Benzo(a)pyrene Exposure Suppressed Osteogenic and Adipogenic Differentiation of Human Bone Marrow-Derived Mesenchymal Stem Cells and Was Associated with Senescence-like Response
5 affiliations
- 1Research Unit in Nutraceuticals and Food Safety, Faculty of Medicine, Thammasat University, Pathumthani 12120, Thailand
- 2Division of Cell Biology, Department of Preclinical Science, Faculty of Medicine, Thammasat University, Pathumthani 12120, Thailand
- 3Division of Biochemistry, Department of Preclinical Science, Faculty of Medicine, Thammasat University, Pathumthani 12120, Thailand
- 4Faculty of Allied Health Sciences, Burapha University, Chonburi 20131, Thailand
- 5Division of Anatomy, Department of Preclinical Science, Faculty of Medicine, Thammasat University, Pathumthani 12120, Thailand
Abstract
Human exposure to benzo(a)pyrene [B(a)P] from contaminated environmental pollutants may induce cellular senescence. Mesenchymal stem cells (MSCs) are responsible for maintaining bone homeostasis, mineralization and integrity. Senescent MSCs may result from exogenous chemical exposure, leading to diminished osteogenic potential and increased bone loss. This study elucidated the toxicological effects of B(a)P exposure in human bone marrow-derived MSCs (BM-hMSCs) under induced osteogenic and adipogenic differentiation by in vitro testing and transcriptomic analyses. Cell viability assays following 1–20 µM of B(a)P showed no toxic effects after 24 to 72 h of exposure. Non-cytotoxic concentrations of B(a)P (1–20 µM) suppressed the differentiation of BM-hMSCs into osteogenic and adipogenic lineages over 7 to 21 days, as indicated by reduced phenotypic parameters and molecular expression of differentiation markers compared with differentiation-induced cells. B(a)P decreased osteoblastic proliferation of signaling Wnt/β-catenin, with increased AhR/AhRR expression, which is related to osteogenic damage. Furthermore, B(a)P increased the expression of senescence markers, includingintracellular β-galactosidase, p21 and the secretory markers IL-1β and IL-6, in osteogenic-differentiated BM-hMSCs. The transcriptomic profile of osteogenic-differentiated BM-hMSCs exposed to 10 µM of B(a)P for 21 days revealed upregulation of stress and inflammatory responses, along with downregulation of cell cycle regulation and genes associated with cellular integrity. RNA-seq profiles also revealed upregulation of senescence-associated markers. Collectively, B(a)P may impair their differentiation capacity and is associated with senescence induction, partly through AhR activation. This study highlights the implications for skeletal health risk of chronic exposure to environmental pollutants by detection of senescent-associated markers.
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BibTeX
@article{jantakee2026benzoapyrene,
title = {{Benzo(a)pyrene Exposure Suppressed Osteogenic and Adipogenic Differentiation of Human Bone Marrow-Derived Mesenchymal Stem Cells and Was Associated with Senescence-like Response}},
author = {Kanyaluck Jantakee and Duangrat Tantikanlayaporn and Chawalit Ngernsombat and Tanapan Siangcham and Kant Sangpairoj},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = nov,
doi = {10.3390/ijms272110026},
url = {https://www.mdpi.com/1422-0067/27/21/10026},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Benzo(a)pyrene Exposure Suppressed Osteogenic and Adipogenic Differentiation of Human Bone Marrow-Derived Mesenchymal Stem Cells and Was Associated with Senescence-like Response
AU - Kanyaluck Jantakee
AU - Duangrat Tantikanlayaporn
AU - Chawalit Ngernsombat
AU - Tanapan Siangcham
AU - Kant Sangpairoj
PY - 2026
DA - 2026/11/09
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms272110026
UR - https://www.mdpi.com/1422-0067/27/21/10026
AB - Human exposure to benzo(a)pyrene [B(a)P] from contaminated environmental pollutants may induce cellular senescence. Mesenchymal stem cells (MSCs) are responsible for maintaining bone homeostasis, mineralization and integrity. Senescent MSCs may result from exogenous chemical exposure, leading to diminished osteogenic potential and increased bone loss. This study elucidated the toxicological effects of B(a)P exposure in human bone marrow-derived MSCs (BM-hMSCs) under induced osteogenic and adipogenic differentiation by in vitro testing and transcriptomic analyses. Cell viability assays following 1–20 µM of B(a)P showed no toxic effects after 24 to 72 h of exposure. Non-cytotoxic concentrations of B(a)P (1–20 µM) suppressed the differentiation of BM-hMSCs into osteogenic and adipogenic lineages over 7 to 21 days, as indicated by reduced phenotypic parameters and molecular expression of differentiation markers compared with differentiation-induced cells. B(a)P decreased osteoblastic proliferation of signaling Wnt/β-catenin, with increased AhR/AhRR expression, which is related to osteogenic damage. Furthermore, B(a)P increased the expression of senescence markers, includingintracellular β-galactosidase, p21 and the secretory markers IL-1β and IL-6, in osteogenic-differentiated BM-hMSCs. The transcriptomic profile of osteogenic-differentiated BM-hMSCs exposed to 10 µM of B(a)P for 21 days revealed upregulation of stress and inflammatory responses, along with downregulation of cell cycle regulation and genes associated with cellular integrity. RNA-seq profiles also revealed upregulation of senescence-associated markers. Collectively, B(a)P may impair their differentiation capacity and is associated with senescence induction, partly through AhR activation. This study highlights the implications for skeletal health risk of chronic exposure to environmental pollutants by detection of senescent-associated markers.
SN - 1422-0067
ER -