# Mesenchymal Stem Cell–Conditioned Media Modulate HUVEC Response to H2O2: Impact on Gene Expression and Potential for Atherosclerosis Intervention

**Authors:** Abdulmajeed Alqasoumi, Mansour Alsharidah, Amer Mahmood, Mona Elsafadi, Osamah Al Rugaie, Khalid M. Mohany, Khalid A. Al-Regaiey, Khaleel I. Alyahya, Alaa A. Alanteet, Norah K. Algarzae, Hanan K. AlGhibiwi, Adel AlHomaidi, Mohammad Abumaree

PMC · DOI: 10.1155/2024/7726493 · 2024-07-17

## TL;DR

This study shows that mesenchymal stem cell media can protect blood vessel cells from oxidative stress and reduce inflammation, which may help treat atherosclerosis.

## Contribution

The novel contribution is demonstrating how hBMSC CM modulates gene expression and protects HUVECs under oxidative stress, offering new insights for atherosclerosis intervention.

## Key findings

- hBMSC CM improved HUVEC viability, proliferation, and migration under oxidative stress.
- The conditioned media modulated inflammatory-related gene expression in HUVECs.

## Abstract

Background: We studied the potential of human bone marrow–derived mesenchymal stem cell conditioned media (hBMSC CM) in protecting endothelial cell properties (viability, proliferation, and migrations) from the deleterious effects produced by the inflammatory environment of H2O2. Additionally, we investigated their impact on the endothelial cells' gene expression of some inflammatory-related genes, namely, TGF-β1, FOS, ATF3, RAF-1, and SMAD3.

Methods: Human umbilical vein endothelial cells (HUVECs) were cultured individually under three conditions: alone, with varying concentrations of H2O2, or with varying concentrations of H2O2 and hBMSC CM. HUVEC adhesion, proliferation, and migration were evaluated using the xCELLigence system. The HUVECs' gene expressions were evaluated by real-time polymerase chain reaction (RT–PCR).

Results: Generally, we observed enhanced HUVEC viability, proliferation, and migration when cultured in media supplemented with H2O2 and hBMSC CM. Furthermore, the CM modulated the expressions of the studied inflammatory-related genes in HUVECs, promoting a more robust cellular response.

Conclusion: This study has illuminated the protective role of hBMSC CM in mitigating the damaging effects of H2O2 on endothelial cell function. Our data demonstrate that hBMSC CM enhances the viability, proliferation, and migration of HUVECs even under oxidative stress conditions. Additionally, the conditioned medium was found to modulate the gene expression of pivotal markers related to inflammation, suggesting a favorable influence on cellular response mechanisms.

## Linked entities

- **Genes:** TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040], FOS (Fos proto-oncogene, AP-1 transcription factor subunit) [NCBI Gene 2353], ATF3 (activating transcription factor 3) [NCBI Gene 467], RAF1 (Raf-1 proto-oncogene, serine/threonine kinase) [NCBI Gene 5894], SMAD3 (SMAD family member 3) [NCBI Gene 4088]
- **Chemicals:** H2O2 (PubChem CID 784)
- **Diseases:** atherosclerosis (MONDO:0005311)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** FOS (Fos proto-oncogene, AP-1 transcription factor subunit) [NCBI Gene 2353] {aka AP-1, C-FOS, p55}, SMAD3 (SMAD family member 3) [NCBI Gene 4088] {aka HSPC193, HsT17436, JV15-2, LDS1C, LDS3, MADH3}, ATF3 (activating transcription factor 3) [NCBI Gene 467], RAF1 (Raf-1 proto-oncogene, serine/threonine kinase) [NCBI Gene 5894] {aka CMD1NN, CRAF, NS5, Raf-1, c-Raf}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}
- **Diseases:** Atherosclerosis (MESH:D050197), inflammation (MESH:D007249)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11268959/full.md

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Source: https://tomesphere.com/paper/PMC11268959