{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,5]],"date-time":"2026-09-05T03:06:36Z","timestamp":1788577596038,"version":"build-2803163510"},"reference-count":44,"publisher":"American Diabetes Association","issue":"2","content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2007,2,1]]},"abstract":"<jats:p>The protein kinase C (PKC)-\u03b2 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-\u03b2\u2013deficient (PKC-\u03b2\u2212\/\u2212) mice. We studied nondiabetic and streptozotocin-induced diabetic PKC-\u03b2\u2212\/\u2212 mice compared with appropriate 129\/SV wild-type mice. After 8 weeks of diabetes, the high-glucose\u2013induced renal and glomerular hypertrophy, as well as the increased expression of extracellular matrix proteins such as collagen and fibronectin, was reduced in PKC-\u03b2\u2212\/\u2212 mice. Furthermore, the high-glucose\u2013induced expression of the profibrotic cytokine transforming growth factor (TGF)-\u03b21 and connective tissue growth factor were significantly diminished in the diabetic PKC-\u03b2\u2212\/\u2212 mice compared with diabetic wild-type mice, suggesting a role of the PKC-\u03b2 isoform in the regulation of renal hypertrophy. Notably, increased urinary albumin-to-creatinine ratio persisted in the diabetic PKC-\u03b2\u2212\/\u2212 mice. The loss of the basement membrane proteoglycan perlecan and the podocyte protein nephrin in the diabetic state was not prevented in the PKC-\u03b2\u2212\/\u2212 mice as previously demonstrated in the nonalbuminuric diabetic PKC-\u03b1\u2212\/\u2212 mice. In summary, the differential effects of PKC-\u03b2 deficiency on diabetes-induced renal hypertrophy and albuminuria suggest that PKC-\u03b2 contributes to high-glucose\u2013induced TGF-\u03b21 expression and renal fibrosis, whereas perlecan, as well as nephrin, expression and albuminuria is regulated by other signaling pathways.<\/jats:p>","DOI":"10.2337\/db06-0891","type":"journal-article","created":{"date-parts":[[2007,1,26]],"date-time":"2007-01-26T20:11:02Z","timestamp":1169842262000},"page":"346-354","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":79,"title":["Deletion of Protein Kinase C-\u03b2 Isoform In Vivo Reduces Renal Hypertrophy but Not Albuminuria in the Streptozotocin-Induced Diabetic Mouse Model"],"prefix":"10.2337","volume":"56","author":[{"given":"Matthias","family":"Meier","sequence":"first","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joon-Keun","family":"Park","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel","family":"Overheu","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Torsten","family":"Kirsch","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carsten","family":"Lindschau","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Faikah","family":"Gueler","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Leitges","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jan","family":"Menne","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hermann","family":"Haller","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1167","reference":[{"key":"2022031208562496400_R1","doi-asserted-by":"crossref","unstructured":"Raptis AE, Viberti G: Pathogenesis of diabetic nephropathy. 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