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A Decrease in Glomerular Endothelial Cells and Endothelial-mesenchymal Transition
during Glomerulosclerosis in the Tensin2-deficient Mice (ICGN strain)
#MMPMID25859060
Kato T
; Mizuno S
; Ito A
Acta Histochem Cytochem
2014[]; 47
(6
): 265-71
PMID25859060
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The ICR-derived glomerulonephritis (ICGN) mouse is a unique model of nephrotic
syndrome, and albuminuria becomes evident in a neonatal stage, due to a genetic
mutation of tensin2. We previously provided evidence that an apparent decrease in
nephrin, caused by tensin2-deficiencient states, leads to podocytopathy,
albuminuria and eventually, chronic renal failure. In general, glomerular
endothelial cells (ECs) function as a barrier through tight attachment of
glomerular basement membrane to podocytes, while decreased ECs can worsen renal
failure. Nevertheless, it is still unknown whether glomerular ECs are altered
under the tensin-2-deficient states during the manifestation of chronic renal
failure. Herein, we examined the changes of glomerular ECs, with focus on the
expression of PECAM-1 and VE-cadherin (EC-specific markers), or of ?-SMA
(myofibroblast marker) in this mouse model by histological methods. Compared with
the non-nephrotic (+/nep) mice, the nephrotic (nep/nep) mice exhibited the
reduced expression of PECAM-1, or of VE-cadherin, in glomerular area. Notably,
some glomerular ECs showed the positive stainings for both PECAM-1 and ?-SMA,
suggesting endothelial-to-mesenchymal transition (EndoMT) during progression of
glomerular sclerosis. This is the first report showing that a decrease in
glomerular ECs, at least in part, via EndoMT is involved in tensin2-deficient
pathological conditions.
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