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Re: IGF-1 Haarwachstum [Beitrag #86708 ist eine Antwort auf Beitrag #86670] :: Tue, 07 August 2007 22:46  
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doc_sung
Beiträge: 405 Registriert: April 2006
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Geile Sache, ich nehm dich beim Wort tino 
@Foxi
Kannst dir ja so lange par Eier und 2 Liter Sojamilch reinpfeiffen, gibt jedenfalls Tinte aufn Füller 
okt. 06 bis feb. 09 ca. 1mg Fin.
nach Absetzen gesteigertes Wohlbefinden + Vitalität, Körperbehharung fast verdoppelt
ab jan. 07 NAC, EASs, B-Vit, Melatonin
ab nov. 09 wieder 0,2 mg Fin. in Ethanol gelöst
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an tino, zu IGF-1-effekten [Beitrag #86748 ist eine Antwort auf Beitrag #86661] :: Wed, 08 August 2007 13:04
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kkoo
Beiträge: 4429 Registriert: November 2005
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IGF-1 als K+channel opener – vielleicht ein Weg, wie IGF-1 Proliferation fördert? Und könnte erklären, wie IGF-1-Doping zu Hypokalämie führen kann: Durch innerzelluläre Konzentrationsveränderung von Ca+ und K+?
IGF-1 activates hEAG K(+) channels through an Akt-dependent signaling pathway in breast cancer cells: Role in cell proliferation.
Borowiec AS, Hague F, Harir N, Guenin S, Guerineau F, Gouilleux F, Roudbaraki M, Lassoued K, Ouadid-Ahidouch H.
J Cell Physiol. 2007 Sep;212(3):690-701.
Insulin-like growth factor-I protects granule neurons from apoptosis and improves ataxia in weaver mice.
Zhong J, Deng J, Phan J, Dlouhy S, Wu H, Yao W, Ye P, D'Ercole AJ, Lee WH.
Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.
Dual effect of insulin-like growth factor on the apical 70-pS K channel in the thick ascending limb of rat kidney.
Wei Y, Chen YJ, Li D, Gu R, Wang WH.
Department of Pharmacology, New York Medical College, Valhalla, NY 10595, USA.
(gibt noch mehr Studien, und auch welche, die zeigen dass IGF-1 K+channels upreguliert – was ja erwartbar ist…)
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Außerdem:
Insulin-like growth factors 1 and 2 induce lymphangiogenesis in vivo.
Björndahl M, Cao R, Nissen LJ, Clasper S, Johnson LA, Xue Y, Zhou Z, Jackson D, Hansen AJ, Cao Y.
Laboratory of Angiogenesis Research, Microbiology and Tumor Biology Center, Karolinska Institute, S-171 77 Stockholm, Sweden.
Insulin-like growth factor I is required for vessel remodeling in the adult brain.
Lopez-Lopez C, LeRoith D, Torres-Aleman I.
Laboratory of Neuroendocrinology, Cajal Institute, Consejo Superior de Investigaciones Cientifícas, 28002 Madrid, Spain.
(gibt auch da noch mehr Studien)
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Interessant auch das Folgene, finde ich. Das könnte zeigen, dass TGF-beta K+channels exprimieren kann, was ein möglicher Weg wäre, wie K+channel opener den Zelltod verhindern?:
Developmental regulation of neuronal K(Ca) channels by TGFbeta1: an essential role for PI3 kinase signaling and membrane insertion.
Lhuillier L, Dryer SE., Department of Biology and Biochemistry, University of Houston, Texas 77204-5513, USA.
TGFbeta1 is a target-derived factor responsible for the developmental expression of large-conductance Ca(2+)-activated K(+) (K(Ca)) channels in ciliary neurons of the chick ciliary ganglion. The acute effects of TGFbeta1 on K(Ca) channels are mediated by posttranslational events and require activation of the MAP kinase Erk. Here we show that TGFbeta1 evokes robust phosphorylation of Akt/PKB, a protein kinase dependent on the products of phosphatidylinositol 3-OH kinase (PI3K). TGFbeta1-evoked stimulation of K(Ca) channels is blocked by the PI3K inhibitors wortmannin and LY294002. These drugs also inhibit TGFbeta1 effects on Akt/PKB phosphorylation but have no effect on TGFbeta1-evoked Erk activation. Application of the MEK1 inhibitor PD98059 blocked TGFbeta1 effects on Erk but had no effect on Akt/PKB phosphorylation. These results indicate that PI3K and Erk represent parallel signaling cascades activated by TGFbeta1 in ciliary neurons. The effects of TGFbeta1 on functional expression of K(Ca) are blocked by the microtubule inhibitors colchicine and nocodazole, by botulinum toxins A and E, and by brefeldin-A, an agent that disrupts the Golgi apparatus. These data indicate that translocation of a membrane protein, possibly Slowpoke (SLO), is required for the acute posttranslational effects of TGFbeta1 on K(Ca) channels. Confocal immunofluorescence studies with three different SLO antisera showed robust expression of SLO in multiple intracellular compartments of embryonic day 9-13 ciliary neurons, including the cell nucleus. These data suggest that TGFbeta1 evokes insertion of SLO channels into the plasma membrane as a result of signaling cascades that entail activation of Erk and PI3K.
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Re: an tino, zu IGF-1-effekten [Beitrag #86750 ist eine Antwort auf Beitrag #86748] :: Wed, 08 August 2007 13:12
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tino
Beiträge: 2762 Registriert: November 2005 Ort: Europa
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Der Effekt von IGF-1 ist sehr sehr multifaktoriell,...K-Channels sind sicher nur ein Bruchteil der Wirkungsweise.Es macht so viel,...es wirkt anabol,antiapoptotisch,endothelschuetzend,TGF-beta hemmend....und und und.
Das TGF-beta einen Nutzen ueber K-Channel opening haben koennte....kann naber nicht bei Haarerkrankungen relevant sein,da TGF-beta hier der groesste Feind ist.Na ja,...Vieles wirkt nicht auf alle Zelltypen gleich.
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Re: an tino, zu IGF-1-effekten [Beitrag #86753 ist eine Antwort auf Beitrag #86750] :: Wed, 08 August 2007 13:40
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kkoo
Beiträge: 4429 Registriert: November 2005
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| tino schrieb am Mit, 08 August 2007 13:12 |
Der Effekt von IGF-1 ist sehr sehr multifaktoriell,...K-Channels sind sicher nur ein Bruchteil der Wirkungsweise.Es macht so viel,...es wirkt anabol,antiapoptotisch,endothelschuetzend,TGF-beta hemmend....und und und.
Das TGF-beta einen Nutzen ueber K-Channel opening haben koennte....kann naber nicht bei Haarerkrankungen relevant sein,da TGF-beta hier der groesste Feind ist.Na ja,...Vieles wirkt nicht auf alle Zelltypen gleich.
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ja, multifaktoriell, aber es kann ja nicht endlos viele pathways geben. z.b. sind antiapoptotisch& endothelschuetzend & TGF-beta hemmend doch das gleiche; es fragt sich nur, an welcher stelle diese effekte ausgelöst werden. ich kann mir vorstellen, dass genau die k-channels eine solche stelle sind (naja, oder sie sind eben auch nur ein nebeneffekt - was ja auch z.b. für minox gilt: wirkt minox, weil es VEGF exprimiert, oder weil es die k+channels öffnet, oder wird nicht etwa VEGF nur dadurch erhöht, WEIL die k+chanels geöffnet werden???)
nein tgf-beta hat, wenn man der studie folgt, keinen "nutzen", sondern schadet, weil es k-channel exprimiert!
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Re: an tino, zu IGF-1-effekten [Beitrag #86755 ist eine Antwort auf Beitrag #86753] :: Wed, 08 August 2007 14:08
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kkoo
Beiträge: 4429 Registriert: November 2005
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was z.b. auch interessant ist: dass spironolcatone antiangiogenetisch wirkt und hyperkaliämie auslöst.... erhöhte k+konzentr. könnte ja channel-blockade bedeuten, was dann genau einen antiangiogenetischen effekt hätte ?
J Hypertens. 2006 Nov;24(11):2207-13.
Antiangiogenic effects of spironolactone and other potassium-sparing diuretics in human umbilical vein endothelial cells and in fibrin gel chambers implanted in rats.
Miternique-Grosse A, Griffon C, Siegel L, Neuville A, Weltin D, Stephan D.
Laboratoire de Recherche sur l'Angiogenèse, Université Louis Pasteur, Faculté de Médecine, Strasbourg F-67085, France.
OBJECTIVE: Potassium-sparing diuretics have different effects on angiogenesis that may mediate some abilities to treat cardiovascular diseases. The aim of the current study was to compare the effects of spironolactone and an active metabolite, canrenone, or a derivative, eplerenone, and amiloride, a diuretic without affecting mineralocorticoid activity, on the proliferation of human umbilical vein endothelial cells (HUVEC) and on angiogenesis in fibrin gel chambers implanted in rats. MATERIALS AND METHODS: We measured the effects of spironolactone, canrenone, eplerenone, and amiloride on the proliferation of HUVEC in the presence or absence of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). We also examined the effects of these compounds on migration and capillary tube formation by HUVEC. Finally, the effects of the compounds on neovessel formation in vivo were investigated by implanting Wistar rats for 14 days with perforated Plexiglas chambers containing rat fibrin. RESULTS: Spironolactone and amiloride inhibited the proliferation of HUVEC, but canrenone and eplerenone had no effect. The inhibitory effect of spironolactone was not prevented by VEGF or bFGF. Aldosterone had no effect on spironolactone-induced inhibition of HUVEC proliferation. Spironolactone induced a dose-dependent reduction of both cell chemotaxis and capillary tube formation. In fibrin gel chambers, spironolactone and amiloride significantly reduced the numbers of both peripheral and central neovessels. Canrenone and eplerenone, in contrast, had no antiangiogenic effect. CONCLUSION: Spironolactone and amiloride significantly inhibited angiogenesis in vitro and in the fibrin gel chamber in vivo. Spironolactone antiangiogenic effects are unrelated to antimineralocorticoid activity.
Br J Pharmacol. 2005 Sep;146(1):146-61.
Spironolactone and its main metabolite canrenoic acid block hKv1.5, Kv4.3 and Kv7.1 + minK channels.
Gómez R, Núñez L, Caballero R, Vaquero M, Tamargo J, Delpón E.
Department of Pharmacology, School of Medicine, Universidad Complutense, Madrid, Spain.
Both spironolactone (SP) and its main metabolite, canrenoic acid (CA), prolong cardiac action potential duration and decrease the Kv11.1 (HERG) current. We examined the effects of SP and CA on cardiac hKv1.5, Kv4.3 and Kv7.1+minK channels that generate the human I(Kur), I(to1) and I(Ks), which contribute to the control of human cardiac action potential duration.hKv1.5 currents were recorded in stably transfected mouse fibroblasts and Kv4.3 and Kv7.1 + minK in transiently transfected Chinese hamster ovary cells using the whole-cell patch clamp. SP (1 microM) and CA (1 nM) inhibited hKv1.5 currents by 23.2 +/- 3.2 and 18.9 +/- 2.7%, respectively, shifted the midpoint of the activation curve to more negative potentials and delayed the time course of tail deactivation.SP (1 microM) and CA (1 nM) inhibited the total charge crossing the membrane through Kv4.3 channels at +50 mV by 27.1 +/- 6.4 and 27.4 +/- 5.7%, respectively, and accelerated the time course of current decay. CA, but not SP, shifted the inactivation curve to more hyperpolarised potentials (V(h)-37.0 +/- 1.8 vs -40.8 +/- 1.6 mV, n = 10, P < 0.05).SP (10 microM) and CA (1 nM) also inhibited Kv7.1 + minK currents by 38.6 +/- 2.3 and 22.1 +/- 1.4%, respectively, without modifying the voltage dependence of channel activation. SP, but not CA, slowed the time course of tail current decay.CA (1 nM) inhibited the I(Kur) (29.2 +/- 5.5%) and the I(to1) (16.1 +/- 3.9%) recorded in mouse ventricular myocytes and the I(K) (21.8 +/- 6.9%) recorded in guinea-pig ventricular myocytes.A mathematical model of human atrial action potentials demonstrated that K(+) blocking effects of CA resulted in a lengthening of action potential duration, both in normal and atrial fibrillation simulated conditions. The results demonstrated that both SP and CA directly block hKv1.5, Kv4.3 and Kv7.1 + minK channels, CA being more potent for these effects. Since peak free plasma concentrations of CA ranged between 3 and 16 nM, these results indicated that blockade of these human cardiac K(+) channels can be observed after administration of therapeutic doses of SP.Blockade of these cardiac K(+) currents, together with the antagonism of the aldosterone proarrhythmic effects produced by SP, might be highly desirable for the treatment of supraventricular arrhythmias.
[Aktualisiert am: Wed, 08 August 2007 14:20]
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