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Pressure suppresses hepatocellular glycogen synthesis through activating the p53/Pten pathway

Junwei Shen1, Yunchen Sun1, Si Shen1

  • 1Department of Gastroenterology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, P.R. China.

Molecular Medicine Reports
|May 7, 2019
PubMed

Insights

Portal hypertension, a complication of chronic liver disease, impairs nervous system metabolism. This study shows mechanical pressure from portal hypertension reduces liver cell glycogen by inhibiting key enzymes and activating specific cellular pathways.

Area of Science:

  • Hepatology
  • Cellular Metabolism
  • Molecular Biology

Background:

  • Portal hypertension is a major complication of chronic liver diseases.
  • It significantly impacts nervous system metabolism.
  • The role of portal hypertension in liver cell metabolism was previously unclear.

Purpose of the Study:

  • To investigate the effect of portal hypertension on hepatocellular metabolism.
  • To elucidate the regulatory mechanisms of glycogen synthesis under pressure.

Main Methods:

  • Used HepG2 and HL-7702 cell lines.
  • Applied increased extracellular pressure.
  • Performed RNA-sequencing (RNA-seq) analysis.
  • Assessed glycogen concentrations and glycogen synthase activity.

Main Results:

  • Increased extracellular pressure significantly decreased hepatocellular glycogen concentrations.
  • Pressure inhibited glycogen synthase activity by reducing glycogen synthase 1 phosphorylation.
  • RNA-seq revealed mechanical pressure activates the p53/phosphatase and tensin homolog pathway, suppressing glycogen synthesis.

Conclusions:

  • Mechanical pressure is associated with altered hepatocellular glycogen metabolism.
  • The p53/phosphatase and tensin homolog pathway is a key regulator of glycogen synthesis under pressure.

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