Abstract
Spinal cord injury (SCI) induces massive cell death, leading to permanent neurological disability. No satisfactory treatment is currently available. Ghrelin, a gastric hormone, is known to stimulate GH release from the hypothalamus and pituitary gland. Here, we report that ghrelin administration improves functional recovery after SCI in part by inhibiting apoptosis of neurons and oligodendrocytes. Ghrelin was not detected in normal, uninjured spinal cords, but spinal cord neurons and oligodendrocytes expressed the ghrelin receptor. Ghrelin significantly inhibited apoptotic cell death of neurons and oligodendrocytes, release of mitochondrial cytochrome c, and activation of caspase-3 after moderate contusion SCI. Ghrelin also significantly increased the level of phosphorylated ERK but decreased the level of phosphorylated p38MAPK. In addition, ghrelin increased the level of ERK-dependent brain-derived neurotrophic factor expression and decreased the level of pronerve growth factor expression. Furthermore, the neuroprotective effects of ghrelin were mediated through the ghrelin receptor. Finally, ghrelin significantly improved functional recovery and reduced the size of the lesion volume and the loss of axons and myelin after injury. These results suggest that ghrelin may represent a potential therapeutic agent after acute SCI in humans.
| Original language | English |
|---|---|
| Pages (from-to) | 3815-3826 |
| Number of pages | 12 |
| Journal | Endocrinology |
| Volume | 151 |
| Issue number | 8 |
| DOIs | |
| Publication status | Published - 2010 Aug 1 |
Fingerprint
All Science Journal Classification (ASJC) codes
- Endocrinology
Cite this
}
Inhibition of apoptotic cell death by ghrelin improves functional recovery after spinal cord injury. / Lee, Jee Y.; Chung, Hyunju; Yoo, Young S.; Oh, Young Jun; Oh, Tae H.; Park, Seungjoon; Yune, Tae Y.
In: Endocrinology, Vol. 151, No. 8, 01.08.2010, p. 3815-3826.Research output: Contribution to journal › Article
TY - JOUR
T1 - Inhibition of apoptotic cell death by ghrelin improves functional recovery after spinal cord injury
AU - Lee, Jee Y.
AU - Chung, Hyunju
AU - Yoo, Young S.
AU - Oh, Young Jun
AU - Oh, Tae H.
AU - Park, Seungjoon
AU - Yune, Tae Y.
PY - 2010/8/1
Y1 - 2010/8/1
N2 - Spinal cord injury (SCI) induces massive cell death, leading to permanent neurological disability. No satisfactory treatment is currently available. Ghrelin, a gastric hormone, is known to stimulate GH release from the hypothalamus and pituitary gland. Here, we report that ghrelin administration improves functional recovery after SCI in part by inhibiting apoptosis of neurons and oligodendrocytes. Ghrelin was not detected in normal, uninjured spinal cords, but spinal cord neurons and oligodendrocytes expressed the ghrelin receptor. Ghrelin significantly inhibited apoptotic cell death of neurons and oligodendrocytes, release of mitochondrial cytochrome c, and activation of caspase-3 after moderate contusion SCI. Ghrelin also significantly increased the level of phosphorylated ERK but decreased the level of phosphorylated p38MAPK. In addition, ghrelin increased the level of ERK-dependent brain-derived neurotrophic factor expression and decreased the level of pronerve growth factor expression. Furthermore, the neuroprotective effects of ghrelin were mediated through the ghrelin receptor. Finally, ghrelin significantly improved functional recovery and reduced the size of the lesion volume and the loss of axons and myelin after injury. These results suggest that ghrelin may represent a potential therapeutic agent after acute SCI in humans.
AB - Spinal cord injury (SCI) induces massive cell death, leading to permanent neurological disability. No satisfactory treatment is currently available. Ghrelin, a gastric hormone, is known to stimulate GH release from the hypothalamus and pituitary gland. Here, we report that ghrelin administration improves functional recovery after SCI in part by inhibiting apoptosis of neurons and oligodendrocytes. Ghrelin was not detected in normal, uninjured spinal cords, but spinal cord neurons and oligodendrocytes expressed the ghrelin receptor. Ghrelin significantly inhibited apoptotic cell death of neurons and oligodendrocytes, release of mitochondrial cytochrome c, and activation of caspase-3 after moderate contusion SCI. Ghrelin also significantly increased the level of phosphorylated ERK but decreased the level of phosphorylated p38MAPK. In addition, ghrelin increased the level of ERK-dependent brain-derived neurotrophic factor expression and decreased the level of pronerve growth factor expression. Furthermore, the neuroprotective effects of ghrelin were mediated through the ghrelin receptor. Finally, ghrelin significantly improved functional recovery and reduced the size of the lesion volume and the loss of axons and myelin after injury. These results suggest that ghrelin may represent a potential therapeutic agent after acute SCI in humans.
UR - http://www.scopus.com/inward/record.url?scp=77954898609&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=77954898609&partnerID=8YFLogxK
U2 - 10.1210/en.2009-1416
DO - 10.1210/en.2009-1416
M3 - Article
VL - 151
SP - 3815
EP - 3826
JO - Endocrinology
JF - Endocrinology
SN - 0013-7227
IS - 8
ER -