Enhanced expression of naofen in kidney of streptozotocin-induced diabetic rats: possible correlation to apoptosis of tubular epithelial cells View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2010-06

AUTHORS

Yuko Sato, Guo-Gang Feng, Lei Huang, Jun-Hua Fan, Chang Li, Jun An, Koji Tsunekawa, Shuji Kurokawa, Yoshihiro Fujiwara, Toru Komatsu, Fumio Kondo, Naohisa Ishikawa

ABSTRACT

BACKGROUND: Hyperglycemia/high glucose may induce apoptosis in diabetic kidney, but the mechanism is not fully understood. Naofen was found as a Shiga toxin (Stx)-2-related protein. Based on renal dysfunction in infection with Stx-producing Escherichia coli and on participation of naofen in apoptosis of human embryonic kidney cells, the present study was undertaken to investigate the mechanism of renal dysfunction in diabetes mellitus with particular reference to naofen. METHODS: In in vivo studies utilizing streptozotocin (STZ)-induced diabetic rats, and also in in vitro cultured rat kidney epithelial (NRK52E) cells, naofen messenger RNA (mRNA) and protein expressions were analyzed. Naofen mRNA location in diabetic kidney was studied by in situ hybridization. Apoptosis was assessed by caspase-3 activity assay. RESULTS: Rat diabetic kidney showed significant increases in caspase-3 activities and naofen mRNA. Naofen was mainly observed at both proximal and distal urinary tubules. Incubation of NRK52E cells in high glucose medium resulted in elevated naofen mRNA expression, whereas neither interleukin-1, interleukin-6, nor tumor necrosis factor-alpha elicited such action. Moreover, treatment of NRK52E cells with naofen small interfering RNA (siRNA) inhibited naofen mRNA expression induced by high glucose and blocked the increase in caspase-3 activity. CONCLUSIONS: These data suggest that naofen expression may be upregulated by hyperglycemia, with possible correlation to apoptosis of tubular epithelial cells and thereby to diabetic nephropathy. More... »

PAGES

205-212

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s10157-010-0276-1

DOI

http://dx.doi.org/10.1007/s10157-010-0276-1

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1008875673

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/20224876


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