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2016 ; 37
(11
): 1423-1431
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Cinacalcet ameliorates aortic calcification in uremic rats via suppression of
endothelial-to-mesenchymal transition
#MMPMID27593220
Wu M
; Tang RN
; Liu H
; Pan MM
; Liu BC
Acta Pharmacol Sin
2016[Nov]; 37
(11
): 1423-1431
PMID27593220
show ga
AIM: Experimental studies found that cinacalcet (CINA) markedly attenuated
vascular calcification in uremic rats, but its underlying mechanisms are still
largely unknown. Recent evidence have demonstrated that endothelial cells (ECs)
participate in ectopic calcification in part by mediating
endothelial-to-mesenchymal transition (EndMT). In this study, we investigated
whether CINA ameliorated aortic calcification in uremic rats via suppression of
EndMT. METHODS: Uremia was induced in rats by feeding rats a 0.75% adenine diet
for 4 weeks. After adenine withdrawal, the rats were maintained on a 1.03%
phosphorus diet for next 8 weeks. At initiation of the adenine diet, rats were
orally administered CINA (10mg/kg one day) for 12 weeks. The aortic expression of
EndMT- and chondrocyte- markers was examined. The effect of elevated PTH on EndMT
was also studied in aortic ECs. RESULTS: In uremic rats, CINA treatment
significantly decreased the serum PTH concentrations, but did not affect the
elevated levels of serum calcium (Ca), phosphorus (P) and Ca×P product. Besides,
CINA significantly attenuated aortic calcification, and inhibited the expression
of chondrocyte markers (SOX9 and COL2A1) and chondrocyte proteoglycan in uremic
aortas. Moreover, CINA treatment largely abolished the up-regulation of
mesenchymal markers (FSP1 and ?-SMA) and down-regulation of the endothelial
marker (CD31), which accompanied aortic calcification in uremic aorta samples. In
vitro, PTH increased the expression of EndMT-markers in a concentration- and
time-dependent manner. CONCLUSION: These findings suggest that strategies aiming
at reducing serum PTH might prevent uremic aortic calcification by abrogating
EndMT.
|Animals
[MESH]
|Aorta/*drug effects/pathology
[MESH]
|Calcimimetic Agents/*pharmacology/therapeutic use
[MESH]
free
free
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