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[Involvement of AKT/eNOS in brain derived neurotrophic factor-induced angiogenesis]

Ya-dan Wang1, Yu Hu, Chun-yan Sun

  • 1Institution of Hematology, Union Hospital Affiliated to Tongii Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

Zhonghua Xue Ye Xue Za Zhi = Zhonghua Xueyexue Zazhi
|December 19, 2006
PubMed
Abstract

Insights

Brain-derived neurotrophic factor (BDNF) promotes angiogenesis via the AKT/eNOS pathway. This pathway presents a potential target for anti-angiogenesis therapies in multiple myeloma.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Context:

  • Angiogenesis plays a critical role in the progression of multiple myeloma.
  • Brain-derived neurotrophic factor (BDNF) has been implicated in various cellular processes, including angiogenesis.
  • Understanding the specific signaling pathways activated by BDNF is crucial for developing targeted therapies.

Purpose:

  • To elucidate the signaling mechanisms by which BDNF stimulates angiogenesis.
  • To investigate the role of the phosphatidylinositol-3-kinase (PI3K)/AKT/endothelial NO synthase (eNOS) pathway in BDNF-induced angiogenesis.
  • To explore the potential of targeting this pathway for anti-angiogenesis therapy in multiple myeloma.

Summary:

  • BDNF activates the PI3K/AKT/eNOS signaling pathway in human umbilical venous epithelial cells (HUVECs) in a time- and dose-dependent manner.
  • BDNF promotes HUVEC migration, tube formation, and NO production, effects inhibited by PI3K inhibitor LY294002 and eNOS inhibitor L-NAME.
  • In vivo studies demonstrated that BDNF enhances capillary ingrowth, which is attenuated by L-NAME treatment, confirming the role of the AKT/eNOS pathway in BDNF-mediated angiogenesis.

Impact:

  • Identifies the AKT/eNOS signaling pathway as a key mediator of BDNF-induced angiogenesis.
  • Provides a novel molecular target for developing anti-angiogenesis strategies against multiple myeloma.
  • Offers potential therapeutic avenues to inhibit tumor growth and metastasis in multiple myeloma by targeting BDNF signaling.

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