Human Wharton's jelly stem cells inhibit endometriosis through apoptosis induction

Saba Hajazimian1, Masoud Maleki1, Shahla Danaei Mehrabad2

  • 1Department of Genetics, Tabriz Branch, Islamic Azad University, Tabriz, Iran.

Reproduction (Cambridge, England)
|March 11, 2020
PubMed

Insights

Human Wharton's jelly stem cells conditioned medium (hWJSC-CM) and cell-free lysate (hWJSC-CL) show potential in treating endometriosis. These stem cell derivatives were found to inhibit endometriosis cell growth, migration, and invasion while promoting apoptosis.

Area of Science:

  • Reproductive biology
  • Stem cell research
  • Oncology

Background:

  • Endometriosis is characterized by endometrial tumors and stroma, with suppressed apoptosis being a key pathological feature.
  • Human Wharton's jelly stem cells (hWJSCs) are known to inhibit cancer cell growth and proliferation by inducing apoptosis.

Purpose of the Study:

  • To investigate the in vitro effects of hWJSCs conditioned medium (hWJSC-CM) and cell-free lysate (hWJSC-CL) on endometriosis cells.
  • To evaluate the impact of hWJSC-CM and hWJSC-CL on endometriosis cell viability, proliferation, morphology, colony formation, migration, invasion, and apoptosis.

Main Methods:

  • Endometriosis cells were treated with varying concentrations of hWJSC-CM and hWJSC-CL.
  • Assays included viability, proliferation, colony formation, migration, invasion, and apoptosis assessments.
  • Gene expression analysis for MMP-2, MMP-9, BAX, BCL-2, SMAC, and SURVIVIN was performed.

Main Results:

  • hWJSC-CM and hWJSC-CL significantly decreased endometriosis cell viability, proliferation, colony formation, migration, and invasion in a dose- and time-dependent manner.
  • Treatment led to increased morphological alterations and apoptosis in endometriosis cells.
  • Reduced migration and invasion were linked to decreased MMP-2 and MMP-9 expression, while apoptosis induction involved regulation of BAX, BCL-2, SMAC, and SURVIVIN.

Conclusions:

  • hWJSC-CM and hWJSC-CL exhibit potential in inhibiting endometriosis cells through multiple physiological mechanisms, including apoptosis induction and modulation of key gene expressions.
  • Further in vivo studies using animal models are warranted to validate these findings and explore therapeutic applications.

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