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NOS1AP O-GlcNAc Modification Involved in Neuron Apoptosis Induced by Excitotoxicity

Liang Zhu1,2, Tao Tao3,4, Dongmei Zhang5,6

  • 1Department of Neurology, Affiliated Hospital of Nantong University, the Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Nantong University, Nantong 226000, China. zhuliang_nt@163.com.

International Journal of Molecular Sciences
|July 22, 2015
PubMed

Insights

O-Linked N-acetylglucosamine (O-GlcNAc) modification of NOS1AP protects neurons during apoptosis. This protective effect is mediated by maintaining the interaction between NOS1AP and nNOS, reducing neuronal cell death.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Neuroscience

Background:

  • O-Linked N-acetylglucosamine (O-GlcNAc) is a dynamic post-translational modification crucial for cellular processes.
  • O-GlcNAc's role in apoptosis and stress response is significant but not fully understood.
  • Nitric oxide synthase adaptor (NOS1AP) is implicated in glutamate-induced neuronal apoptosis.

Purpose of the Study:

  • To investigate the role of O-GlcNAc modification on NOS1AP in neuronal apoptosis.
  • To identify O-GlcNAc sites on NOS1AP and their functional significance.

Main Methods:

  • Mass spectrometry to identify O-GlcNAc sites on NOS1AP.
  • Mutation of identified O-GlcNAc sites on NOS1AP.
  • Assessment of NOS1AP-nNOS interaction and neuronal apoptosis levels.

Main Results:

  • Identified five O-GlcNAc sites on NOS1AP (Ser47, Ser183, Ser204, Ser269, Ser271).
  • Observed increased O-GlcNAc modification of NOS1AP during glutamate-induced apoptosis.
  • Demonstrated that O-GlcNAc modification of NOS1AP enhances its interaction with nNOS.
  • Showed that reduced O-GlcNAc modification of NOS1AP exacerbates neuronal apoptosis.

Conclusions:

  • O-GlcNAc modification of NOS1AP plays a protective role in glutamate-induced neuronal apoptosis.
  • This protection is linked to the maintenance of NOS1AP and nNOS interaction.
  • Targeting O-GlcNAc modification of NOS1AP may offer therapeutic potential for neurodegenerative conditions.
Keywords:
NOS1APO-GlcNAc modificationexcitotoxicity

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