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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Tác giả chính: Nguyễn, Thị Huỳnh Nga
Định dạng: Journal article
Ngôn ngữ:English
Được phát hành: 2022
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Truy cập trực tuyến:http://scholar.dlu.edu.vn/handle/123456789/1575
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id oai:scholar.dlu.edu.vn:123456789-1575
record_format dspace
institution Thư viện Trường Đại học Đà Lạt
collection Thư viện số
language English
topic Neural stem cells, Staurosporine, Etoposide Apoptosis BDNF NGF
spellingShingle Neural stem cells, Staurosporine, Etoposide Apoptosis BDNF NGF
Nguyễn, Thị Huỳnh Nga
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
description 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.
format Journal article
author Nguyễn, Thị Huỳnh Nga
author_facet Nguyễn, Thị Huỳnh Nga
author_sort Nguyễn, Thị Huỳnh Nga
title 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
title_short 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
title_full 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
title_fullStr 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
title_full_unstemmed 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
title_sort 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
publishDate 2022
url http://scholar.dlu.edu.vn/handle/123456789/1575
_version_ 1768306090536075264
spelling oai:scholar.dlu.edu.vn:123456789-15752022-11-09T06:40:22Z 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 Nguyễn, Thị Huỳnh Nga Neural stem cells, Staurosporine, Etoposide Apoptosis BDNF NGF 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. 2022-11-09T04:34:46Z 2022-11-09T04:34:46Z 2009 Journal article Bài báo đăng trên tạp chí thuộc ISI, bao gồm book chapter Khoa học y, dược http://scholar.dlu.edu.vn/handle/123456789/1575 10.1007/s11064-008-9848-9 en 1. Kuan C-Y, Roth KA, Flavell RA et al (2000) Mechanisms of programmed cell death in the developing brain. Trends Neurosci 23:291–297. doi:10.1016/S0166-2236(00)01581-2 2. Snyder EY, Deitcher DL, Walsh C et al (1992) Multipotent neural cell lines can engraft and participate in development of mouse cerebellum. Cell 68:33–51. doi:10.1016/0092-8674(92) 90204-P 3. Snyder EY, Yoon C, Flax JD et al (1997) Multipotent neural precursors can differentiate toward replacement of neurons undergoing targeted apoptotic degeneration in adult mouse neocortex. 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