1. Academic Validation
  2. GIP-GIPR promotes neurite outgrowth of cortical neurons in Akt dependent manner

GIP-GIPR promotes neurite outgrowth of cortical neurons in Akt dependent manner

  • Biochem Biophys Res Commun. 2021 Jan 1;534:121-127. doi: 10.1016/j.bbrc.2020.11.120.
Long Teng 1 Tuchen Guan 1 Beibei Guo 1 Chao Ma 1 Ge Lin 1 Ronghua Wu 1 Man Xu 1 Mei Liu 2 Yan Liu 3
Affiliations

Affiliations

  • 1 Key Laboratory of Neuroregeneration of Jiangsu Province and Ministry of Education, Co-innovation Center of Neuroregeneration, Nantong University, China.
  • 2 Key Laboratory of Neuroregeneration of Jiangsu Province and Ministry of Education, Co-innovation Center of Neuroregeneration, Nantong University, China. Electronic address: liumei@ntu.edu.cn.
  • 3 Key Laboratory of Neuroregeneration of Jiangsu Province and Ministry of Education, Co-innovation Center of Neuroregeneration, Nantong University, China. Electronic address: liuyan@ntu.edu.cn.
Abstract

The intrinsic capacity of axonal growth is varied among the neurons form different tissues or different developmental stages. In this study, we established an in vitro model to compare the axonal growth of neurons from embryonic 18 days, post-natal 1 day and post-natal 3 days rat. The E18 neurons showed powerful ability of neuritogenensis and axon outgrowth and the ability decreased rapidly along with development. The transcriptome profile of these neurons revealed a set of genes positively correlated with the capacity of neurite outgrowth. Glucose-dependent insulinotropic polypeptide receptor (GIPR) is identified as a gene to promote neurite outgrowth, which was approved by siRNA knock down assay in E18 neuron. Glucose-dependent insulinotropic polypeptide (GIP), a ligand of GIPR secreted from enteroendocrine K cells, is well-known for its role in nutrient sensing and intake. To verify the effect of GIP-GIPR signal on neurite outgrowth, we administrated GIP to stimulate the E18 neurons, the results showed that GIP significantly improved extension of axon. We further revealed that GIP increased Rac1/Cdc42 phosphorylation in Akt dependent manner. In summary, our study established an in vitro model to screen the genes involved in neurite outgrowth, and we provided mechanical insight on the GIP-GIPR axis to promote axonal outgrowth.

Keywords

Akt pathway; Cortical neuron; Glucose-dependent insulinotropic polypeptide; Glucose-dependent insulinotropic polypeptide receptor; Neurite outgrowth; Rac1/Cdc42.

Figures
Products