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10.1111/j.1582-4934.2009.00910.x http://scihub22266oqcxt.onion/10.1111/j.1582-4934.2009.00910.x C3822805!3822805!19778355     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Cell+Mol+Med 2011 ; 15 (2): 414-22 Nephropedia Template TP {{tp|p=19778355|t=2011. Calcineurin A-? is required for hypertrophy but not matrix expansion in the diabetic kidney |pdf=|usr=}}{{19778355}} gab.com Text Calcineurin A- is required for hypertrophy but not matrix expansion in the diabetic kidney JO: J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=19778355 #FOAvip Calcineurin is an important signalling protein that regulates a number of molecular and cellular processes. Previously, we found that inhibition of calcineurin with cyclosporine reduced renal hypertrophy and blocked glomerular matrix expansion in the diabetic kidney. Isoforms of the catalytic subunit of calcineurin are reported to have tissue specific expression and functions. In particular, the ? isoform has been implicated in cardiac and skeletal muscle hypertrophy. Therefore, we examined the role of calcineurin ? in diabetic renal hypertrophy and glomerular matrix expansion. Type I diabetes was induced in wild-type and ??/? mice and then renal function, extracellular matrix expansion and hypertrophy were evaluated. The absence of ? produced a significant decrease in total calcineurin activity in the inner medulla (IM) and reduced nuclear factor of activated T-cells (NFATc) activity. Loss of ? did not alter diabetic renal dysfunction assessed by glomerular filtration rate, urine albumin excretion and blood urea nitrogen. Similarly, matrix expansion in the whole kidney and glomerulus was not different between diabetic wild-type and ??/? mice. In contrast, whole kidney and glomerular hypertrophy were significantly reduced in diabetic ??/? mice. Moreover, ??/? renal fibroblasts demonstrated impaired phosphorylation of Erk1/Erk2, c-Jun N-terminal kinases (JNK) and mammalian target of rapamycin (mTOR) following stimulation with transforming growth factor-? and did not undergo hypertrophy with 48 hrs culture in high glucose. In conclusion, loss of the ? isoform of calcineurin is sufficient to reproduce beneficial aspects of cyclosporine on diabetic renal hypertrophy but not matrix expansion. Therefore, while multiple signals appear to regulate matrix, calcineurin ? appears to be a central mechanism involved in organ hypertrophy. Twit Text FOAVip Calcineurin A- is required for hypertrophy but not matrix expansion in the diabetic kidney ????J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=19778355 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19778355 #FOAvip English Wikipedia <ref>{{Cite pmid|19778355}}</ref> Calcineurin A-? is required for hypertrophy but not matrix expansion in the diabetic kidney #MMPMID19778355 Reddy RN; Knotts TL; Roberts BR; Molkentin JD; Price SR; Gooch JL J Cell Mol Med 2011[Feb]; 15 (2): 414-22 PMID19778355show ga Calcineurin is an important signalling protein that regulates a number of molecular and cellular processes. Previously, we found that inhibition of calcineurin with cyclosporine reduced renal hypertrophy and blocked glomerular matrix expansion in the diabetic kidney. Isoforms of the catalytic subunit of calcineurin are reported to have tissue specific expression and functions. In particular, the ? isoform has been implicated in cardiac and skeletal muscle hypertrophy. Therefore, we examined the role of calcineurin ? in diabetic renal hypertrophy and glomerular matrix expansion. Type I diabetes was induced in wild-type and ??/? mice and then renal function, extracellular matrix expansion and hypertrophy were evaluated. The absence of ? produced a significant decrease in total calcineurin activity in the inner medulla (IM) and reduced nuclear factor of activated T-cells (NFATc) activity. Loss of ? did not alter diabetic renal dysfunction assessed by glomerular filtration rate, urine albumin excretion and blood urea nitrogen. Similarly, matrix expansion in the whole kidney and glomerulus was not different between diabetic wild-type and ??/? mice. In contrast, whole kidney and glomerular hypertrophy were significantly reduced in diabetic ??/? mice. Moreover, ??/? renal fibroblasts demonstrated impaired phosphorylation of Erk1/Erk2, c-Jun N-terminal kinases (JNK) and mammalian target of rapamycin (mTOR) following stimulation with transforming growth factor-? and did not undergo hypertrophy with 48 hrs culture in high glucose. In conclusion, loss of the ? isoform of calcineurin is sufficient to reproduce beneficial aspects of cyclosporine on diabetic renal hypertrophy but not matrix expansion. Therefore, while multiple signals appear to regulate matrix, calcineurin ? appears to be a central mechanism involved in organ hypertrophy. äCalcineurin A-? is required for hypertrophy but not matrix expansion i(epmc).pdf DeepDyve Pubget Overpricing