An AD-Related Neuroprotector Rescues Transformed Rat Retinal Ganglion Cells from CoCl2-Induced Apoptosis

Department of Ophthalmology, Shengjing Hospital, China Medical University, Sanhao street 36, Heping district, Shenyang 110004, Liaoning Province, China.
Journal of Molecular Neuroscience (Impact Factor: 2.34). 01/2012; 47(1):144-9. DOI: 10.1007/s12031-011-9701-5
Source: PubMed


Some ocular diseases characterized by apoptotic death of retinal ganglion cells (RGCs) and Alzheimer's disease (AD) are chronic neurodegenerative disorders and have similarities in neuropathology. Humanin (HN) is known for its ability to suppress neuronal death induced by AD-related insults. In present study, we investigated the neuroprotective effects of HN on hypoxia-induced toxicity in RGC-5 cells. Hypoxia mimetic compound cobalt chloride (CoCl₂) could increase the cell viability loss and apoptosis, whereas HN can significantly attenuate these effects. This finding may provide new therapeutics for the retinal neurodegenerative diseases targeting neuroprotection.

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    • "The effects of HIF-1α on the expressions of many downstream genes, especially those involved in cell-cycle control and cell proliferation and death, are well established [15,16]. Moreover, HIF-1α stabilizers, such as cobalt chloride (CoCl2), are able to mimic hypoxia and are used in RGC programmed cell death models [17-20]. They are also able to induce the expression of β-amyloid precursor protein (APP) in RGCs as well as hypoxia [21], and they specifically upregulate Hsp27 after retinal ischemic preconditioning and prevent retinal ischemic damage both in vitro (RGC-5 cell line) and in vivo (rat retina) through HIF-1α activation [22]. "
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