Conditioned medium from human adipose-derived mesenchymal stromal cells can modulate cell migration and morphology of keratinocytes in vitro.
Rodrigues C., Paim TC., Zanatelli C., Prignon EVS., Azevedo JG., Naasani LIS.
Laboratory Study on Chronic Wound, published in Hum Cell (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
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- Study type
- Laboratory Study
- Journal
- Hum Cell (2026)
- Country
- Japan
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41629724
- PMCID
- PMC12864314
- DOI
- 10.1007/s13577-026-01353-9
Abstract (original English)
The regenerative ability of the skin is orchestrated by different types of cells, including mesenchymal stromal cells (MSCs). Their role in wound healing is being widely studied due to their capacity to produce a secretome able to modulate their microenvironment. In this context, MSCs factors can be isolated using in vitro cell culture and be experimentally tested for a series of clinical conditions, such as skin repair. In this study, we produced conditioned medium (MSC-CM) using primary cultures from human adipose-derived MSCs. This medium was used as treatment in a culture of keratinocytes cell line from adult human skin (HaCaT) to investigate the modulation of their dynamics. We analyzed cell proliferation, migration, and changes on cell morphology by labeling the actin filaments and nuclei. The factors released by MSCs were able to improve both the proliferation and migration of keratinocytes. In addition, there was an increase in the amount of actin stress fibers, filopodia protrusions, and nuclei irregularities. The MSCs secretome modified the migratory patterns of keratinocytes, being observable through their morphological changes. At least in part, this modulation was caused by the TGF-β1 signaling, considering that its antagonist, SB 431542, lead to a reduction of approximately 76% in the migration of HaCaT cells through the porous membranes of transwell chambers. Tog
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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