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Functional Interrogation of Adult Hypothalamic Neurogenesis with Focal Radiological Inhibition
11:45

Functional Interrogation of Adult Hypothalamic Neurogenesis with Focal Radiological Inhibition

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[Apoptosis regulation in hypothalamic neurosecretory cells of HER2/neu transgenic mice in ontogenesis]

E D Bazhanova, V N Molodtsov, I G Popovich

    Advances in Gerontology = Uspekhi Gerontologii
    |April 4, 2008
    PubMed

    Insights

    HER2/neu overexpression prevents apoptosis in aging neuroendocrine cells, unlike in wild-type mice. This involves suppressed p53 pathways and maintained 17beta-estradiol, promoting cell survival.

    Area of Science:

    • Molecular Biology
    • Neuroendocrinology
    • Oncology

    Context:

    • The human epidermal growth factor receptor 2 (HER2/neu) is implicated in carcinogenesis and promotes cell survival by inhibiting apoptosis.
    • Aging is often associated with increased cellular apoptosis, particularly in neuroendocrine systems.

    Purpose:

    • To investigate the regulation of apoptosis in hypothalamic neurosecretory cells of HER2/neu transgenic mice during aging.
    • To compare apoptosis levels, protein expression (Bax, c-Raf), and functional activity (vasopressin) in aging wild-type and HER2/neu transgenic mice.

    Summary:

    • Apoptosis of neuroendocrine cells increases with age in wild-type mice but not in HER2/neu transgenic mice.
    • HER2/neu transgenic mice exhibit suppressed p53-dependent apoptosis, decreased caspase-8, and dysregulated Bcl-2/Mcl-1 synthesis.
    • Bax concentration decreases, c-Raf-1 expression remains unchanged, and 17beta-estradiol levels are maintained in aged HER2/neu mice, contributing to neurosecretory cell survival.

    Impact:

    • This study reveals a novel mechanism of apoptosis suppression in aging neuroendocrine cells mediated by HER2/neu.
    • Findings suggest that HER2/neu overexpression and sustained 17beta-estradiol contribute to enhanced neurosecretory cell survival in aged transgenic mice.
    • Understanding these pathways could inform therapeutic strategies targeting age-related neuroendocrine dysfunction and cancer.

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