General fitness, health and nutrition · Public discussion

Klotho / iron / oxidative stress

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General fitness, health and nutrition
Published
6 November 2005
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8 November 2005
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  1. Biology of Aging: Hormonal Suppression of Aging in Mice

    A defect in Klotho gene expression in mice accelerates the
    degeneration of multiple age-sensitive traits. New work
    demonstrates that overexpression of Klotho in mice extends life
    span. Klotho protein functions as a circulating hormone that
    binds to a cell-surface receptor and represses intracellular
    signals of insulin and insulin-like growth factor-1, an
    evolutionarily conserved mechanism for extending life span.
    Alleviation of aging-like phenotypes in Klotho-deficient mice was
    observed by perturbing insulin and IGF1 signaling, suggesting
    that Klotho-mediated inhibition of insulin and IGF1 signaling
    contributes to its anti-aging properties. Klotho protein may
    function as an anti-aging hormone in mammals.
    Full report at http://scienceweek.com/2005/sw051111-5.htm
    ---------------------------------------------------------------------------------

    Iron chelation and a free radical scavenger suppress angiotensin
    II-induced downregulation of klotho, an anti-aging gene, in rat.

    Saito K, Ishizaka N, Mitani H, Ohno M, Nagai R
    FEBS Lett. 2003 Sep 11; 551(1-3): 58-62

    Administration of angiotensin II to rats decreases renal expression of
    klotho, an aging-related gene, and also causes abnormal iron deposition
    in renal cells. Here we have examined the effects of iron overload and
    iron chelation on renal expression of klotho in untreated rats and rats
    treated with angiotensin II. Administration of iron-dextran caused a
    downregulation of klotho expression, and iron chelation suppressed the
    angiotensin II-induced downregulation of this gene. In addition, a free
    radical scavenger (T-0970), which effectively decreased plasma levels
    of 8-epi-prostaglandin F(2alpha) (8-epi-PGF(2alpha)), suppressed
    angiotensin II-induced downregulation of klotho. Collectively, these
    findings suggest that abnormal iron metabolism and increased oxidative
    stress are involved in the mechanism of angiotensin II-mediated
    modulation of klotho expression.

    Who loves ya.
    Tom

    Jesus Was A Vegetarian!
    http://jesuswasavegetarian.7h.com

    Man Is A Herbivore!
    http://pages.ivillage.com/ironjustice/manisaherbivore

    DEAD PEOPLE WALKING
    http://pages.ivillage.com/ironjustice/deadpeoplewalking

  2. Can't remember if this has been posted here.

    Cardiovasc Res. 2004 Nov 1;64(2):331-6. Related Articles, Links
    Click here to read
    HMG-CoA reductase inhibitors up-regulate anti-aging klotho mRNA via
    RhoA inactivation in IMCD3 cells.

    Narumiya H, Sasaki S, Kuwahara N, Irie H, Kusaba T, Kameyama H,
    Tamagaki K, Hatta T, Takeda K, Matsubara H.

    Department of Hypertension and Nephrology, Kyoto Prefectural
    University School of Medicine, 465 Kajii-cho Kawaramachi Hirokoji, Kyoto
    602-8566, Japan. [email hidden]

    OBJECTIVE: Klotho is thought to play a critical role in the
    development of age-related disorders including arteriosclerosis. Statins
    may exert vascular protective effects, independent of the lowering of
    plasma cholesterol levels. We investigated the impact of statins on mRNA
    expression of the age-suppressor gene, klotho in mIMCD3 cells. METHODS
    AND RESULTS: Klotho mRNA levels were evaluated with real-time RT-PCR.
    Atorvastatin and pitavastatin increased the expression of klotho mRNA in
    a dose-dependent manner. This stimulatory effect was abolished by the
    addition of mevalonate, GGPP and FPP, essential molecules for
    isoprenylation of the small GTPase Rho. As was the case with the statin
    treatment, inhibition of Rho-kinase by Y27632 up-regulated klotho mRNA.
    In contrast to the statin treatment, stimulation with angiotensin II
    down-regulated klotho mRNA expression without obvious morphological
    changes. Furthermore, pretreatment with atorvastatin blunted the
    angiotensin II-induced response and ameliorated the decrease in klotho
    mRNA expression towards basal levels. RhoA activity was further
    evaluated by detection of its translocation. Angiotensin II activated
    RhoA, whereas statins potently inactivated RhoA and blocked RhoA
    activation by angiotensin II. CONCLUSION: Statins inactivate the RhoA
    pathway, resulting in over-expression of klotho mRNA, which may
    contribute to the novel pleiotropic effects of statins towards vascular
    protection.

    PMID: 15485693 [PubMed - indexed for MEDLINE]

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