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15(S)-hydroxyeicosatetraenoic acid–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2 expression
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| Zeitschriftentitel: | Blood |
|---|---|
| Personen und Körperschaften: | , , , , , , , , |
| In: | Blood, 115, 2010, 10, S. 2105-2116 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Society of Hematology
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| Schlagwörter: |
| author_facet |
Kundumani-Sridharan, Venkatesh Niu, Jixiao Wang, Dong Van Quyen, Dong Zhang, Qiuhua Singh, Nikhlesh K. Subramani, Jaganathan Karri, Saradasri Rao, Gadiparthi N. Kundumani-Sridharan, Venkatesh Niu, Jixiao Wang, Dong Van Quyen, Dong Zhang, Qiuhua Singh, Nikhlesh K. Subramani, Jaganathan Karri, Saradasri Rao, Gadiparthi N. |
|---|---|
| author |
Kundumani-Sridharan, Venkatesh Niu, Jixiao Wang, Dong Van Quyen, Dong Zhang, Qiuhua Singh, Nikhlesh K. Subramani, Jaganathan Karri, Saradasri Rao, Gadiparthi N. |
| spellingShingle |
Kundumani-Sridharan, Venkatesh Niu, Jixiao Wang, Dong Van Quyen, Dong Zhang, Qiuhua Singh, Nikhlesh K. Subramani, Jaganathan Karri, Saradasri Rao, Gadiparthi N. Blood 15(S)-hydroxyeicosatetraenoic acid–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2 expression Cell Biology Hematology Immunology Biochemistry |
| author_sort |
kundumani-sridharan, venkatesh |
| spelling |
Kundumani-Sridharan, Venkatesh Niu, Jixiao Wang, Dong Van Quyen, Dong Zhang, Qiuhua Singh, Nikhlesh K. Subramani, Jaganathan Karri, Saradasri Rao, Gadiparthi N. 0006-4971 1528-0020 American Society of Hematology Cell Biology Hematology Immunology Biochemistry http://dx.doi.org/10.1182/blood-2009-09-241802 <jats:title>Abstract</jats:title><jats:p>To understand the mechanisms underlying 15(S)-hydroxyeicosatetraenoic acid [15(S)-HETE]–induced angiogenesis, we studied the role of Egr-1. 15(S)-HETE induced Egr-1 expression in a time-dependent manner in human dermal microvascular endothelial cells (HDMVECs). Blockade of Egr-1 via forced expression of its dominant-negative mutant attenuated 15(S)-HETE–induced HDMVEC migration and tube formation as well as Matrigel plug angiogenesis. 15(S)-HETE–induced Egr-1 expression requires Src activation. In addition, adenovirus-mediated expression of dominant-negative mutant of Src blocked 15(S)-HETE's effects on migration and tube formation of HDMVECs and Matrigel plug angiogenesis. 15(S)-HETE induced fibroblast growth factor-2 (FGF-2) expression rapidly via Src-mediated production of Egr-1. Cloning and mutational analysis of FGF-2 promoter revealed that Egr-1 binding site proximal to transcription start site is required for 15(S)-HETE–induced FGF-2 expression. Neutralizing antibody-mediated suppression of FGF-2 function also attenuated the effects of 15(S)-HETE on HDMVEC migration and tube formation as well as Matrigel plug angiogenesis. Furthermore, in contrast to wild-type mice, 12/15-LOX−/− mice exhibited decreased Matrigel plug angiogenesis in response to AA, which was rescued by 15(S)-HETE. On the basis of these observations, we conclude that 15(S)-HETE–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2. These findings may suggest that 15(S)-HETE could be a potential endogenous regulator of pathologic angiogenesis associated with atherosclerosis and restenosis.</jats:p> 15(S)-hydroxyeicosatetraenoic acid–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2 expression Blood |
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10.1182/blood-2009-09-241802 |
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Online Free |
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Biologie Medizin Chemie und Pharmazie |
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ElectronicArticle |
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American Society of Hematology, 2010 |
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American Society of Hematology, 2010 |
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| title |
15(S)-hydroxyeicosatetraenoic acid–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2 expression |
| title_unstemmed |
15(S)-hydroxyeicosatetraenoic acid–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2 expression |
| title_full |
15(S)-hydroxyeicosatetraenoic acid–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2 expression |
| title_fullStr |
15(S)-hydroxyeicosatetraenoic acid–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2 expression |
| title_full_unstemmed |
15(S)-hydroxyeicosatetraenoic acid–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2 expression |
| title_short |
15(S)-hydroxyeicosatetraenoic acid–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2 expression |
| title_sort |
15(s)-hydroxyeicosatetraenoic acid–induced angiogenesis requires src-mediated egr-1–dependent rapid induction of fgf-2 expression |
| topic |
Cell Biology Hematology Immunology Biochemistry |
| url |
http://dx.doi.org/10.1182/blood-2009-09-241802 |
| publishDate |
2010 |
| physical |
2105-2116 |
| description |
<jats:title>Abstract</jats:title><jats:p>To understand the mechanisms underlying 15(S)-hydroxyeicosatetraenoic acid [15(S)-HETE]–induced angiogenesis, we studied the role of Egr-1. 15(S)-HETE induced Egr-1 expression in a time-dependent manner in human dermal microvascular endothelial cells (HDMVECs). Blockade of Egr-1 via forced expression of its dominant-negative mutant attenuated 15(S)-HETE–induced HDMVEC migration and tube formation as well as Matrigel plug angiogenesis. 15(S)-HETE–induced Egr-1 expression requires Src activation. In addition, adenovirus-mediated expression of dominant-negative mutant of Src blocked 15(S)-HETE's effects on migration and tube formation of HDMVECs and Matrigel plug angiogenesis. 15(S)-HETE induced fibroblast growth factor-2 (FGF-2) expression rapidly via Src-mediated production of Egr-1. Cloning and mutational analysis of FGF-2 promoter revealed that Egr-1 binding site proximal to transcription start site is required for 15(S)-HETE–induced FGF-2 expression. Neutralizing antibody-mediated suppression of FGF-2 function also attenuated the effects of 15(S)-HETE on HDMVEC migration and tube formation as well as Matrigel plug angiogenesis. Furthermore, in contrast to wild-type mice, 12/15-LOX−/− mice exhibited decreased Matrigel plug angiogenesis in response to AA, which was rescued by 15(S)-HETE. On the basis of these observations, we conclude that 15(S)-HETE–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2. These findings may suggest that 15(S)-HETE could be a potential endogenous regulator of pathologic angiogenesis associated with atherosclerosis and restenosis.</jats:p> |
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| author | Kundumani-Sridharan, Venkatesh, Niu, Jixiao, Wang, Dong, Van Quyen, Dong, Zhang, Qiuhua, Singh, Nikhlesh K., Subramani, Jaganathan, Karri, Saradasri, Rao, Gadiparthi N. |
| author_facet | Kundumani-Sridharan, Venkatesh, Niu, Jixiao, Wang, Dong, Van Quyen, Dong, Zhang, Qiuhua, Singh, Nikhlesh K., Subramani, Jaganathan, Karri, Saradasri, Rao, Gadiparthi N., Kundumani-Sridharan, Venkatesh, Niu, Jixiao, Wang, Dong, Van Quyen, Dong, Zhang, Qiuhua, Singh, Nikhlesh K., Subramani, Jaganathan, Karri, Saradasri, Rao, Gadiparthi N. |
| author_sort | kundumani-sridharan, venkatesh |
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| description | <jats:title>Abstract</jats:title><jats:p>To understand the mechanisms underlying 15(S)-hydroxyeicosatetraenoic acid [15(S)-HETE]–induced angiogenesis, we studied the role of Egr-1. 15(S)-HETE induced Egr-1 expression in a time-dependent manner in human dermal microvascular endothelial cells (HDMVECs). Blockade of Egr-1 via forced expression of its dominant-negative mutant attenuated 15(S)-HETE–induced HDMVEC migration and tube formation as well as Matrigel plug angiogenesis. 15(S)-HETE–induced Egr-1 expression requires Src activation. In addition, adenovirus-mediated expression of dominant-negative mutant of Src blocked 15(S)-HETE's effects on migration and tube formation of HDMVECs and Matrigel plug angiogenesis. 15(S)-HETE induced fibroblast growth factor-2 (FGF-2) expression rapidly via Src-mediated production of Egr-1. Cloning and mutational analysis of FGF-2 promoter revealed that Egr-1 binding site proximal to transcription start site is required for 15(S)-HETE–induced FGF-2 expression. Neutralizing antibody-mediated suppression of FGF-2 function also attenuated the effects of 15(S)-HETE on HDMVEC migration and tube formation as well as Matrigel plug angiogenesis. Furthermore, in contrast to wild-type mice, 12/15-LOX−/− mice exhibited decreased Matrigel plug angiogenesis in response to AA, which was rescued by 15(S)-HETE. On the basis of these observations, we conclude that 15(S)-HETE–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2. These findings may suggest that 15(S)-HETE could be a potential endogenous regulator of pathologic angiogenesis associated with atherosclerosis and restenosis.</jats:p> |
| doi_str_mv | 10.1182/blood-2009-09-241802 |
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| imprint | American Society of Hematology, 2010 |
| imprint_str_mv | American Society of Hematology, 2010 |
| institution | DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161 |
| issn | 0006-4971, 1528-0020 |
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| language | English |
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| mega_collection | American Society of Hematology (CrossRef) |
| physical | 2105-2116 |
| publishDate | 2010 |
| publishDateSort | 2010 |
| publisher | American Society of Hematology |
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| series | Blood |
| source_id | 49 |
| spelling | Kundumani-Sridharan, Venkatesh Niu, Jixiao Wang, Dong Van Quyen, Dong Zhang, Qiuhua Singh, Nikhlesh K. Subramani, Jaganathan Karri, Saradasri Rao, Gadiparthi N. 0006-4971 1528-0020 American Society of Hematology Cell Biology Hematology Immunology Biochemistry http://dx.doi.org/10.1182/blood-2009-09-241802 <jats:title>Abstract</jats:title><jats:p>To understand the mechanisms underlying 15(S)-hydroxyeicosatetraenoic acid [15(S)-HETE]–induced angiogenesis, we studied the role of Egr-1. 15(S)-HETE induced Egr-1 expression in a time-dependent manner in human dermal microvascular endothelial cells (HDMVECs). Blockade of Egr-1 via forced expression of its dominant-negative mutant attenuated 15(S)-HETE–induced HDMVEC migration and tube formation as well as Matrigel plug angiogenesis. 15(S)-HETE–induced Egr-1 expression requires Src activation. In addition, adenovirus-mediated expression of dominant-negative mutant of Src blocked 15(S)-HETE's effects on migration and tube formation of HDMVECs and Matrigel plug angiogenesis. 15(S)-HETE induced fibroblast growth factor-2 (FGF-2) expression rapidly via Src-mediated production of Egr-1. Cloning and mutational analysis of FGF-2 promoter revealed that Egr-1 binding site proximal to transcription start site is required for 15(S)-HETE–induced FGF-2 expression. Neutralizing antibody-mediated suppression of FGF-2 function also attenuated the effects of 15(S)-HETE on HDMVEC migration and tube formation as well as Matrigel plug angiogenesis. Furthermore, in contrast to wild-type mice, 12/15-LOX−/− mice exhibited decreased Matrigel plug angiogenesis in response to AA, which was rescued by 15(S)-HETE. On the basis of these observations, we conclude that 15(S)-HETE–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2. These findings may suggest that 15(S)-HETE could be a potential endogenous regulator of pathologic angiogenesis associated with atherosclerosis and restenosis.</jats:p> 15(S)-hydroxyeicosatetraenoic acid–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2 expression Blood |
| spellingShingle | Kundumani-Sridharan, Venkatesh, Niu, Jixiao, Wang, Dong, Van Quyen, Dong, Zhang, Qiuhua, Singh, Nikhlesh K., Subramani, Jaganathan, Karri, Saradasri, Rao, Gadiparthi N., Blood, 15(S)-hydroxyeicosatetraenoic acid–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2 expression, Cell Biology, Hematology, Immunology, Biochemistry |
| title | 15(S)-hydroxyeicosatetraenoic acid–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2 expression |
| title_full | 15(S)-hydroxyeicosatetraenoic acid–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2 expression |
| title_fullStr | 15(S)-hydroxyeicosatetraenoic acid–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2 expression |
| title_full_unstemmed | 15(S)-hydroxyeicosatetraenoic acid–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2 expression |
| title_short | 15(S)-hydroxyeicosatetraenoic acid–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2 expression |
| title_sort | 15(s)-hydroxyeicosatetraenoic acid–induced angiogenesis requires src-mediated egr-1–dependent rapid induction of fgf-2 expression |
| title_unstemmed | 15(S)-hydroxyeicosatetraenoic acid–induced angiogenesis requires Src-mediated Egr-1–dependent rapid induction of FGF-2 expression |
| topic | Cell Biology, Hematology, Immunology, Biochemistry |
| url | http://dx.doi.org/10.1182/blood-2009-09-241802 |