NEURO-PROTECTIVE EFFECT OF GROWTH HORMONE (GH) IN CHICKEN CEREBELLAR CELL CULTURES: A POSSIBLE ANTI-APOPTOTIC ROLE OF GH DURING THE HYPOXIA INJURY
-
1
Universidad Nacional Autonoma de Mexico, Institute of Neurobiology, Dept. of Molecular and Cellular Neurobiology, Mexico
-
2
University of California, Irvine, Dept. Neurobiology and Behavior, United States
Recent reports indicate that growth hormone (GH) and its receptor (GHR) are expressed in the Central Nervous System (CNS) of several species, where it may act as a neuroprotective factor in addition to its capacity to stimulate growth and development of the brain. A common insult that can cause severe damage on the CNS is ischemia, which can be induced by hypoxia and low glucose condition (HLG). We studied the possible neuroprotective role of GH in a model of ischemic neuronal injury (HLG) using primary cultures of cerebellar neurons. The viability of cerebellar neurons exposed to HLG decreased to 38.4±7.2% compared to the control (97.8%), and it increased to 66±12.8% after GH (1 nM) treatment. Likewise, the addition of GH (1 nM) decreased the number of apoptotic cells marked by TUNEL (15.3±2.2%) when compared with those exposed only to HLG (68.1±12.1%). GH treatment (1 nM) was also capable to reduce the activity of caspase 3 1.5 times (4.8±0.9 units) in cerebellar neurons exposed to HLG (7.5±1.3 units). Furthermore, addition of GH induced the activation of the PI3K/Akt pathway during the HLG insult, and this activation was blocked by Wortmannin (a PI3K/Akt inhibitor), suggesting that GH exerts its effects through this signaling pathway. Also, the antiapoptotic Bcl-2 protein increased following GH treatment in HLG exposed cells. On the other hand, the addition of 10 nM 15kDa GH variant (which is the most abundant isoform in the chicken cerebellum) also increased cell viability (63.2±11.9%) compared to HLG exposed cultures (28.4±6.2%), and was able to reduce caspase 3 activity by one third (to 5.1±1.2 units). These results indicate that locally expressed GH may act as an autocrine/paracrine survival factor that preserves cellular viability and inhibits apoptotic cell death.
Acknowledgements
Supported by PAPIIT-DGAPA, UNAM 210209; CONACYT F1-60296, 118353 and 51044
Keywords:
antiapoptotic effects of growth hormone,
Caspase 3,
cerebellar growth hormone,
hypoxia and low glucose conditions,
Ischemia,
neuroprotective effects of growth hormone,
PI3K/Akt pathway,
wortmaninn
Conference:
NASCE 2011: The inaugural meeting of the North American Society for Comparative Endocrinology, Ann Arbor, United States, 13 Jul - 16 Jul, 2011.
Presentation Type:
Poster
Topic:
General neuroendocrinology
Citation:
Alba-Betancourt
C,
Luna-Acosta
J,
Ramírez-Martínez
CE,
Courtois
G,
Carranza
ME,
Martínez-Coria
H,
Arámburo
C and
Luna
M
(2011). NEURO-PROTECTIVE EFFECT OF GROWTH HORMONE (GH) IN CHICKEN CEREBELLAR CELL CULTURES: A POSSIBLE ANTI-APOPTOTIC ROLE OF GH DURING THE HYPOXIA INJURY.
Front. Endocrinol.
Conference Abstract:
NASCE 2011: The inaugural meeting of the North American Society for Comparative Endocrinology.
doi: 10.3389/conf.fendo.2011.04.00104
Copyright:
The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers.
They are made available through the Frontiers publishing platform as a service to conference organizers and presenters.
The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated.
Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed.
For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions.
Received:
23 Jul 2011;
Published Online:
09 Aug 2011.
*
Correspondence:
Dr. Maricela Luna, Universidad Nacional Autonoma de Mexico, Institute of Neurobiology, Dept. of Molecular and Cellular Neurobiology, Queretaro, Queretaro, 76230, Mexico, lunam@servidor.unam.mx