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rdf:type |
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lifeskim:mentions |
umls-concept:C0001925,
umls-concept:C0020564,
umls-concept:C0022646,
umls-concept:C0025914,
umls-concept:C0026336,
umls-concept:C0026809,
umls-concept:C0257291,
umls-concept:C0392756,
umls-concept:C0597298,
umls-concept:C1442161,
umls-concept:C1515655
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pubmed:issue |
2
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pubmed:dateCreated |
2007-1-29
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pubmed:abstractText |
The protein kinase C (PKC)-beta isoform has been implicated to play a pivotal role in the development of diabetic kidney disease. We tested this hypothesis by inducing diabetic nephropathy in PKC-beta-deficient (PKC-beta(-/-)) mice. We studied nondiabetic and streptozotocin-induced diabetic PKC-beta(-/-) mice compared with appropriate 129/SV wild-type mice. After 8 weeks of diabetes, the high-glucose-induced renal and glomerular hypertrophy, as well as the increased expression of extracellular matrix proteins such as collagen and fibronectin, was reduced in PKC-beta(-/-) mice. Furthermore, the high-glucose-induced expression of the profibrotic cytokine transforming growth factor (TGF)-beta1 and connective tissue growth factor were significantly diminished in the diabetic PKC-beta(-/-) mice compared with diabetic wild-type mice, suggesting a role of the PKC-beta isoform in the regulation of renal hypertrophy. Notably, increased urinary albumin-to-creatinine ratio persisted in the diabetic PKC-beta(-/-) mice. The loss of the basement membrane proteoglycan perlecan and the podocyte protein nephrin in the diabetic state was not prevented in the PKC-beta(-/-) mice as previously demonstrated in the nonalbuminuric diabetic PKC-alpha(-/-) mice. In summary, the differential effects of PKC-beta deficiency on diabetes-induced renal hypertrophy and albuminuria suggest that PKC-beta contributes to high-glucose-induced TGF-beta1 expression and renal fibrosis, whereas perlecan, as well as nephrin, expression and albuminuria is regulated by other signaling pathways.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Collagen Type IV,
http://linkedlifedata.com/resource/pubmed/chemical/Creatinine,
http://linkedlifedata.com/resource/pubmed/chemical/Fibronectins,
http://linkedlifedata.com/resource/pubmed/chemical/Heparan Sulfate Proteoglycans,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Isoforms,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/RNA,
http://linkedlifedata.com/resource/pubmed/chemical/Streptozocin,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta1,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factors,
http://linkedlifedata.com/resource/pubmed/chemical/nephrin,
http://linkedlifedata.com/resource/pubmed/chemical/perlecan
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0012-1797
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
56
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
346-54
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:17259378-Albuminuria,
pubmed-meshheading:17259378-Animals,
pubmed-meshheading:17259378-Chromosome Deletion,
pubmed-meshheading:17259378-Collagen Type IV,
pubmed-meshheading:17259378-Creatinine,
pubmed-meshheading:17259378-Diabetes Mellitus, Experimental,
pubmed-meshheading:17259378-Diabetic Nephropathies,
pubmed-meshheading:17259378-Fibronectins,
pubmed-meshheading:17259378-Fibrosis,
pubmed-meshheading:17259378-Heparan Sulfate Proteoglycans,
pubmed-meshheading:17259378-Hypertrophy,
pubmed-meshheading:17259378-Kidney,
pubmed-meshheading:17259378-Membrane Proteins,
pubmed-meshheading:17259378-Mice,
pubmed-meshheading:17259378-Mice, Knockout,
pubmed-meshheading:17259378-Organ Size,
pubmed-meshheading:17259378-Protein Isoforms,
pubmed-meshheading:17259378-Protein Kinase C,
pubmed-meshheading:17259378-RNA,
pubmed-meshheading:17259378-Streptozocin,
pubmed-meshheading:17259378-Transforming Growth Factor beta1,
pubmed-meshheading:17259378-Vascular Endothelial Growth Factors
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pubmed:year |
2007
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pubmed:articleTitle |
Deletion of protein kinase C-beta isoform in vivo reduces renal hypertrophy but not albuminuria in the streptozotocin-induced diabetic mouse model.
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pubmed:affiliation |
Department of Nephrology, Hannover Medical School, Carl-Neuberg Strasse 1, 30625 Hannover, Germany. meier.matthias@mh-hannover.de
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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