Regulation of vascular endothelial growth factor expression by insulin-like growth factor-II in human keratinocytes, differential involvement of mitogen-activated protein kinases and feedback inhibition of protein kinase C
Background Vascular endothelial growth factor (VEGF) is overexpressed in hyperproliferative diseases such as psoriasis and cancer, which are characterized by an increased angiogenesis. It was reported that insulin-like growth factor (IGF)-II is highly expressed during hepatocarcinogenesis and is in...
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| Autor*in: |
Kim, H.J. [verfasserIn] Kim, T-Y. [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 2005 |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2005 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: British journal of dermatology - Oxford : Wiley-Blackwell, 1892, 152(2005), 3, Seite 0 |
| Übergeordnetes Werk: |
volume:152 ; year:2005 ; number:3 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1111/j.1365-2133.2004.06397.x |
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NLEJ242107125 |
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| 520 | |a Background Vascular endothelial growth factor (VEGF) is overexpressed in hyperproliferative diseases such as psoriasis and cancer, which are characterized by an increased angiogenesis. It was reported that insulin-like growth factor (IGF)-II is highly expressed during hepatocarcinogenesis and is increased in psoriatic lesions. The increase in IGF-II is believed to be associated with the pathogenesis of these diseases by increasing angiogenesis.Objectives In order to investigate the relationship between IGF-II and angiogenesis-related VEGF, VEGF expression in the IGF-II-treated human keratinocytes was monitored and the IGF-II signalling pathways were examined with respect to VEGF expression.Methods Northern blot analysis for the VEGF mRNA levels and an enzyme-linked immunosorbent assay for the VEGF protein were performed to determine if IGF-II (100 ng mL−1) can increase the VEGF expression levels with or without a pretreatment with protein inhibitors in primary normal human keratinocytes and HaCaT cells.Results The mRNA and protein levels of VEGF by IGF-II were increased in a time-dependent manner and reached the maximum level 2 h and 8 h after the IGF-II treatment, respectively. However, this increase was abrogated by pretreatment with an extracellular signal-regulated kinase (ERK) inhibitor but not by a p38 inhibitor. The IGF-II-mediated VEGF induction was also effectively inhibited by a pretreatment with the tyrosine kinase inhibitor and Src inhibitor. The PI3–kinase inhibitor also inhibited the expression of VEGF by IGF-II. However, the phospholipase C (PLC) and protein kinase C (PKC) inhibitors did not block the increases of VEGF mRNA level and its protein level by IGF-II, and the PKC inhibitor instead increased VEGF expression by IGF-II.Conclusions These results suggest that the tyrosine kinase–Src–ERK1/2 pathway and the PI3–kinase pathway are involved in IGF-II-mediated VEGF expression, but PKC is negatively associated in the IGF-II-mediated VEGF expression. | ||
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10.1111/j.1365-2133.2004.06397.x doi (DE-627)NLEJ242107125 DE-627 ger DE-627 rakwb Kim, H.J. verfasserin aut Regulation of vascular endothelial growth factor expression by insulin-like growth factor-II in human keratinocytes, differential involvement of mitogen-activated protein kinases and feedback inhibition of protein kinase C Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Background Vascular endothelial growth factor (VEGF) is overexpressed in hyperproliferative diseases such as psoriasis and cancer, which are characterized by an increased angiogenesis. It was reported that insulin-like growth factor (IGF)-II is highly expressed during hepatocarcinogenesis and is increased in psoriatic lesions. The increase in IGF-II is believed to be associated with the pathogenesis of these diseases by increasing angiogenesis.Objectives In order to investigate the relationship between IGF-II and angiogenesis-related VEGF, VEGF expression in the IGF-II-treated human keratinocytes was monitored and the IGF-II signalling pathways were examined with respect to VEGF expression.Methods Northern blot analysis for the VEGF mRNA levels and an enzyme-linked immunosorbent assay for the VEGF protein were performed to determine if IGF-II (100 ng mL−1) can increase the VEGF expression levels with or without a pretreatment with protein inhibitors in primary normal human keratinocytes and HaCaT cells.Results The mRNA and protein levels of VEGF by IGF-II were increased in a time-dependent manner and reached the maximum level 2 h and 8 h after the IGF-II treatment, respectively. However, this increase was abrogated by pretreatment with an extracellular signal-regulated kinase (ERK) inhibitor but not by a p38 inhibitor. The IGF-II-mediated VEGF induction was also effectively inhibited by a pretreatment with the tyrosine kinase inhibitor and Src inhibitor. The PI3–kinase inhibitor also inhibited the expression of VEGF by IGF-II. However, the phospholipase C (PLC) and protein kinase C (PKC) inhibitors did not block the increases of VEGF mRNA level and its protein level by IGF-II, and the PKC inhibitor instead increased VEGF expression by IGF-II.Conclusions These results suggest that the tyrosine kinase–Src–ERK1/2 pathway and the PI3–kinase pathway are involved in IGF-II-mediated VEGF expression, but PKC is negatively associated in the IGF-II-mediated VEGF expression. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| ERK1/2 Kim, T-Y. verfasserin aut In British journal of dermatology Oxford : Wiley-Blackwell, 1892 152(2005), 3, Seite 0 Online-Ressource (DE-627)NLEJ24392786X (DE-600)2004086-6 1365-2133 nnns volume:152 year:2005 number:3 pages:0 http://dx.doi.org/10.1111/j.1365-2133.2004.06397.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 152 2005 3 0 |
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10.1111/j.1365-2133.2004.06397.x doi (DE-627)NLEJ242107125 DE-627 ger DE-627 rakwb Kim, H.J. verfasserin aut Regulation of vascular endothelial growth factor expression by insulin-like growth factor-II in human keratinocytes, differential involvement of mitogen-activated protein kinases and feedback inhibition of protein kinase C Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Background Vascular endothelial growth factor (VEGF) is overexpressed in hyperproliferative diseases such as psoriasis and cancer, which are characterized by an increased angiogenesis. It was reported that insulin-like growth factor (IGF)-II is highly expressed during hepatocarcinogenesis and is increased in psoriatic lesions. The increase in IGF-II is believed to be associated with the pathogenesis of these diseases by increasing angiogenesis.Objectives In order to investigate the relationship between IGF-II and angiogenesis-related VEGF, VEGF expression in the IGF-II-treated human keratinocytes was monitored and the IGF-II signalling pathways were examined with respect to VEGF expression.Methods Northern blot analysis for the VEGF mRNA levels and an enzyme-linked immunosorbent assay for the VEGF protein were performed to determine if IGF-II (100 ng mL−1) can increase the VEGF expression levels with or without a pretreatment with protein inhibitors in primary normal human keratinocytes and HaCaT cells.Results The mRNA and protein levels of VEGF by IGF-II were increased in a time-dependent manner and reached the maximum level 2 h and 8 h after the IGF-II treatment, respectively. However, this increase was abrogated by pretreatment with an extracellular signal-regulated kinase (ERK) inhibitor but not by a p38 inhibitor. The IGF-II-mediated VEGF induction was also effectively inhibited by a pretreatment with the tyrosine kinase inhibitor and Src inhibitor. The PI3–kinase inhibitor also inhibited the expression of VEGF by IGF-II. However, the phospholipase C (PLC) and protein kinase C (PKC) inhibitors did not block the increases of VEGF mRNA level and its protein level by IGF-II, and the PKC inhibitor instead increased VEGF expression by IGF-II.Conclusions These results suggest that the tyrosine kinase–Src–ERK1/2 pathway and the PI3–kinase pathway are involved in IGF-II-mediated VEGF expression, but PKC is negatively associated in the IGF-II-mediated VEGF expression. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| ERK1/2 Kim, T-Y. verfasserin aut In British journal of dermatology Oxford : Wiley-Blackwell, 1892 152(2005), 3, Seite 0 Online-Ressource (DE-627)NLEJ24392786X (DE-600)2004086-6 1365-2133 nnns volume:152 year:2005 number:3 pages:0 http://dx.doi.org/10.1111/j.1365-2133.2004.06397.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 152 2005 3 0 |
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10.1111/j.1365-2133.2004.06397.x doi (DE-627)NLEJ242107125 DE-627 ger DE-627 rakwb Kim, H.J. verfasserin aut Regulation of vascular endothelial growth factor expression by insulin-like growth factor-II in human keratinocytes, differential involvement of mitogen-activated protein kinases and feedback inhibition of protein kinase C Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Background Vascular endothelial growth factor (VEGF) is overexpressed in hyperproliferative diseases such as psoriasis and cancer, which are characterized by an increased angiogenesis. It was reported that insulin-like growth factor (IGF)-II is highly expressed during hepatocarcinogenesis and is increased in psoriatic lesions. The increase in IGF-II is believed to be associated with the pathogenesis of these diseases by increasing angiogenesis.Objectives In order to investigate the relationship between IGF-II and angiogenesis-related VEGF, VEGF expression in the IGF-II-treated human keratinocytes was monitored and the IGF-II signalling pathways were examined with respect to VEGF expression.Methods Northern blot analysis for the VEGF mRNA levels and an enzyme-linked immunosorbent assay for the VEGF protein were performed to determine if IGF-II (100 ng mL−1) can increase the VEGF expression levels with or without a pretreatment with protein inhibitors in primary normal human keratinocytes and HaCaT cells.Results The mRNA and protein levels of VEGF by IGF-II were increased in a time-dependent manner and reached the maximum level 2 h and 8 h after the IGF-II treatment, respectively. However, this increase was abrogated by pretreatment with an extracellular signal-regulated kinase (ERK) inhibitor but not by a p38 inhibitor. The IGF-II-mediated VEGF induction was also effectively inhibited by a pretreatment with the tyrosine kinase inhibitor and Src inhibitor. The PI3–kinase inhibitor also inhibited the expression of VEGF by IGF-II. However, the phospholipase C (PLC) and protein kinase C (PKC) inhibitors did not block the increases of VEGF mRNA level and its protein level by IGF-II, and the PKC inhibitor instead increased VEGF expression by IGF-II.Conclusions These results suggest that the tyrosine kinase–Src–ERK1/2 pathway and the PI3–kinase pathway are involved in IGF-II-mediated VEGF expression, but PKC is negatively associated in the IGF-II-mediated VEGF expression. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| ERK1/2 Kim, T-Y. verfasserin aut In British journal of dermatology Oxford : Wiley-Blackwell, 1892 152(2005), 3, Seite 0 Online-Ressource (DE-627)NLEJ24392786X (DE-600)2004086-6 1365-2133 nnns volume:152 year:2005 number:3 pages:0 http://dx.doi.org/10.1111/j.1365-2133.2004.06397.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 152 2005 3 0 |
| allfieldsGer |
10.1111/j.1365-2133.2004.06397.x doi (DE-627)NLEJ242107125 DE-627 ger DE-627 rakwb Kim, H.J. verfasserin aut Regulation of vascular endothelial growth factor expression by insulin-like growth factor-II in human keratinocytes, differential involvement of mitogen-activated protein kinases and feedback inhibition of protein kinase C Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Background Vascular endothelial growth factor (VEGF) is overexpressed in hyperproliferative diseases such as psoriasis and cancer, which are characterized by an increased angiogenesis. It was reported that insulin-like growth factor (IGF)-II is highly expressed during hepatocarcinogenesis and is increased in psoriatic lesions. The increase in IGF-II is believed to be associated with the pathogenesis of these diseases by increasing angiogenesis.Objectives In order to investigate the relationship between IGF-II and angiogenesis-related VEGF, VEGF expression in the IGF-II-treated human keratinocytes was monitored and the IGF-II signalling pathways were examined with respect to VEGF expression.Methods Northern blot analysis for the VEGF mRNA levels and an enzyme-linked immunosorbent assay for the VEGF protein were performed to determine if IGF-II (100 ng mL−1) can increase the VEGF expression levels with or without a pretreatment with protein inhibitors in primary normal human keratinocytes and HaCaT cells.Results The mRNA and protein levels of VEGF by IGF-II were increased in a time-dependent manner and reached the maximum level 2 h and 8 h after the IGF-II treatment, respectively. However, this increase was abrogated by pretreatment with an extracellular signal-regulated kinase (ERK) inhibitor but not by a p38 inhibitor. The IGF-II-mediated VEGF induction was also effectively inhibited by a pretreatment with the tyrosine kinase inhibitor and Src inhibitor. The PI3–kinase inhibitor also inhibited the expression of VEGF by IGF-II. However, the phospholipase C (PLC) and protein kinase C (PKC) inhibitors did not block the increases of VEGF mRNA level and its protein level by IGF-II, and the PKC inhibitor instead increased VEGF expression by IGF-II.Conclusions These results suggest that the tyrosine kinase–Src–ERK1/2 pathway and the PI3–kinase pathway are involved in IGF-II-mediated VEGF expression, but PKC is negatively associated in the IGF-II-mediated VEGF expression. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| ERK1/2 Kim, T-Y. verfasserin aut In British journal of dermatology Oxford : Wiley-Blackwell, 1892 152(2005), 3, Seite 0 Online-Ressource (DE-627)NLEJ24392786X (DE-600)2004086-6 1365-2133 nnns volume:152 year:2005 number:3 pages:0 http://dx.doi.org/10.1111/j.1365-2133.2004.06397.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 152 2005 3 0 |
| allfieldsSound |
10.1111/j.1365-2133.2004.06397.x doi (DE-627)NLEJ242107125 DE-627 ger DE-627 rakwb Kim, H.J. verfasserin aut Regulation of vascular endothelial growth factor expression by insulin-like growth factor-II in human keratinocytes, differential involvement of mitogen-activated protein kinases and feedback inhibition of protein kinase C Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Background Vascular endothelial growth factor (VEGF) is overexpressed in hyperproliferative diseases such as psoriasis and cancer, which are characterized by an increased angiogenesis. It was reported that insulin-like growth factor (IGF)-II is highly expressed during hepatocarcinogenesis and is increased in psoriatic lesions. The increase in IGF-II is believed to be associated with the pathogenesis of these diseases by increasing angiogenesis.Objectives In order to investigate the relationship between IGF-II and angiogenesis-related VEGF, VEGF expression in the IGF-II-treated human keratinocytes was monitored and the IGF-II signalling pathways were examined with respect to VEGF expression.Methods Northern blot analysis for the VEGF mRNA levels and an enzyme-linked immunosorbent assay for the VEGF protein were performed to determine if IGF-II (100 ng mL−1) can increase the VEGF expression levels with or without a pretreatment with protein inhibitors in primary normal human keratinocytes and HaCaT cells.Results The mRNA and protein levels of VEGF by IGF-II were increased in a time-dependent manner and reached the maximum level 2 h and 8 h after the IGF-II treatment, respectively. However, this increase was abrogated by pretreatment with an extracellular signal-regulated kinase (ERK) inhibitor but not by a p38 inhibitor. The IGF-II-mediated VEGF induction was also effectively inhibited by a pretreatment with the tyrosine kinase inhibitor and Src inhibitor. The PI3–kinase inhibitor also inhibited the expression of VEGF by IGF-II. However, the phospholipase C (PLC) and protein kinase C (PKC) inhibitors did not block the increases of VEGF mRNA level and its protein level by IGF-II, and the PKC inhibitor instead increased VEGF expression by IGF-II.Conclusions These results suggest that the tyrosine kinase–Src–ERK1/2 pathway and the PI3–kinase pathway are involved in IGF-II-mediated VEGF expression, but PKC is negatively associated in the IGF-II-mediated VEGF expression. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| ERK1/2 Kim, T-Y. verfasserin aut In British journal of dermatology Oxford : Wiley-Blackwell, 1892 152(2005), 3, Seite 0 Online-Ressource (DE-627)NLEJ24392786X (DE-600)2004086-6 1365-2133 nnns volume:152 year:2005 number:3 pages:0 http://dx.doi.org/10.1111/j.1365-2133.2004.06397.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 152 2005 3 0 |
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It was reported that insulin-like growth factor (IGF)-II is highly expressed during hepatocarcinogenesis and is increased in psoriatic lesions. The increase in IGF-II is believed to be associated with the pathogenesis of these diseases by increasing angiogenesis.Objectives In order to investigate the relationship between IGF-II and angiogenesis-related VEGF, VEGF expression in the IGF-II-treated human keratinocytes was monitored and the IGF-II signalling pathways were examined with respect to VEGF expression.Methods Northern blot analysis for the VEGF mRNA levels and an enzyme-linked immunosorbent assay for the VEGF protein were performed to determine if IGF-II (100 ng mL−1) can increase the VEGF expression levels with or without a pretreatment with protein inhibitors in primary normal human keratinocytes and HaCaT cells.Results The mRNA and protein levels of VEGF by IGF-II were increased in a time-dependent manner and reached the maximum level 2 h and 8 h after the IGF-II treatment, respectively. 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regulation of vascular endothelial growth factor expression by insulin-like growth factor-ii in human keratinocytes, differential involvement of mitogen-activated protein kinases and feedback inhibition of protein kinase c |
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Regulation of vascular endothelial growth factor expression by insulin-like growth factor-II in human keratinocytes, differential involvement of mitogen-activated protein kinases and feedback inhibition of protein kinase C |
| abstract |
Background Vascular endothelial growth factor (VEGF) is overexpressed in hyperproliferative diseases such as psoriasis and cancer, which are characterized by an increased angiogenesis. It was reported that insulin-like growth factor (IGF)-II is highly expressed during hepatocarcinogenesis and is increased in psoriatic lesions. The increase in IGF-II is believed to be associated with the pathogenesis of these diseases by increasing angiogenesis.Objectives In order to investigate the relationship between IGF-II and angiogenesis-related VEGF, VEGF expression in the IGF-II-treated human keratinocytes was monitored and the IGF-II signalling pathways were examined with respect to VEGF expression.Methods Northern blot analysis for the VEGF mRNA levels and an enzyme-linked immunosorbent assay for the VEGF protein were performed to determine if IGF-II (100 ng mL−1) can increase the VEGF expression levels with or without a pretreatment with protein inhibitors in primary normal human keratinocytes and HaCaT cells.Results The mRNA and protein levels of VEGF by IGF-II were increased in a time-dependent manner and reached the maximum level 2 h and 8 h after the IGF-II treatment, respectively. However, this increase was abrogated by pretreatment with an extracellular signal-regulated kinase (ERK) inhibitor but not by a p38 inhibitor. The IGF-II-mediated VEGF induction was also effectively inhibited by a pretreatment with the tyrosine kinase inhibitor and Src inhibitor. The PI3–kinase inhibitor also inhibited the expression of VEGF by IGF-II. However, the phospholipase C (PLC) and protein kinase C (PKC) inhibitors did not block the increases of VEGF mRNA level and its protein level by IGF-II, and the PKC inhibitor instead increased VEGF expression by IGF-II.Conclusions These results suggest that the tyrosine kinase–Src–ERK1/2 pathway and the PI3–kinase pathway are involved in IGF-II-mediated VEGF expression, but PKC is negatively associated in the IGF-II-mediated VEGF expression. |
| abstractGer |
Background Vascular endothelial growth factor (VEGF) is overexpressed in hyperproliferative diseases such as psoriasis and cancer, which are characterized by an increased angiogenesis. It was reported that insulin-like growth factor (IGF)-II is highly expressed during hepatocarcinogenesis and is increased in psoriatic lesions. The increase in IGF-II is believed to be associated with the pathogenesis of these diseases by increasing angiogenesis.Objectives In order to investigate the relationship between IGF-II and angiogenesis-related VEGF, VEGF expression in the IGF-II-treated human keratinocytes was monitored and the IGF-II signalling pathways were examined with respect to VEGF expression.Methods Northern blot analysis for the VEGF mRNA levels and an enzyme-linked immunosorbent assay for the VEGF protein were performed to determine if IGF-II (100 ng mL−1) can increase the VEGF expression levels with or without a pretreatment with protein inhibitors in primary normal human keratinocytes and HaCaT cells.Results The mRNA and protein levels of VEGF by IGF-II were increased in a time-dependent manner and reached the maximum level 2 h and 8 h after the IGF-II treatment, respectively. However, this increase was abrogated by pretreatment with an extracellular signal-regulated kinase (ERK) inhibitor but not by a p38 inhibitor. The IGF-II-mediated VEGF induction was also effectively inhibited by a pretreatment with the tyrosine kinase inhibitor and Src inhibitor. The PI3–kinase inhibitor also inhibited the expression of VEGF by IGF-II. However, the phospholipase C (PLC) and protein kinase C (PKC) inhibitors did not block the increases of VEGF mRNA level and its protein level by IGF-II, and the PKC inhibitor instead increased VEGF expression by IGF-II.Conclusions These results suggest that the tyrosine kinase–Src–ERK1/2 pathway and the PI3–kinase pathway are involved in IGF-II-mediated VEGF expression, but PKC is negatively associated in the IGF-II-mediated VEGF expression. |
| abstract_unstemmed |
Background Vascular endothelial growth factor (VEGF) is overexpressed in hyperproliferative diseases such as psoriasis and cancer, which are characterized by an increased angiogenesis. It was reported that insulin-like growth factor (IGF)-II is highly expressed during hepatocarcinogenesis and is increased in psoriatic lesions. The increase in IGF-II is believed to be associated with the pathogenesis of these diseases by increasing angiogenesis.Objectives In order to investigate the relationship between IGF-II and angiogenesis-related VEGF, VEGF expression in the IGF-II-treated human keratinocytes was monitored and the IGF-II signalling pathways were examined with respect to VEGF expression.Methods Northern blot analysis for the VEGF mRNA levels and an enzyme-linked immunosorbent assay for the VEGF protein were performed to determine if IGF-II (100 ng mL−1) can increase the VEGF expression levels with or without a pretreatment with protein inhibitors in primary normal human keratinocytes and HaCaT cells.Results The mRNA and protein levels of VEGF by IGF-II were increased in a time-dependent manner and reached the maximum level 2 h and 8 h after the IGF-II treatment, respectively. However, this increase was abrogated by pretreatment with an extracellular signal-regulated kinase (ERK) inhibitor but not by a p38 inhibitor. The IGF-II-mediated VEGF induction was also effectively inhibited by a pretreatment with the tyrosine kinase inhibitor and Src inhibitor. The PI3–kinase inhibitor also inhibited the expression of VEGF by IGF-II. However, the phospholipase C (PLC) and protein kinase C (PKC) inhibitors did not block the increases of VEGF mRNA level and its protein level by IGF-II, and the PKC inhibitor instead increased VEGF expression by IGF-II.Conclusions These results suggest that the tyrosine kinase–Src–ERK1/2 pathway and the PI3–kinase pathway are involved in IGF-II-mediated VEGF expression, but PKC is negatively associated in the IGF-II-mediated VEGF expression. |
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Regulation of vascular endothelial growth factor expression by insulin-like growth factor-II in human keratinocytes, differential involvement of mitogen-activated protein kinases and feedback inhibition of protein kinase C |
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