MCP-1 Upregulates Amylin Expression in Murine Pancreatic β Cells through ERK/JNK-AP1 and NF-κB Related Signaling Pathways Independent of CCR2
2011

MCP-1 Increases Amylin Production in Pancreatic Cells

publication Evidence: moderate

Author Information

Author(s): Cai Kun, Qi Dongfei, Hou Xinwei, Wang Oumei, Chen Juan, Deng Bo, Qian Lihua, Liu Xiaolong, Le Yingying

Primary Institution: Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Graduate School of the Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China

Hypothesis

Does MCP-1 affect amylin expression in pancreatic β-cells and what are the underlying mechanisms?

Conclusion

MCP-1 induces amylin expression through specific signaling pathways independent of CCR2.

Supporting Evidence

  • MCP-1 specifically induces amylin expression in β-cells.
  • MCP-1 increases proamylin and intermediate forms of amylin at the protein level.
  • The inductive effect of MCP-1 on amylin mRNA is more potent in pancreatic islets than in MIN6 cells.
  • MCP-1-induced amylin expression is mediated through ERK1/2 and JNK signaling pathways.

Takeaway

MCP-1 is a protein that helps cells communicate during inflammation, and it can make pancreatic cells produce more amylin, which is linked to diabetes.

Methodology

The study used murine pancreatic β-cell line MIN6 and pancreatic islets to examine the effect of MCP-1 on amylin expression through various biochemical assays.

Limitations

The study primarily focused on murine models, which may not fully represent human physiology.

Statistical Information

P-Value

116 pM

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0019559

Want to read the original?

Access the complete publication on the publisher's website

View Original Publication