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Titolo:
Hyperosmolality activates Akt and regulates apoptosis in renal tubular cells
Autore:
Terada, Y; Inoshita, S; Hanada, S; Shimamura, H; Kuwahara, M; Ogawa, W; Kasuga, M; Sasaki, S; Marumo, F;
Indirizzi:
Tokyo Med & Dent Univ, Bunkyo Ku, Tokyo 1138519, Japan Tokyo Med & Dent Univ Tokyo Japan 1138519 unkyo Ku, Tokyo 1138519, Japan Kobe Univ, Sch Med, Dept Internal Med 2, Kobe, Hyogo, Japan Kobe Univ Kobe Hyogo Japan Med, Dept Internal Med 2, Kobe, Hyogo, Japan
Titolo Testata:
KIDNEY INTERNATIONAL
fascicolo: 2, volume: 60, anno: 2001,
pagine: 553 - 567
SICI:
0085-2538(200108)60:2<553:HAAARA>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-B; RAT MESANGIAL CELLS; PHOSPHATIDYLINOSITOL 3-KINASE; IN-VITRO; ORGANIC OSMOLYTES; SURVIVAL; STRESS; DEATH; PHOSPHORYLATION; TRANSCRIPTION;
Keywords:
serine-threonine kinase; cell signaling; phosphatidylinositol 3-kinase; MDCK cells; phosphorylation; dehydration; renal medulla collecting duct; osmotic stress;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Terada, Y Tokyo Med & Dent Univ, Bunkyo Ku, 1-5-45 Yushima, Tokyo 1138519,Japan Tokyo Med & Dent Univ 1-5-45 Yushima Tokyo Japan 1138519 Japan
Citazione:
Y. Terada et al., "Hyperosmolality activates Akt and regulates apoptosis in renal tubular cells", KIDNEY INT, 60(2), 2001, pp. 553-567

Abstract

Background. The novel serine-threonine kinase Akt is a critical enzyme in cell survival. We investigated the roles of the Akt pathway and apoptotic signals in (1) Madin-Darby canine kidney (MDCK) cells in a hyperosmotic condition in vitro and (2) in the inner medulla of dehydrated rat in vivo. Methods. The in vivo experiments were performed in 24- and 48-hour water-restricted rats. Hyperosmolality-stimulated Akt phosphorylation was examinedin MDCK cells, Phosphatidylinositol 3-kinase (PI3-K) inhibitors, the dominant-negative mutant of PI3-K, the dominant-negative mutant of Akt, and the dominant-active form of Akt were used to examine the roles of the PI3-K/Aktpathways in renal tubular cell apoptosis. Results. The amount of phosphorylated Akt protein was increased in the inner medulla of dehydrated rats. Hyperosmolality induced by the addition of NaCl, urea, and raffinose phosphorylated Akt in MDCK cells in an osmolality-dependent manner. PI3-K inhibitors and the dominant-negative mutant of PI3-K inhibited the hyperosmolality-induced phosphorylation of Akt. Raising themedia osmolality from a normal level to 500 or 600 mOsm/kg H2O final osmolality elicited apoptotic changes such as nucleosomal laddering of DNA and an increment of caspase-3 activity and increased activity in the cell death enzyme-linked immunosorbent assay. Dominant-active Akt prevented the mild hyperosmolality-induced apoptosis, while inhibition of the PI3-K/Akt pathways promoted apoptosis. Conclusion. The Akt pathway is activated by hyperosmolality in vitro and in vivo. and activation of Akt prevents the mild hyperosmolality-induced apoptotic changes in MDCK cells. PI3-K/Akt pathways are involved in a hypertonic condition that confers the balance between cell survival and apoptosis.

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Documento generato il 19/09/20 alle ore 18:05:35