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Transcript
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Oral or Poster Cat: Molecular cardiology, Basic Research
PATHOLOGICAL EFFECT OF ENDOTHELIAL-TO-MESENCHYMAL
TRANSITION ON THE CYSTIC KIDNEY
B.H. Kim, M.Y. Park, J.H. Park
Sookmyung Women's University, Yongsan-gu, Seoul, Korea
Objectives: We research on pathological effects of endothelial to mesenchymal transition
(EndMT) on cystic kidney. Furthermore, we try to find novel genes inducing endMT on
it.
Background: EndMT is a phenomenon that an endothelial cell loses its characteristic and
acquires mesenchymal cell specific feature. It is known to be crucial for heart
development. However, as it was found that endMT was involved in the cardiac fibrosis
in 2007, pathological effect of endMT has been unveiled in other organs. Kidney is the
organ composing urinary system. A functional and structural unit of the kidney is called
nephron, which consists of epithelial tubules and blood vessels. Majority of kidney
diseases entail renal fibrosis which impairs renal function. In 2008, it was reported that
renal fibrosis considerably results from endMT.
Methods: We got mRNA and protein from mouse cystic kidney tissues. Expression level
of mesenchymal markers was checked by real time RT PCR and western blot. Extent of
endMT was observed by immunostaining with antibodies for mesenchymal markers
(FSP1, Vim, etc.) and endothelial cell marker (CD31).
Results: Expression level of mesenchymal markers in mouse cystic kidney was higher
than that in mouse normal kidney. Furthermore, endMT occurred much more in the cystic
kidney tissue.
Conclusions Like other chronic kidney disease, cystic kidney entails renal fibrosis.
EndMT considerably contributes to renal fibrosis in the cystic kidney. To find out the
novel inducer gene for endMT can help understanding its pathological effect on the cystic
kidney.