Tags

Type your tag names separated by a space and hit enter

Estradiol protects PC12 cells against CoCl2-induced apoptosis.
Brain Res Bull. 2008 Aug 15; 76(6):579-85.BR

Abstract

In hypoxic/ischemic conditions, neuronal apoptotic events are occurred, resulting in neuronal diseases. Estradiol is a female sex hormone with steroid structure known to provide neuroprotection through multiple mechanisms in the central nervous system. This study was aimed to investigate the signal transduction pathway leading to the inhibitory effects of estradiol against cobalt chloride (CoCl(2))-mediated hypoxic death in PC12 cells. Estradiol inhibits CoCl(2)-induced cell death with genomic DNA fragmentation and morphologic changes such as cell shrinkage and condensed nuclei. Pre-incubation of estradiol prior to CoCl(2) treatment attenuated CoCl(2)-mediated the reactive oxygen species (ROS) production and limited the activities of the caspase cascades, such as caspase-8, -9 and -3. Furthermore, estradiol downregulated the Bax:Bcl-2 ratio and decreased the release of cytochrome c from the mitochondria into the cytosol in CoCl(2)-treated cells, indicating that estradiol affect on mitochondrial pathway. Estradiol attenuated also CoCl(2)-induced upregulation of Fas-ligand (Fas-L) and truncated of Bid in sequence of death receptor-mediated pathway. In addition, estradiol increased the phosphorylation of Akt in CoCl(2)-treated cells, demonstrating that estradiol has no affect on upstream signaling through the PI3K/Akt in inhibition of CoCl(2)-induced apoptosis in PC12 cells. Taken together, estradiol was found to have a neuroprotective effect against CoCl(2)-induced apoptosis of PC12 cells by the attenuating ROS production and the modulating apoptotic signal pathway through Bcl-2 family, cytochrome c, Fas/Fas-L as well as PI3K/Akt pathway.

Authors+Show Affiliations

Dental Science Research Institute, 2nd Stage of Brain Korea 21 Project for School of Dentistry, Chonnam National University School of Dentistry, Gwangju 500-757, South Korea. jjy@chonnam.ac.krNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18598848

Citation

Jung, Ji Yeon, et al. "Estradiol Protects PC12 Cells Against CoCl2-induced Apoptosis." Brain Research Bulletin, vol. 76, no. 6, 2008, pp. 579-85.
Jung JY, Roh KH, Jeong YJ, et al. Estradiol protects PC12 cells against CoCl2-induced apoptosis. Brain Res Bull. 2008;76(6):579-85.
Jung, J. Y., Roh, K. H., Jeong, Y. J., Kim, S. H., Lee, E. J., Kim, M. S., Oh, W. M., Oh, H. K., & Kim, W. J. (2008). Estradiol protects PC12 cells against CoCl2-induced apoptosis. Brain Research Bulletin, 76(6), 579-85. https://doi.org/10.1016/j.brainresbull.2008.04.006
Jung JY, et al. Estradiol Protects PC12 Cells Against CoCl2-induced Apoptosis. Brain Res Bull. 2008 Aug 15;76(6):579-85. PubMed PMID: 18598848.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Estradiol protects PC12 cells against CoCl2-induced apoptosis. AU - Jung,Ji Yeon, AU - Roh,Kwang Hoon, AU - Jeong,Yeon Jin, AU - Kim,Sun Hun, AU - Lee,Eun Ju, AU - Kim,Min Seok, AU - Oh,Won Mann, AU - Oh,Hee Kyun, AU - Kim,Won Jae, Y1 - 2008/05/16/ PY - 2007/10/17/received PY - 2008/03/12/revised PY - 2008/04/11/accepted PY - 2008/7/5/pubmed PY - 2008/8/20/medline PY - 2008/7/5/entrez SP - 579 EP - 85 JF - Brain research bulletin JO - Brain Res. Bull. VL - 76 IS - 6 N2 - In hypoxic/ischemic conditions, neuronal apoptotic events are occurred, resulting in neuronal diseases. Estradiol is a female sex hormone with steroid structure known to provide neuroprotection through multiple mechanisms in the central nervous system. This study was aimed to investigate the signal transduction pathway leading to the inhibitory effects of estradiol against cobalt chloride (CoCl(2))-mediated hypoxic death in PC12 cells. Estradiol inhibits CoCl(2)-induced cell death with genomic DNA fragmentation and morphologic changes such as cell shrinkage and condensed nuclei. Pre-incubation of estradiol prior to CoCl(2) treatment attenuated CoCl(2)-mediated the reactive oxygen species (ROS) production and limited the activities of the caspase cascades, such as caspase-8, -9 and -3. Furthermore, estradiol downregulated the Bax:Bcl-2 ratio and decreased the release of cytochrome c from the mitochondria into the cytosol in CoCl(2)-treated cells, indicating that estradiol affect on mitochondrial pathway. Estradiol attenuated also CoCl(2)-induced upregulation of Fas-ligand (Fas-L) and truncated of Bid in sequence of death receptor-mediated pathway. In addition, estradiol increased the phosphorylation of Akt in CoCl(2)-treated cells, demonstrating that estradiol has no affect on upstream signaling through the PI3K/Akt in inhibition of CoCl(2)-induced apoptosis in PC12 cells. Taken together, estradiol was found to have a neuroprotective effect against CoCl(2)-induced apoptosis of PC12 cells by the attenuating ROS production and the modulating apoptotic signal pathway through Bcl-2 family, cytochrome c, Fas/Fas-L as well as PI3K/Akt pathway. SN - 1873-2747 UR - https://www.unboundmedicine.com/medline/citation/18598848/Estradiol_protects_PC12_cells_against_CoCl2_induced_apoptosis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0361-9230(08)00167-6 DB - PRIME DP - Unbound Medicine ER -