The DOI matches its Crossref record; 40 of the 40 references it cites were found in a registry or an index.
Human mesenchymal stem cells stimulated by TNF-α, LPS, or hypoxia produce growth factors by an NFκB- but not JNK-dependent mechanism
Abstract
Understanding the mechanisms by which adult stem cells produce growth factors may represent an important way to optimize their beneficial paracrine and autocrine effects. Components of the wound milieu may stimulate growth factor production to promote stem cell-mediated repair. We hypothesized that tumor necrosis factor-α (TNF-α), endotoxin (LPS), or hypoxia may activate human mesenchymal stem cells (MSCs) to increase release of vascular endothelial growth factor (VEGF), fibroblast growth factor 2 (FGF2), insulin-like growth factor 1 (IGF-1), or hepatocyte growth factor (HGF) and that nuclear factor-κB (NFκB), c-Jun NH 2-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK) mediates growth factor production from human MSCs. To study this, human MSCs were harvested, passaged, divided into four groups (100,000 cells, triplicates) and treated as follows: 1) with vehicle; 2) with stimulant alone [24 h LPS (200 ng/ml), 24 h TNF-α (50 ng/ml), or 24 h hypoxia (1% O 2)]; 3) with inhibitor alone [NFκB (PDTC, 1 mM), JNK (TI-JIP, 10 μM), or ERK (ERK Inhibitor II, 25 μM)]; and 4) with stimulant and the various inhibitors. After 24 h incubation, MSC activation was determined by measuring supernatants for VEGF, FGF2, IGF-1, or HGF (ELISA). TNF-α, LPS, and hypoxia significantly increased human MSC VEGF, FGF2, HGF, and IGF-1 production versus controls. Stem cells exposed to injury demonstrated increased activation of NFκB, ERK, and JNK. VEGF, FGF2, and HGF expression was significantly reduced by NFκB inhibition (50% decrease) but not ERK or JNK inhibition. Moreover, ERK, JNK, and NFκB inhibitor alone did not activate MSC VEGF expression over controls. Various stressors activate human MSCs to increase VEGF, FGF2, HGF, and IGF-1 expression, which depends on an NFkB mechanism.
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Cites
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Cited by
Mesenchymal stromal cell secretome: influencing therapeutic potential by cellular pre-conditioning
Ferreira, J. R., Teixeira, G. Q., Santos, S. G., Barbosa, M. A., Almeida-Porada, G., & Gonçalves, R. M. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.02837 · Cited by 572
Modulation of the Inflammatory Response and Bone Healing
Maruyama, M., Rhee, C., Utsunomiya, T., Zhang, N., Ueno, M., Yao, Z., & Goodman, S. B. (2020) · Frontiers in Endocrinology · doi:10.3389/fendo.2020.00386 · Cited by 541
c-Jun N-terminal kinase (JNK) signaling: Recent advances and challenges
Bogoyevitch, M. A., Ngoei, K. R. W., Zhao, T. T., Yeap, Y. Y. C., & Ng, D. C. H. (2010) · Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics · doi:10.1016/j.bbapap.2009.11.002 · Cited by 323
Suk, K. T., Yoon, J., Kim, M. Y., Kim, C. W., Kim, J. K., Park, H., Hwang, S. G., Kim, D. J., Lee, B. S., Lee, S. H., et al. (2016) · Hepatology · doi:10.1002/hep.28693 · Cited by 303
The wound-healing and antioxidant effects of adipose-derived stem cells
Kim, W.-S., Park, B.-S., & Sung, J.-H. (2009) · Expert Opinion on Biological Therapy · doi:10.1517/14712590903039684 · Cited by 294
Metadata
- Authors
- Crisostomo, P. R., Wang, Y., Markel, T. A., Wang, M., Lahm, T., & Meldrum, D. R.
- Venue
- American Journal of Physiology-Cell Physiology
- Publisher
- American Physiological Society
- Published
- 2008-03
- Volume
- 294
- Issue
- 3
- Pages
- C675-C682
- ISSN
- 0363-6143 (ISSN-L)
- 1522-1563
- OpenAlex
- W2171630160
- Cited by
- 459
- References
- 40
- FWCI
- 12.46
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: Human mesenchymal stem cells stimulated by TNF-α, LPS, or hypoxia produce growth factors by an NFκB- but not JNK-dependent mechanism. https://app.cochat.ai/papers/10.1152/ajpcell.00437.2007
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- Crisostomo, P. R., Wang, Y., Markel, T. A., Wang, M., Lahm, T., & Meldrum, D. R. (2008). Human mesenchymal stem cells stimulated by TNF-α, LPS, or hypoxia produce growth factors by an NFκB- but not JNK-dependent mechanism. American Journal of Physiology-Cell Physiology. https://doi.org/10.1152/ajpcell.00437.2007
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