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Updated: Sep 29, 2025

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
Mechanical signals induces reprogramming of mature adipocytes through the YAP/TAZ-binding motif
Lan Liu1, Xingke Liu1, Mengchang Liu1
1Department of Plastic and Burn Surgery, Affiliated Hospital of Southwest Medical University, National Key Clinical Construction Specialty, Wound Repair and Regeneration Laboratory, Luzhou, Sichuan Province, 646000, No. 25 Taiping Street, Jiangyang District, Luzhou, Sichuan Province, China.
Abstract:
Tissue engineering technology will be the main approach to tissue regeneration in the future and are promising for the treatment of large-area burns and refractory wounds. Dedifferentiated fat cells (DFAT) derived from mature adipocytes (MAs) as a seed cell have great potential in cell therapy and tissue engineering for the treatment of a variety of clinical diseases because of their wider availability, stronger proliferation ability, multidirectional redifferentiation potential, higher cell purity, lower heterogeneity, and greater biosafety profile. However, the triggering mechanism for MAs reprogramming in vitro is unclear. In this study, MAs were successfully induced to dedifferentiate into DFAT in a short time in vitro using an "improved ceiling culture method". Flow cytometry, adipogenic, and osteogenic differentiation experiments verified that DFAT cells present the biological characteristics of stem cells. In addition, changing the stiffness of the extracellular matrix can inhibit the dedifferentiation of MAs to DFAT, and increase the expression of Yes-associated protein/transcriptional co-activator with the PDZ-binding motif (YAP/TAZ), nuclear translocation, and the expression of reprogramming transcription factors. In conclusion, extracellular matrix stiffness can induce MAs to dedifferentiate into DFAT in vitro, and can directly transmit mechanical force signals to the nucleus via YAP/TAZ binding to trigger the expression of stem cell-related reprogramming factors.
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