Jun
|
|
pubmed:issn |
1615-9861
|
|
pubmed:author |
|
|
pubmed:issnType |
Electronic
|
|
pubmed:volume |
8
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
2407-19
|
|
pubmed:meshHeading |
pubmed-meshheading:18563736-Animals,
pubmed-meshheading:18563736-Bleomycin,
pubmed-meshheading:18563736-Calreticulin,
pubmed-meshheading:18563736-Cell Line, Transformed,
pubmed-meshheading:18563736-Cells, Cultured,
pubmed-meshheading:18563736-Collagen,
pubmed-meshheading:18563736-Desmin,
pubmed-meshheading:18563736-Disease Models, Animal,
pubmed-meshheading:18563736-Epithelial Cells,
pubmed-meshheading:18563736-Female,
pubmed-meshheading:18563736-Fibrosis,
pubmed-meshheading:18563736-Gene Expression Regulation,
pubmed-meshheading:18563736-Humans,
pubmed-meshheading:18563736-Immunohistochemistry,
pubmed-meshheading:18563736-Kidney Tubules, Proximal,
pubmed-meshheading:18563736-Male,
pubmed-meshheading:18563736-Mice,
pubmed-meshheading:18563736-Mice, Inbred C57BL,
pubmed-meshheading:18563736-Mice, Mutant Strains,
pubmed-meshheading:18563736-Models, Biological,
pubmed-meshheading:18563736-Proteomics,
pubmed-meshheading:18563736-Pulmonary Fibrosis,
pubmed-meshheading:18563736-Rats,
pubmed-meshheading:18563736-Rats, Wistar,
pubmed-meshheading:18563736-Time Factors,
pubmed-meshheading:18563736-Transforming Growth Factor beta
|
|
pubmed:year |
2008
|
|
pubmed:articleTitle |
Altered expression of calreticulin during the development of fibrosis.
|
|
pubmed:affiliation |
Department of Basic Research, Biomedical Research Foundation of the Academy of Athens, Athens, Greece.
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|
