Vascular endothelial growth factor increases the intracellular magnesium

Area of Science:

• Cell Biology
• Molecular Biology
• Biochemistry

Background:

• Angiogenesis, the formation of new blood vessels, is crucial for development and disease.
• Vascular endothelial growth factor (VEGF) is a key regulator of angiogenesis, but its precise molecular mechanisms are not fully understood.
• Intracellular magnesium (Mg2+) is vital for numerous cellular functions.

Purpose of the Study:

• To investigate the effect of VEGF on intracellular Mg2+ concentration ([Mg2+]i) in human umbilical vein endothelial cells (HUVECs).
• To elucidate the signaling pathways involved in VEGF-mediated changes in [Mg2+]i.

Main Methods:

• Treatment of HUVECs with VEGF-A165.
• Measurement of intracellular Mg2+ concentrations.
• Inhibition of specific signaling pathways using SU1498, tyrosine kinase inhibitors, PI3K inhibitors, PLCgamma inhibitors, and MAPK inhibitors.

Main Results:

• VEGF-A165 significantly increased [Mg2+]i in HUVECs in a dose-dependent manner.
• The VEGF-induced increase in [Mg2+]i was abolished by inhibitors of tyrosine kinase, PI3K, and PLCgamma.
• Inhibitors of mitogen-activated protein kinase (MAPK) pathways did not affect the VEGF-induced [Mg2+]i increase.

Conclusions:

• VEGF-A165 elevates intracellular Mg2+ levels in endothelial cells.
• This elevation is mediated by the activation of tyrosine kinase, PI3K, and PLCgamma signaling cascades.
• VEGF-A165 likely mobilizes Mg2+ from intracellular stores through these specific pathways, contributing to its role in angiogenesis.