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10.1152/ajprenal.00567.2009 http://scihub22266oqcxt.onion/10.1152/ajprenal.00567.2009 C4380486!4380486 !20071461     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=20071461 &cmd=llinks): Failed to open stream: HTTP request failed! 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Impact of Cyclin B2 and Cell division cycle 2 on tubular hyperplasia in progressive chronic renal failure rats |pdf=|usr=}}{{20071461 }} gab.com Text Impact of Cyclin B2 and Cell division cycle 2 on tubular hyperplasia in progressive chronic renal failure rats JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=20071461 #FOAvip To clarify the specific molecular events of progressive tubular damage in chronic renal failure (CRF), we conducted microarray analyses using isolated proximal tubules from subtotally nephrectomized (Nx) rats as a model of CRF. Our results clearly demonstrated time-dependent changes in gene expression profiles localized to proximal tubules. The expression of mitosis-specific genes Cyclin B2 and Cell division cycle 2 (Cdc2) was significantly and selectively increased in the proximal tubules during the compensated period but decreased to basal level in the end-stage period. Administration of everolimus, a potent inhibitor of mammalian target of rapamycin, markedly reduced compensatory hypertrophy and hyperplasia of epithelial cells, which was accompanied by complete abolishment of the expression of Cyclin B2 and Cdc2 enhancement; renal function was then severely decreased. Treatment with the Cdc2 inhibitor 2-cyanoethyl alsterpaullone clearly decreased epithelial cell hyperplasia, based on staining of phosphorylated histone H3 and Ki-67, while hypertrophy was not inhibited. In conclusion, we have demonstrated roles of Cyclin B2 and Cdc2 in the epithelial hyperplasia in response to Nx. These results advance the knowledge of the contribution of cell cycle regulators, especially M phase, in pathophysiology of tubular restoration and/or degeneration, and these two molecules are suggested to be a marker for the proliferation of proximal tubular cells in CRF. Twit Text FOAVip Impact of Cyclin B2 and Cell division cycle 2 on tubular hyperplasia in progressive chronic renal failure rats ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=20071461 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=20071461 #FOAvip English Wikipedia <ref>{{Cite pmid|20071461 }}</ref> Impact of Cyclin B2 and Cell division cycle 2 on tubular hyperplasia in progressive chronic renal failure rats #MMPMID20071461 Nishihara K ; Masuda S ; Nakagawa S ; Yonezawa A ; Ichimura T ; Bonventre JV ; Inui K Am J Physiol Renal Physiol 2010[Apr]; 298 (4 ): F923-34 PMID20071461 show ga To clarify the specific molecular events of progressive tubular damage in chronic renal failure (CRF), we conducted microarray analyses using isolated proximal tubules from subtotally nephrectomized (Nx) rats as a model of CRF. Our results clearly demonstrated time-dependent changes in gene expression profiles localized to proximal tubules. The expression of mitosis-specific genes Cyclin B2 and Cell division cycle 2 (Cdc2) was significantly and selectively increased in the proximal tubules during the compensated period but decreased to basal level in the end-stage period. Administration of everolimus, a potent inhibitor of mammalian target of rapamycin, markedly reduced compensatory hypertrophy and hyperplasia of epithelial cells, which was accompanied by complete abolishment of the expression of Cyclin B2 and Cdc2 enhancement; renal function was then severely decreased. Treatment with the Cdc2 inhibitor 2-cyanoethyl alsterpaullone clearly decreased epithelial cell hyperplasia, based on staining of phosphorylated histone H3 and Ki-67, while hypertrophy was not inhibited. In conclusion, we have demonstrated roles of Cyclin B2 and Cdc2 in the epithelial hyperplasia in response to Nx. These results advance the knowledge of the contribution of cell cycle regulators, especially M phase, in pathophysiology of tubular restoration and/or degeneration, and these two molecules are suggested to be a marker for the proliferation of proximal tubular cells in CRF. |Animals [MESH] |CDC2 Protein Kinase [MESH] |Cell Cycle Proteins/genetics/*metabolism [MESH] |Cell Cycle/genetics [MESH] |Cyclin B2/genetics/*metabolism [MESH] |Cyclin-Dependent Kinases [MESH] |Everolimus [MESH] |Hyperplasia/metabolism/pathology [MESH] |Immunosuppressive Agents/pharmacology [MESH] |Intracellular Signaling Peptides and Proteins/antagonists & inhibitors/metabolism [MESH] |Kidney Failure, Chronic/*metabolism/pathology [MESH] |Kidney Tubules/metabolism/*pathology [MESH] |Male [MESH] |Mitosis/physiology [MESH] |Protein Array Analysis [MESH] |Protein Serine-Threonine Kinases/antagonists & inhibitors/metabolism [MESH] |Rats [MESH] |Rats, Wistar [MESH] |Reproducibility of Results [MESH] |Sirolimus/analogs & derivatives/pharmacology [MESH] |TOR Serine-Threonine Kinases [MESH]Impact of Cyclin B2 and Cell division cycle 2 on tubular hyperplasia i(epmc).pdf DeepDyve Pubget Overpricing