Characterizing medullary and human mesenchymal stem cell-derived adipocytes.
Mackay DL., Tesar PJ., Liang LN., Haynesworth SE.
Laboratory Study, published in J Cell Physiol (2006) — 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
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- J Cell Physiol (2006)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 16482529
- DOI
- 10.1002/jcp.20617
Abstract (original English)
Throughout postnatal years, medullary adipocytes (MAs) increase in both number and size; however, knowledge of these cells pales in comparison to that of other adipocyte depots. It is widely hypothesized that MAs derive from multipotent progenitor cells of the bone marrow, such as human mesenchymal stem cells (hMSCs). Nevertheless, there is a paucity of comparative, molecular-level studies in support of this hypothesis. In the present article, RTPCR was used to examine similarities and differences in gene expression among MAs, hMSC-derived adipocytes, and subcutaneous adipocytes. While little or no message for lineage-specific markers was detected in undifferentiated hMSCs, the data demonstrate that hMSC-derived adipocytes, MAs, and subcutaneous adipocytes commonly express mRNA encoding for adipogenic transcription factors (PPARgamma2, C/EBPalpha, and SREBP1), adipokines (adipsin, leptin, APM1, and angiotensinogen), and lipid-metabolizing agents (aP2 and LPL), among other genes. None of the cell populations examined expressed a detectable level of the brown fat marker UCP1. This suggests highly similar gene expression between human subcutaneous and MAs, not previously substantiated to this degree. Coupled with the hMSC-derived adipocyte analysis, these data provide a framework ultimately for characterizing MAs and identifying their origin and function.
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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