Vascular endothelial growth factor rescues HN33 neural cells from death induced by serum withdrawal

Lin Jin Kun Lin Jin, Ou Mao Xiao Ou Mao, D. A. Greenberg

Research output: Contribution to journalArticle

112 Citations (Scopus)

Abstract

Vascular endothelial growth factor (VEGF) is an angiogenic factor with neurotrophic effects in the peripheral nervous system. To determine if VEGF can also promote the survival of central neurons, we examined its effect on HN33 (mouse hippocampal neuron x neuroblastoma) cells deprived of serum. Serum-deprived HN33 cells expressed VEGFR-2 receptors, which, in the presence of VEGF, interacted with the downstream signaling molecules phosphatidylinositol 3'-kinase and phospho-Akt, as demonstrated by immunoprecipitation and Western blotting. Treatment of serum-deprived HN33 cells with VEGF also stimulated the phosphorylation of IκB-α and nuclear translocation of the transcription factor NF-κB. Withdrawal of serum for 24 h reduced HN33 cell viability by ~50% in the absence of VEGF, but by only ~20% in the presence of 100 ng/mL of VEGF. These findings support a neurotrophic role for VEGF in the central nervous system, which may be mediated through VEGFR-2 receptors, the protein kinases phosphatidylinositol 3'-kinase and Akt, and the transcription factor NK-κB. Thus, VEGF, like other neurotrophic factors, could exert protective effects in acute or chronic neurodegenerative disorders.

Original languageEnglish
Pages (from-to)197-203
Number of pages7
JournalJournal of Molecular Neuroscience
Volume14
Issue number3
StatePublished - 11 Sep 2000

Fingerprint

Vascular Endothelial Growth Factor A
Cell Death
Serum
Phosphatidylinositol 3-Kinase
Vascular Endothelial Growth Factor Receptor-2
Vascular Endothelial Growth Factor B
Transcription Factors
Neurons
Angiogenesis Inducing Agents
Peripheral Nervous System
Nerve Growth Factors
Neuroblastoma
Immunoprecipitation
Neurodegenerative Diseases
Protein Kinases
Cell Survival
Central Nervous System
Western Blotting
Phosphorylation

Keywords

  • Akt
  • Growth factors
  • HN33 cells
  • Phosphatidylinositol 3'-kinase
  • VEGF
  • VEGFR-2 receptor

Cite this

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abstract = "Vascular endothelial growth factor (VEGF) is an angiogenic factor with neurotrophic effects in the peripheral nervous system. To determine if VEGF can also promote the survival of central neurons, we examined its effect on HN33 (mouse hippocampal neuron x neuroblastoma) cells deprived of serum. Serum-deprived HN33 cells expressed VEGFR-2 receptors, which, in the presence of VEGF, interacted with the downstream signaling molecules phosphatidylinositol 3'-kinase and phospho-Akt, as demonstrated by immunoprecipitation and Western blotting. Treatment of serum-deprived HN33 cells with VEGF also stimulated the phosphorylation of IκB-α and nuclear translocation of the transcription factor NF-κB. Withdrawal of serum for 24 h reduced HN33 cell viability by ~50{\%} in the absence of VEGF, but by only ~20{\%} in the presence of 100 ng/mL of VEGF. These findings support a neurotrophic role for VEGF in the central nervous system, which may be mediated through VEGFR-2 receptors, the protein kinases phosphatidylinositol 3'-kinase and Akt, and the transcription factor NK-κB. Thus, VEGF, like other neurotrophic factors, could exert protective effects in acute or chronic neurodegenerative disorders.",
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Vascular endothelial growth factor rescues HN33 neural cells from death induced by serum withdrawal. / Kun Lin Jin, Lin Jin; Xiao Ou Mao, Ou Mao; Greenberg, D. A.

In: Journal of Molecular Neuroscience, Vol. 14, No. 3, 11.09.2000, p. 197-203.

Research output: Contribution to journalArticle

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