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2016 ; 16
(1
): 30
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Impairment of Wnt11 function leads to kidney tubular abnormalities and secondary
glomerular cystogenesis
#MMPMID27582005
Nagy II
; Xu Q
; Naillat F
; Ali N
; Miinalainen I
; Samoylenko A
; Vainio SJ
BMC Dev Biol
2016[Aug]; 16
(1
): 30
PMID27582005
show ga
BACKGROUND: Wnt11 is a member of the Wnt family of secreted signals controlling
the early steps in ureteric bud (UB) branching. Due to the reported lethality of
Wnt11 knockout embryos in utero, its role in later mammalian kidney organogenesis
remains open. The presence of Wnt11 in the emerging tubular system suggests that
it may have certain roles later in the development of the epithelial ductal
system. RESULTS: The Wnt11 knockout allele was backcrossed with the C57Bl6 strain
for several generations to address possible differences in penetrance of the
kidney phenotypes. Strikingly, around one third of the null mice with this inbred
background survived to the postnatal stages. Many of them also reached adulthood,
but urine and plasma analyses pointed out to compromised kidney function.
Consistent with these data the tubules of the C57Bl6 Wnt11 (-/-) mice appeared to
be enlarged, and the optical projection tomography indicated changes in tubular
convolution. Moreover, the C57Bl6 Wnt11 (-/-) mice developed secondary glomerular
cysts not observed in the controls. The failure of Wnt11 signaling reduced the
expression of several genes implicated in kidney development, such as Wnt9b,
Six2, Foxd1 and Hox10. Also Dvl2, an important PCP pathway component, was
downregulated by more than 90 % due to Wnt11 deficiency in both the E16.5 and NB
kidneys. Since all these genes take part in the control of UB, nephron and
stromal progenitor cell differentiation, their disrupted expression may
contribute to the observed anomalies in the kidney tubular system caused by Wnt11
deficiency. CONCLUSIONS: The Wnt11 signal has roles at the later stages of kidney
development, namely in coordinating the development of the tubular system. The
C57Bl6 Wnt11 (-/-) mouse generated here provides a model for studying the
mechanisms behind tubular anomalies and glomerular cyst formation.
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