Increased IGFBP2 Levels by Placenta-Derived Mesenchymal Stem Cells Enhance Glucose Metabolism in a TAA-Injured Rat

Dae-Hyun Lee1,2, Hyeri Park1, Jun-Hyeong You1

  • 1Department of Bioinspired Science, CHA University, Seongnam-si 13488, Republic of Korea.

Insights

Placental-derived mesenchymal stem cells (PD-MSCs) improve ovarian function by enhancing glucose metabolism via the IGFBP2-AMPK pathway. This research highlights a novel therapeutic target for ovarian dysfunction.

Area of Science:

  • Endocrinology
  • Metabolic Research
  • Stem Cell Biology

Background:

  • Impaired glucose metabolism and insulin resistance are linked to ovarian dysfunction.
  • The role of glucose metabolism in ovarian health requires further investigation.

Purpose of the Study:

  • To investigate the effect of placental-derived mesenchymal stem cells (PD-MSCs) on ovarian glucose metabolism via the IGFBP2-AMPK signaling pathway.
  • To explore the correlation between enhanced glucose metabolism and improved ovarian function.

Main Methods:

  • A rat model of ovarian injury was induced using thioacetamide (TAA).
  • PD-MSCs were transplanted into rats, and key gene and protein expressions (IGFBP2, AMPK, GLUT4) were analyzed.
  • Ex vivo cocultivation experiments were performed to validate the effects of PD-MSCs and recombinant proteins.

Main Results:

  • PD-MSC transplantation significantly increased IGFBP2, AMPK, and GLUT4 expression compared to controls.
  • Follicular development markers and sex hormone levels (AMH, FSH, E2) were elevated in the PD-MSC group.
  • Cocultivation confirmed that PD-MSCs and recombinant proteins upregulate IGFBP2-AMPK signaling and glucose metabolism factors.

Conclusions:

  • PD-MSCs enhance ovarian glucose metabolism and function through the IGFBP2-AMPK signaling pathway.
  • Increased IGFBP2 levels are crucial for mediating these beneficial effects.
  • This pathway represents a potential therapeutic target for ovarian dysfunction related to metabolic disturbances.

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