大鼠腎小球支持細胞表現fractalkine之訊息傳遞機轉及其病態生理角色之探討(2/2)
Other Title
Signal transduction mechanisms and pathophysiologic roles of fractalkine
expression by rat mesangial cells (2/2)
expression by rat mesangial cells (2/2)
Date Issued
2003
Date
2003
Author(s)
陳永銘
DOI
912314B002335
Abstract
Background. Fractalkine is a CX3C chemokine for mononuclear cells that has been
implicated in the recruitment and accumulation of monocytes seen in glomerular
diseases. This study investigated the sequential expression of fractalkine in rat anti-Thy1
nephritis, and the effect of fractakine blockade on the severity of anti-Thy1
nephritis.
Methods. Rat anti-Thy1 glomerulonephritis was induced as described previously.
Group A rats received monoclonal anti-Thy1 antibodies and daily 1X PBS injection;
group B rats received monoclonal anti-Thy1 antibodies and daily 1X PBS injection
(days 1-2) and rabbit anti-rat fractalkine injection (days 3-5); group C rats received
monoclonal anti-Thy1 antibodies and daily rabbit anti-rat fractalkine injection (days
1-5). Fractalkine mRNA and protein were analyzed by Northern and Western blotting.
Renal histomorphology was examined by H&E staining, glomerular macrophage and
T cell infiltration were studied by immunohistochemical staining. Results. Group A rats showed an appreciable increase in urinary protein excretion,
glomerulosclerosis, and matrix gene expression at days 5 of the nephritis, when
compared with normal control rats. In addition, the nephritic rats showed an increase
in glomerular fractalkine gene expression during days 1 to 5 of the disease. A parallel
in crease in glomerular fractalkine protein expression was also seen during days 3 to 5.
Urinary fractalkine excretion could be seen during days 3 to 5 of the nephritis. The
administration of rabbit anti-rat fractalkine antibodies, whether between days 3 and 5
(group B), or during days 1 and 5 (group C), did not affect the severity of the nephritis.
Conclusion. The present data shows that fractalkine is upregulated during the course
of anti-Thy1 nephritis. However, blocking fractalkine activity with a commercially-available
polyclonal antibody did not ameliorate the severity of the disease.
Publisher
臺北市：國立臺灣大學醫學院內科
Type
report
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