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10.1100/tsw.2008.108 http://scihub22266oqcxt.onion/10.1100/tsw.2008.108 C5849071!5849071!18758661     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 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 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       ScientificWorldJournal 2008 ; 8 (ä): 835-44 Nephropedia Template TP {{tp|p=18758661|t=2008. Evaluation of Renal Gene Expression of Protein Kinase C (PKC) Isoforms in Diabetic and Nondiabetic Proliferative Glomerular Diseases |pdf=|usr=}}{{18758661}} gab.com Text Evaluation of Renal Gene Expression of Protein Kinase C (PKC) Isoforms in Diabetic and Nondiabetic Proliferative Glomerular Diseases JO: ScientificWorldJournal http://www.kidney.de/pget.php?&tw=1&pmid=18758661 #FOAvip The protein kinase C (PKC) family consists of 13 members categorized as conventional or novel depending on whether diacylglycerol, calcium, or phosphatidylserine is required for activation. High glucose leads to activation of different forms of PKC across tissue types, thus determining the kind of diabetes-induced organ damage. PKC ? was reported to have a positive role in B-lymphocyte activity through activation of NF-?B, leading to various immune disorders. We examined renal expression of two PKC isoforms ? and ? in renal biopsies of patients with diabetic nephropathy, lupus nephritis (LN) (Class 3-4), and mesangioproliferative glomerulonephritis (MPGN) to explore the role of each isoform in different glomerular diseases. PKC ? and ? gene expression was studied by quantitative real-time reverse transcription-PCR in 20 patients with type 2 diabetes and proteinuria (serum creatinine 2.04 ± 0.85 mg/dl, 24-h urinary protein 3.61 ± 1.75 g, eGFR 37.85 ± 17.89 ml/min/1.73 m2), 20 patients with proliferative LN (serum creatinine 1.67 ± 1.50 mg/dl, 24-h urinary protein 4.46 ± 5.01 g, eGFR 69.62 ± 40.93 ml/min/1.73 m2), and 20 patients with MPGN (serum creatinine 3.32 ± 2.79 mg/dl, 24-h urinary protein 4.65 ± 4.11 g, eGFR 32.62 ± 29.56 ml/min/1.73 m2). Normal tissues from the normal pole of four kidneys removed because of renal tumor served as controls. PKC ? gene expression was significantly increased in diabetic kidneys compared to LN and MPGN (316.95 ± 152.94 µg/ml vs. 185.97 ± 32.13 and 195.46 ± 46.45 µg/ml, p < 0.05). PKC ? gene expression was significantly increased in the LN and MPGN groups compared to the diabetic nephropathy group (41.01 ± 14.03 and 39.93 ± 16.41 µg/ml, respectively, vs. 18.20 ± 4.91 µg/ml, p < 0.05). Significant correlation was noted between the PKC ? gene concentrations and proteinuria in diabetic patients. Renal expression of PKC ? and ? genes in control tissues were significantly lower compared to diabetic kidneys, LN, and MPGN groups (32.31 ± 0.36 and 4.67 ± 2.41 µg/ml, respectively, p < 0.001). The study revealed enhanced renal gene expression of both PKC isoforms ? and ? in diabetic kidney tissues, LN, and MPGN, but in different patterns. PKC ? gene expression was significantly increased in diabetic patients with chronic kidney disease. The increased expression of the PKC ? gene in LN and MPGN highlights its role in regulation of the immune system. This may represent potential therapeutic targets for prevention of progressive kidney injury in diabetic and proliferative glomerular diseases. Twit Text FOAVip Evaluation of Renal Gene Expression of Protein Kinase C (PKC) Isoforms in Diabetic and Nondiabetic Proliferative Glomerular Diseases ????ScientificWorldJournal http://www.kidney.de/pget.php?&tw=1&pmid=18758661 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=18758661 #FOAvip English Wikipedia <ref>{{Cite pmid|18758661}}</ref> Evaluation of Renal Gene Expression of Protein Kinase C (PKC) Isoforms in Diabetic and Nondiabetic Proliferative Glomerular Diseases #MMPMID18758661 Ibrahim S; Rashed L; Fadda S ScientificWorldJournal 2008[]; 8 (ä): 835-44 PMID18758661show ga The protein kinase C (PKC) family consists of 13 members categorized as conventional or novel depending on whether diacylglycerol, calcium, or phosphatidylserine is required for activation. High glucose leads to activation of different forms of PKC across tissue types, thus determining the kind of diabetes-induced organ damage. PKC ? was reported to have a positive role in B-lymphocyte activity through activation of NF-?B, leading to various immune disorders. We examined renal expression of two PKC isoforms ? and ? in renal biopsies of patients with diabetic nephropathy, lupus nephritis (LN) (Class 3-4), and mesangioproliferative glomerulonephritis (MPGN) to explore the role of each isoform in different glomerular diseases. PKC ? and ? gene expression was studied by quantitative real-time reverse transcription-PCR in 20 patients with type 2 diabetes and proteinuria (serum creatinine 2.04 ± 0.85 mg/dl, 24-h urinary protein 3.61 ± 1.75 g, eGFR 37.85 ± 17.89 ml/min/1.73 m2), 20 patients with proliferative LN (serum creatinine 1.67 ± 1.50 mg/dl, 24-h urinary protein 4.46 ± 5.01 g, eGFR 69.62 ± 40.93 ml/min/1.73 m2), and 20 patients with MPGN (serum creatinine 3.32 ± 2.79 mg/dl, 24-h urinary protein 4.65 ± 4.11 g, eGFR 32.62 ± 29.56 ml/min/1.73 m2). Normal tissues from the normal pole of four kidneys removed because of renal tumor served as controls. PKC ? gene expression was significantly increased in diabetic kidneys compared to LN and MPGN (316.95 ± 152.94 µg/ml vs. 185.97 ± 32.13 and 195.46 ± 46.45 µg/ml, p < 0.05). PKC ? gene expression was significantly increased in the LN and MPGN groups compared to the diabetic nephropathy group (41.01 ± 14.03 and 39.93 ± 16.41 µg/ml, respectively, vs. 18.20 ± 4.91 µg/ml, p < 0.05). Significant correlation was noted between the PKC ? gene concentrations and proteinuria in diabetic patients. Renal expression of PKC ? and ? genes in control tissues were significantly lower compared to diabetic kidneys, LN, and MPGN groups (32.31 ± 0.36 and 4.67 ± 2.41 µg/ml, respectively, p < 0.001). The study revealed enhanced renal gene expression of both PKC isoforms ? and ? in diabetic kidney tissues, LN, and MPGN, but in different patterns. PKC ? gene expression was significantly increased in diabetic patients with chronic kidney disease. The increased expression of the PKC ? gene in LN and MPGN highlights its role in regulation of the immune system. This may represent potential therapeutic targets for prevention of progressive kidney injury in diabetic and proliferative glomerular diseases. äEvaluation of Renal Gene Expression of Protein Kinase C (PKC) Isoforms(epmc).pdf DeepDyve Pubget Overpricing