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Netrin-1 induces angiogenesis via a DCC-dependent ERK1/2-eNOS feed-forward mechanism
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| Zeitschriftentitel: | Proceedings of the National Academy of Sciences |
|---|---|
| Personen und Körperschaften: | , |
| In: | Proceedings of the National Academy of Sciences, 103, 2006, 17, S. 6530-6535 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Proceedings of the National Academy of Sciences
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| Schlagwörter: |
| author_facet |
Nguyen, Andrew Cai, Hua Nguyen, Andrew Cai, Hua |
|---|---|
| author |
Nguyen, Andrew Cai, Hua |
| spellingShingle |
Nguyen, Andrew Cai, Hua Proceedings of the National Academy of Sciences Netrin-1 induces angiogenesis via a DCC-dependent ERK1/2-eNOS feed-forward mechanism Multidisciplinary |
| author_sort |
nguyen, andrew |
| spelling |
Nguyen, Andrew Cai, Hua 0027-8424 1091-6490 Proceedings of the National Academy of Sciences Multidisciplinary http://dx.doi.org/10.1073/pnas.0511011103 <jats:p> Netrin-1 is critical for axonal pathfinding which shares similarities with formation of vascular network. Here we report that netrin-1 induction of angiogenesis is mediated by an increase in endothelial nitric oxide (NO <jats:sup>•</jats:sup> ) production, which occurs via a DCC-dependent, ERK1/2-eNOS feed-forward mechanism. Exposure of mature aortic endothelial cells to netrin-1 resulted in a potent, dose-dependent increase in NO <jats:sup>•</jats:sup> production, detected by electron spin resonance. Scavenging NO <jats:sup>•</jats:sup> with 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO) abolished netrin-1 stimulated angiogenesis. Netrin-1-stimulated NO <jats:sup>•</jats:sup> production or angiogenesis was inhibited by DCC antibody, DCC small interfering RNA (siRNA), specific inhibitors (PD98059, U0126), or siRNAs for MEK1/2. PTIO attenuated ERK1/2 phosphorylation, indicating a feed-forward mechanism. Netrin-1 induced a time-dependent phosphorylation of eNOS <jats:sub>s1179, s116</jats:sub> and a rapid dephosphorylation of eNOS <jats:sub>t497</jats:sub> . Only eNOS <jats:sub>s1179</jats:sub> was sensitive to U0126 or PTIO. These data characterized a mechanism whereby netrin-1 promotes angiogenesis, which may broadly relate to cardiovascular, neuronal and cancer physiology. </jats:p> Netrin-1 induces angiogenesis via a DCC-dependent ERK1/2-eNOS feed-forward mechanism Proceedings of the National Academy of Sciences |
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Proceedings of the National Academy of Sciences, 2006 |
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Proceedings of the National Academy of Sciences, 2006 |
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| title |
Netrin-1 induces angiogenesis via a DCC-dependent ERK1/2-eNOS feed-forward mechanism |
| title_unstemmed |
Netrin-1 induces angiogenesis via a DCC-dependent ERK1/2-eNOS feed-forward mechanism |
| title_full |
Netrin-1 induces angiogenesis via a DCC-dependent ERK1/2-eNOS feed-forward mechanism |
| title_fullStr |
Netrin-1 induces angiogenesis via a DCC-dependent ERK1/2-eNOS feed-forward mechanism |
| title_full_unstemmed |
Netrin-1 induces angiogenesis via a DCC-dependent ERK1/2-eNOS feed-forward mechanism |
| title_short |
Netrin-1 induces angiogenesis via a DCC-dependent ERK1/2-eNOS feed-forward mechanism |
| title_sort |
netrin-1 induces angiogenesis via a dcc-dependent erk1/2-enos feed-forward mechanism |
| topic |
Multidisciplinary |
| url |
http://dx.doi.org/10.1073/pnas.0511011103 |
| publishDate |
2006 |
| physical |
6530-6535 |
| description |
<jats:p>
Netrin-1 is critical for axonal pathfinding which shares similarities with formation of vascular network. Here we report that netrin-1 induction of angiogenesis is mediated by an increase in endothelial nitric oxide (NO
<jats:sup>•</jats:sup>
) production, which occurs via a DCC-dependent, ERK1/2-eNOS feed-forward mechanism. Exposure of mature aortic endothelial cells to netrin-1 resulted in a potent, dose-dependent increase in NO
<jats:sup>•</jats:sup>
production, detected by electron spin resonance. Scavenging NO
<jats:sup>•</jats:sup>
with 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO) abolished netrin-1 stimulated angiogenesis. Netrin-1-stimulated NO
<jats:sup>•</jats:sup>
production or angiogenesis was inhibited by DCC antibody, DCC small interfering RNA (siRNA), specific inhibitors (PD98059, U0126), or siRNAs for MEK1/2. PTIO attenuated ERK1/2 phosphorylation, indicating a feed-forward mechanism. Netrin-1 induced a time-dependent phosphorylation of eNOS
<jats:sub>s1179, s116</jats:sub>
and a rapid dephosphorylation of eNOS
<jats:sub>t497</jats:sub>
. Only eNOS
<jats:sub>s1179</jats:sub>
was sensitive to U0126 or PTIO. These data characterized a mechanism whereby netrin-1 promotes angiogenesis, which may broadly relate to cardiovascular, neuronal and cancer physiology.
</jats:p> |
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| author | Nguyen, Andrew, Cai, Hua |
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| author_sort | nguyen, andrew |
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| container_title | Proceedings of the National Academy of Sciences |
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| description | <jats:p> Netrin-1 is critical for axonal pathfinding which shares similarities with formation of vascular network. Here we report that netrin-1 induction of angiogenesis is mediated by an increase in endothelial nitric oxide (NO <jats:sup>•</jats:sup> ) production, which occurs via a DCC-dependent, ERK1/2-eNOS feed-forward mechanism. Exposure of mature aortic endothelial cells to netrin-1 resulted in a potent, dose-dependent increase in NO <jats:sup>•</jats:sup> production, detected by electron spin resonance. Scavenging NO <jats:sup>•</jats:sup> with 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO) abolished netrin-1 stimulated angiogenesis. Netrin-1-stimulated NO <jats:sup>•</jats:sup> production or angiogenesis was inhibited by DCC antibody, DCC small interfering RNA (siRNA), specific inhibitors (PD98059, U0126), or siRNAs for MEK1/2. PTIO attenuated ERK1/2 phosphorylation, indicating a feed-forward mechanism. Netrin-1 induced a time-dependent phosphorylation of eNOS <jats:sub>s1179, s116</jats:sub> and a rapid dephosphorylation of eNOS <jats:sub>t497</jats:sub> . Only eNOS <jats:sub>s1179</jats:sub> was sensitive to U0126 or PTIO. These data characterized a mechanism whereby netrin-1 promotes angiogenesis, which may broadly relate to cardiovascular, neuronal and cancer physiology. </jats:p> |
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| imprint_str_mv | Proceedings of the National Academy of Sciences, 2006 |
| institution | DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14 |
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| spelling | Nguyen, Andrew Cai, Hua 0027-8424 1091-6490 Proceedings of the National Academy of Sciences Multidisciplinary http://dx.doi.org/10.1073/pnas.0511011103 <jats:p> Netrin-1 is critical for axonal pathfinding which shares similarities with formation of vascular network. Here we report that netrin-1 induction of angiogenesis is mediated by an increase in endothelial nitric oxide (NO <jats:sup>•</jats:sup> ) production, which occurs via a DCC-dependent, ERK1/2-eNOS feed-forward mechanism. Exposure of mature aortic endothelial cells to netrin-1 resulted in a potent, dose-dependent increase in NO <jats:sup>•</jats:sup> production, detected by electron spin resonance. Scavenging NO <jats:sup>•</jats:sup> with 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO) abolished netrin-1 stimulated angiogenesis. Netrin-1-stimulated NO <jats:sup>•</jats:sup> production or angiogenesis was inhibited by DCC antibody, DCC small interfering RNA (siRNA), specific inhibitors (PD98059, U0126), or siRNAs for MEK1/2. PTIO attenuated ERK1/2 phosphorylation, indicating a feed-forward mechanism. Netrin-1 induced a time-dependent phosphorylation of eNOS <jats:sub>s1179, s116</jats:sub> and a rapid dephosphorylation of eNOS <jats:sub>t497</jats:sub> . Only eNOS <jats:sub>s1179</jats:sub> was sensitive to U0126 or PTIO. These data characterized a mechanism whereby netrin-1 promotes angiogenesis, which may broadly relate to cardiovascular, neuronal and cancer physiology. </jats:p> Netrin-1 induces angiogenesis via a DCC-dependent ERK1/2-eNOS feed-forward mechanism Proceedings of the National Academy of Sciences |
| spellingShingle | Nguyen, Andrew, Cai, Hua, Proceedings of the National Academy of Sciences, Netrin-1 induces angiogenesis via a DCC-dependent ERK1/2-eNOS feed-forward mechanism, Multidisciplinary |
| title | Netrin-1 induces angiogenesis via a DCC-dependent ERK1/2-eNOS feed-forward mechanism |
| title_full | Netrin-1 induces angiogenesis via a DCC-dependent ERK1/2-eNOS feed-forward mechanism |
| title_fullStr | Netrin-1 induces angiogenesis via a DCC-dependent ERK1/2-eNOS feed-forward mechanism |
| title_full_unstemmed | Netrin-1 induces angiogenesis via a DCC-dependent ERK1/2-eNOS feed-forward mechanism |
| title_short | Netrin-1 induces angiogenesis via a DCC-dependent ERK1/2-eNOS feed-forward mechanism |
| title_sort | netrin-1 induces angiogenesis via a dcc-dependent erk1/2-enos feed-forward mechanism |
| title_unstemmed | Netrin-1 induces angiogenesis via a DCC-dependent ERK1/2-eNOS feed-forward mechanism |
| topic | Multidisciplinary |
| url | http://dx.doi.org/10.1073/pnas.0511011103 |