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10.1681/ASN.2008020233 http://scihub22266oqcxt.onion/10.1681/ASN.2008020233 18776121!2573015!18776121     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Soc+Nephrol 2008 ; 19 (11): 2150-8 Nephropedia Template TP {{tp|p=18776121|t=2008. Podocyte-specific deletion of dicer alters cytoskeletal dynamics and causes glomerular disease |pdf=|usr=}}{{18776121}} gab.com Text Podocyte-specific deletion of dicer alters cytoskeletal dynamics and causes glomerular disease JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=18776121 #FOAvip MicroRNAs (miRNAs) regulate gene expression by binding the 3' untranslated region of mRNAs. To define their role in glomerular function, miRNA biogenesis was disrupted in mouse podocytes using a conditional Dicer allele. Mutant mice developed proteinuria by 3 wk after birth and progressed rapidly to end-stage kidney disease. Podocyte pathology included effacement, vacuolization, and hypertrophy with crescent formation. Despite normal expression of WT1, podocytes underwent dedifferentiation, exemplified by cytoskeletal disruption with early transcriptional downregulation of synaptopodin. These abnormalities differed from Cd2ap(-/-) mice, indicating they were not a general consequence of glomerular disease. Glomerular labeling of ezrin, moesin, and gelsolin was altered at 3 wk, but expression of nestin and alpha-actinin was unchanged. Abnormal cell proliferation or apoptosis was not responsible for the glomerular injury. Mutant podocytes were incapable of synthesizing mature miRNA, as revealed by their loss of miR-30a. In contrast, expression of glomerular endothelial and mesangial cell miRNAs (miR-126 and miR-145, respectively) was unchanged. These findings demonstrate a critical role for miRNA in glomerular function and suggest a pathway that may participate in the pathogenesis of kidney diseases of podocyte origin. The unique architecture of podocytes may make them especially susceptible to cytoskeletal alterations initiated by aberrant miRNA dynamics. Twit Text FOAVip Podocyte-specific deletion of dicer alters cytoskeletal dynamics and causes glomerular disease ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=18776121 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=18776121 #FOAvip English Wikipedia <ref>{{Cite pmid|18776121}}</ref> Podocyte-specific deletion of dicer alters cytoskeletal dynamics and causes glomerular disease #MMPMID18776121 Harvey SJ; Jarad G; Cunningham J; Goldberg S; Schermer B; Harfe BD; McManus MT; Benzing T; Miner JH J Am Soc Nephrol 2008[Nov]; 19 (11): 2150-8 PMID18776121show ga MicroRNAs (miRNAs) regulate gene expression by binding the 3' untranslated region of mRNAs. To define their role in glomerular function, miRNA biogenesis was disrupted in mouse podocytes using a conditional Dicer allele. Mutant mice developed proteinuria by 3 wk after birth and progressed rapidly to end-stage kidney disease. Podocyte pathology included effacement, vacuolization, and hypertrophy with crescent formation. Despite normal expression of WT1, podocytes underwent dedifferentiation, exemplified by cytoskeletal disruption with early transcriptional downregulation of synaptopodin. These abnormalities differed from Cd2ap(-/-) mice, indicating they were not a general consequence of glomerular disease. Glomerular labeling of ezrin, moesin, and gelsolin was altered at 3 wk, but expression of nestin and alpha-actinin was unchanged. Abnormal cell proliferation or apoptosis was not responsible for the glomerular injury. Mutant podocytes were incapable of synthesizing mature miRNA, as revealed by their loss of miR-30a. In contrast, expression of glomerular endothelial and mesangial cell miRNAs (miR-126 and miR-145, respectively) was unchanged. These findings demonstrate a critical role for miRNA in glomerular function and suggest a pathway that may participate in the pathogenesis of kidney diseases of podocyte origin. The unique architecture of podocytes may make them especially susceptible to cytoskeletal alterations initiated by aberrant miRNA dynamics. |Animals[MESH] |Apoptosis[MESH] |Cell Differentiation[MESH] |Cell Proliferation[MESH] |Cytoskeleton/metabolism[MESH] |DEAD-box RNA Helicases/*deficiency/genetics/metabolism[MESH] |Endoribonucleases/*deficiency/genetics/metabolism[MESH] |Kidney Diseases/enzymology/*etiology/genetics/pathology[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |MicroRNAs/biosynthesis/genetics[MESH] |Podocytes/*enzymology/pathology[MESH] |RNA Processing, Post-Transcriptional[MESH]Podocyte-specific deletion of dicer alters cytoskeletal dynamics and c(epmc).pdf DeepDyve Pubget Overpricing