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Characterizing medullary and human mesenchymal stem cell-derived adipocytes
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...
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Published in: | Journal of cellular physiology 2006-06, Vol.207 (3), p.722-728 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 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 (PPARγ2, C/EBPα, 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. J. Cell. Physiol. © 2006 Wiley‐Liss, Inc. |
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ISSN: | 0021-9541 1097-4652 |
DOI: | 10.1002/jcp.20617 |