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Role of mammalian target of rapamycin signaling in compensatory renal hypertrophy.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Chen, Jian-Kang Chen, Jianchun Neilson, Eric G. Harris, Raymond C. |
| Copyright Year | 2005 |
| Abstract | Loss of functioning nephrons stimulates the growth of residual kidney tissue to augment work capacity and maintain normal renal function. This growth largely occurs by hypertrophy rather than from hyperplasia of the remaining nephrons. The signaling mechanisms that increase RNA and protein synthesis during compensatory renal hypertrophy are unknown. This study found that the remaining kidney hypertrophied 42% by 16 d after unilateral nephrectomy (UNX) in DBA/2 mice. Immunoblotting analysis revealed increased phosphorylation of the 40S ribosomal protein S6 (rpS6) and the eukaryotic translation initiation factor (eIF) 4E-binding protein 1 (4E-BP1), the two downstream effectors of the mammalian target of rapamycin (mTOR). The highly specific mTOR inhibitor rapamycin blocked UNX-increased phosphorylation of both rpS6 and 4E-BP1. UNX increased the content of not only 40S and 60S ribosomal subunits but also 80S monosomes and polysomes in the remaining kidney. Administration of rapamycin decreased UNX-induced polysome formation and shifted the polysome profile in the direction of monosomes and ribosomal subunits. Pretreatment of the mice with rapamycin inhibited UNX-induced hypertrophy. These studies demonstrate that activation of the mTOR signaling pathway in the remaining kidney after UNX plays an essential role in modulating RNA and protein synthesis during development of compensatory renal hypertrophy. |
| Starting Page | 256 |
| Ending Page | 256 |
| Page Count | 1 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://jasn.asnjournals.org/content/16/5/1384.full.pdf |
| PubMed reference number | 15788477v1 |
| Volume Number | 16 |
| Issue Number | 5 |
| Journal | Journal of the American Society of Nephrology : JASN |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | F Factor FRAP1 protein, human Kidney Diseases Mammals Mice, Inbred DBA Nephrectomy Nephrons Peptide Initiation Factors Polyribosomes Protein Biosynthesis Renal Tissue Ribosomal Proteins Ribosome Subunits Signal Transduction Sirolimus Transcription Initiation Translation Initiation mTOR Inhibitor renal hypertrophy |
| Content Type | Text |
| Resource Type | Article |
