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10.1681/ASN.2015040366 http://scihub22266oqcxt.onion/10.1681/ASN.2015040366 C5004641!5004641!26823550     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26823550&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Soc+Nephrol 2016 ; 27 (9): 2685-700 Nephropedia Template TP {{tp|p=26823550|t=2016. Cathepsin D in Podocytes Is Important in the Pathogenesis of Proteinuria and CKD |pdf=|usr=}}{{26823550}} gab.com Text Cathepsin D in Podocytes Is Important in the Pathogenesis of Proteinuria and CKD JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=26823550 #FOAvip Studies have revealed many analogies between podocytes and neurons, and these analogies may be key to elucidating the pathogenesis of podocyte injury. Cathepsin D (CD) is a representative aspartic proteinase in lysosomes. Central nervous system neurons in CD-deficient mice exhibit a form of lysosomal storage disease with a phenotype resembling neuronal ceroid lipofuscinoses. In the kidney, the role of CD in podocytes has not been fully explored. Herein, we generated podocyte?specific CD?knockout mice that developed proteinuria at 5 months of age and ESRD by 20?22 months of age. Immunohistochemical analysis of these mice showed apoptotic podocyte death followed by proteinuria and glomerulosclerosis with aging. Using electron microscopy, we identified, in podocytes, granular osmiophilic deposits (GRODs), autophagosome/autolysosome-like bodies, and fingerprint profiles, typical hallmarks of CD-deficient neurons. CD deficiency in podocytes also led to the cessation of autolysosomal degradation and accumulation of proteins indicative of autophagy impairment and the mitochondrial ATP synthase subunit c accumulation in the GRODs, again similar to changes reported in CD-deficient neurons. Furthermore, both podocin and nephrin, two essential components of the slit diaphragm, translocated to Rab7? and lysosome?associated membrane glycoprotein 1?positive amphisomes/autolysosomes that accumulated in podocyte cell bodies in podocyte?specific CD?knockout mice. We hypothesize that defective lysosomal activity resulting in foot process effacement caused this accumulation of podocin and nephrin. Overall, our results suggest that loss of CD in podocytes causes autophagy impairment, triggering the accumulation of toxic subunit c?positive lipofuscins as well as slit diaphragm proteins followed by apoptotic cell death. Twit Text FOAVip Cathepsin D in Podocytes Is Important in the Pathogenesis of Proteinuria and CKD ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=26823550 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26823550 #FOAvip English Wikipedia <ref>{{Cite pmid|26823550}}</ref> Cathepsin D in Podocytes Is Important in the Pathogenesis of Proteinuria and CKD #MMPMID26823550 Yamamoto-Nonaka K; Koike M; Asanuma K; Takagi M; Oliva Trejo JA; Seki T; Hidaka T; Ichimura K; Sakai T; Tada N; Ueno T; Uchiyama Y; Tomino Y J Am Soc Nephrol 2016[Sep]; 27 (9): 2685-700 PMID26823550show ga Studies have revealed many analogies between podocytes and neurons, and these analogies may be key to elucidating the pathogenesis of podocyte injury. Cathepsin D (CD) is a representative aspartic proteinase in lysosomes. Central nervous system neurons in CD-deficient mice exhibit a form of lysosomal storage disease with a phenotype resembling neuronal ceroid lipofuscinoses. In the kidney, the role of CD in podocytes has not been fully explored. Herein, we generated podocyte?specific CD?knockout mice that developed proteinuria at 5 months of age and ESRD by 20?22 months of age. Immunohistochemical analysis of these mice showed apoptotic podocyte death followed by proteinuria and glomerulosclerosis with aging. Using electron microscopy, we identified, in podocytes, granular osmiophilic deposits (GRODs), autophagosome/autolysosome-like bodies, and fingerprint profiles, typical hallmarks of CD-deficient neurons. CD deficiency in podocytes also led to the cessation of autolysosomal degradation and accumulation of proteins indicative of autophagy impairment and the mitochondrial ATP synthase subunit c accumulation in the GRODs, again similar to changes reported in CD-deficient neurons. Furthermore, both podocin and nephrin, two essential components of the slit diaphragm, translocated to Rab7? and lysosome?associated membrane glycoprotein 1?positive amphisomes/autolysosomes that accumulated in podocyte cell bodies in podocyte?specific CD?knockout mice. We hypothesize that defective lysosomal activity resulting in foot process effacement caused this accumulation of podocin and nephrin. Overall, our results suggest that loss of CD in podocytes causes autophagy impairment, triggering the accumulation of toxic subunit c?positive lipofuscins as well as slit diaphragm proteins followed by apoptotic cell death. äCathepsin D in Podocytes Is Important in the Pathogenesis of Proteinur(epmc).pdf DeepDyve Pubget Overpricing