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10.1186/s12861-016-0131-z http://scihub22266oqcxt.onion/10.1186/s12861-016-0131-z C5007805!5007805!27582005     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       BMC+Dev+Biol 2016 ; 16 (1): ä Nephropedia Template TP {{tp|p=27582005|t=2016. Impairment of Wnt11 function leads to kidney tubular abnormalities and secondary glomerular cystogenesis |pdf=|usr=}}{{27582005}} gab.com Text Impairment of Wnt11 function leads to kidney tubular abnormalities and secondary glomerular cystogenesis JO: BMC Dev Biol http://www.kidney.de/pget.php?&tw=1&pmid=27582005 #FOAvip 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. Electronic supplementary material: The online version of this article (doi:10.1186/s12861-016-0131-z) contains supplementary material, which is available to authorized users. Twit Text FOAVip Impairment of Wnt11 function leads to kidney tubular abnormalities and secondary glomerular cystogenesis ????BMC Dev Biol http://www.kidney.de/pget.php?&tw=1&pmid=27582005 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27582005 #FOAvip English Wikipedia <ref>{{Cite pmid|27582005}}</ref> 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[]; 16 (1): ä PMID27582005show 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. Electronic supplementary material: The online version of this article (doi:10.1186/s12861-016-0131-z) contains supplementary material, which is available to authorized users. äImpairment of Wnt11 function leads to kidney tubular abnormalities and(epmc).pdf DeepDyve Pubget Overpricing