## Abstract Migration of chondrocytes and mesenchymal stem cells (MSCs) may be important in cartilage development, tissue response to injury, and in tissue engineering. This study analyzed growth factors and cytokines for their ability to induce migration of human articular chondrocytes and bone ma
Characterizing medullary and human mesenchymal stem cell-derived adipocytes
✍ Scribed by Danielle L. MacKay; Paul J. Tesar; Li-Nuo Liang; Stephen E. Haynesworth
- Publisher
- John Wiley and Sons
- Year
- 2006
- Tongue
- English
- Weight
- 356 KB
- Volume
- 207
- Category
- Article
- ISSN
- 0021-9541
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
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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