Neuroprotection by NGF and BDNF against neurotoxin-exerted apoptotic death in neural stem cells are mediated through Trk receptors, activating PI3-kinase and MAPK pathways
Neural stem cells (NSC) undergo apoptotic cell death during development of nervous system and in adult. However, little is known about the biochemical regulation of neuroprotection by neurotrophin in these cells. In this report, we demonstrate that Staurosporine (STS) and Etoposide (ETS) induce...
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| Định dạng: | Journal article |
| Ngôn ngữ: | English |
| Được phát hành: |
2022
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| Những chủ đề: | |
| Truy cập trực tuyến: | http://scholar.dlu.edu.vn/handle/123456789/1575 |
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| Thư viện lưu trữ: | Thư viện Trường Đại học Đà Lạt |
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| Tóm tắt: | Neural stem cells (NSC) undergo apoptotic cell
death during development of nervous system and in adult.
However, little is known about the biochemical regulation
of neuroprotection by neurotrophin in these cells. In this
report, we demonstrate that Staurosporine (STS) and Etoposide
(ETS) induced apoptotic cell death of NSC by a
mechanism requiring Caspase 3 activation, poly (ADPribose)
polymerase and Lamin A/C cleavage. Although
C17.2 cells revealed higher mRNA level of p75 neurotrophin
receptor (p75NTR) compared with TrkA or TrkB
receptor, neuroprotective effect of both nerve growth factor
(NGF) and brain-derived growth factor (BDNF) mediated
through the activation of tropomyosin receptor kinase (Trk)
receptors. Moreover, both NGF and BDNF induced the
activation of the phosphatidylinositide 3 kinase (PI3K)/Akt
and the mitogen-activated protein kinase (MAPK) pathway.
Inhibition of Trk receptor by K252a reduced PARP
cleavage as well as cell viability, whereas inhibition of
p75NTR did not affect the effect of neurotrophin on neurotoxic
insults. Thus our studies indicate that the protective
effect of NGF and BDNF in NSC against apoptotic stimuli
is mediated by the PI3K/Akt and MAPK signaling pathway
via Trk receptors. |
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