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Nierenfunktion Kinase-defizienter Mäuse

von Dr. Diana Sandulache

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[1.] Dsa/Fragment 036 01 - Diskussion
Zuletzt bearbeitet: 2016-08-06 10:38:07 WiseWoman
Boini 2006, Dsa, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop

Typus
KomplettPlagiat
Bearbeiter
Hindemith
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 36, Zeilen: 1ff (entire page)
Quelle: Boini 2006
Seite(n): 18, 19, Zeilen: 18: 8ff; 19: 1ff
At least part of the stimulatory effect of aldosterone on SGK1 appears to be mediated by activation of the MR, as indicated by findings in primary rabbit collecting duct cells in vitro (Narey-Fejes-Toth et al., (1999) [sic] J Biol Chem) and kidneys in vivo (Bhargava A. et al., (2001) Endocrinology). Consistently, physiologically relevant concentrations of aldosterone are sufficient to significantly induce SGK1 mRNA in the renal cortex and outer medulla (Muller OG. et al., (2003) J Am Soc Nephrol). The physiological importance of aldosterone in SGK induction is also supported by the fact that dietary Na+ restriction, which physiologically increases plasma aldosterone, induces SGK1 mRNA in the renal cortex (Farjah M. et al., (2003) Hypertension). The aldosterone-dependent induction of SGK1 occurs specifically in the ENaC-positive cells of the ASDN, whereas SGK1 expression in other nephron portions such as the thick ascending limb or the proximal tubule is not increased by aldosterone. Likewise, the high level of expression of SGK1 in the renal papilla is not further stimulated by aldosterone, suggesting that SGK1 expression at this site is controlled by factors other than aldosterone. The renal papilla plays an important role for the urinary concentration mechanism, and the cells in the renal papilla can be exposed to a large variation in extracellular osmolarity depending on the requirements for diuresis to antidiuresis. SGK1 expression is strongly modulated by osmotic cell shrinkage and swelling (Waldegger S. et al., (1997) Proc Natl Acad Sci USA; Rozansky DJ. et al., (2002) Am J Renal Physiol), and it is therefore conceivable that SGK1 participates in the functional adaptation of the renal papilla cells to fluctuation of extracellular osmolarity.

Consistent with this notion, recent data suggest that SGK1 mediates the osmotic induction of the type A natriuretic peptide receptor (NPR-A) in rat inner MCD cells (Chen S. et al., (2004) Hypertension). Aldosterone also controls SGK1 expression in the distal colon (Coric CM. et al., (2004) Am J Physiol Gastrointest Liver Physiol; Bhargava A. et al., (2001) Endocrinology). Aldosterone-dependent Na+ reabsorption at this site may help to limit extrarenal Na+ losses during conditions of dietary Na+ restriction. Transepithelial Na+ transport is achieved mainly by epithelial cells that are situated at the tips of colonic crypts and that express high levels of ENaC (Coric CM. et al., (2004) Am J Physiol Gastrointest Liver Physiol) and SGK1 (Waldegger S. et al., (1999) Gastroenterology; Coric CM. et al., (2004) Am J Physiol Gastrointest Liver Physiol). In spite of these data pointing to aldosterone-dependent regulation of ENaC via SGK1, recent Western blot and immunohistochemical studies on rat kidney and colon, which reported no or rather modest aldosterone-dependent induction of SGK1 at the protein level, were interpreted to question the significance of aldosterone-dependent induction of SGK1 for ENaC-mediated Na+ transport regulation (Coric CM. et al., (2004) Am J Physiol Gastrointest Liver Physiol). Support for a functional significance of SGK1 in regulation of transepithelial Na+ transport comes from experiments in X. laevis A6 cells and in mouse M1 CCD cells.

Transfection of A6 or M1 cells with SGK1 leads to an increase in transepithelial Na+ transport, whereas transfection of a dominant-negative “kinase-dead” SGK1 mutant or an antisense SGK1 transcript abolishes dexamethasone- and/or insulin-dependent regulation of transepithelial Na+ transport (Alvarez de Rosa D. et al., (2003) J Physiol; Faletti CJ. et al., (2002) Am J Physiol Cell Physiol). Likewise, the use of interfering RNA to knockdown SGK1 expression in A6 cells results in a significant reduction in SGK1 protein levels and a ~50% reduction in dexamethasone-induced short-circuit currents (Bhargava A. et al., (2001) Endocrinology). Consistent with these in vitro findings, experiments in SGK1 KO (sgk1−/−) mice supported the importance of SGK1 for aldosterone-dependent regulation of renal Na+ transport (Wulff et al., (2002) J Clin Invest).

At least part of the stimulatory effect of aldosterone on SGK1 appears to be mediated by activation of the MR, as indicated by findings in primary rabbit collecting duct cells in vitro (Naray-Fejes-Toth et al., 1999) and kidneys in vivo (Bhargava et al., 2001). Consistently, physiologically relevant concentrations of aldosterone are sufficient to significantly induce SGK1 mRNA in the renal cortex and outer medulla (Muller et al., 2003). The physiological importance of aldosterone in SGK induction is also supported by the fact that dietary Na+ restriction, which physiologically increases plasma aldosterone, induces SGK1 mRNA in the renal cortex (Farjah et al., 2003). The aldosterone-dependent induction of SGK1 occurs specifically in the ENaC-positive cells of the ASDN, whereas SGK1 expression in other nephron portions such as the thick ascending limb or the proximal tubule is not increased by aldosterone. Likewise, the high level of expression of SGK1 in the renal papilla is not further stimulated by aldosterone, suggesting that SGK1 expression at this site is controlled by factors other than aldosterone. The renal papilla plays an important role for the urinary concentration mechanism, and the cells in the renal papilla can be exposed to a large variation in extracellular osmolarity depending on the requirements for diuresis to antidiuresis. SGK1 expression is strongly modulated by osmotic cell shrinkage and swelling (Waldegger et al., 1997; Rozansky et al., 2002), and it is therefore conceivable that SGK1 participates in the functional adaptation of the renal papilla cells to fluctuation of extracellular osmolarity. Consistent with this notion, recent data suggest that SGK1 mediates the osmotic induction of the type A natriuretic peptide receptor (NPR-A) in rat inner MCD cells (Chen et al., 2004). Aldosterone also controls SGK1 expression in the distal colon (Coric et al., 2004; Bhargava et al., 2001). Aldosterone-dependent Na+ reabsorption at this site may help to limit extrarenal Na+ losses during conditions of dietary Na+ restriction. Transepithelial Na+ transport is achieved mainly by epithelial cells that are situated at the tips of colonic crypts and that express high levels of

[page 19]

ENaC (Coric et al., 2004) and Sgk1 (Waldegger et al., 1999; Coric et al., 2004). In spite of these data pointing to aldosterone-dependent regulation of ENaC via SGK1, recent Western blot and immunohistochemical studies on rat kidney and colon, which reported no or rather modest aldosterone-dependent induction of SGK1 at the protein level, were interpreted to question the significance of aldosterone-dependent induction of SGK1 for ENaC-mediated Na+ transport regulation (Coric et al., 2004). Support for a functional significance of SGK1 in regulation of transepithelial Na+ transport comes from experiments in X. laevis A6 cells and in mouse M1 CCD cells. Transfection of A6 or M1 cells with SGK1 leads to an increase in transepithelial Na+ transport, whereas transfection of a dominant-negative “kinase-dead” SGK1 mutant or an antisense SGK1 transcript abolishes dexamethasone- and/or insulin-dependent regulation of transepithelial Na+ transport (Alvarez de Rosa et al., 2003; Faletti et al., 2002). Likewise, the use of interfering RNA to knockdown SGK1 expression in A6 cells results in a significant reduction in SGK1 protein levels and a ~50% reduction in dexamethasone-induced short-circuit currents (Bhargava et al., 2004). Consistent with these in vitro findings, experiments in SGK1 KO (sgk1-/-) mice supported the importance of SGK1 for aldosterone-dependent regulation of renal Na+ transport (Wulff et al., 2002).

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(Hindemith), WiseWoman


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