Adipose tissue engineering with cells in engineered matrices

Abstract

Tissue engineering has shown promise for the development of constructs to facilitate large volume soft tissue augmentation in reconstructive and cosmetic plastic surgery. This article reviews the key progress to date in the field of adipose tissue engineering. In order to effectively design a soft tissue substitute, it is critical to understand the native tissue environment and function. As such, the basic physiology of adipose tissue is described and the process of adipogenesis is discussed. In this article, we have focused on tissue engineering using a cell-seeded scaffold approach, where engineered extracellular matrix substitutes are seeded with exogenous cells that may contribute to the regenerative response. The strengths and limitations of each of the possible cell sources for adipose tissue engineering, including adipose-derived stem cells, are detailed. We briefly highlight some of the results from the major studies to date, involving a range of synthetic and naturally derived scaffolds. While these studies have shown that adipose tissue regeneration is possible, more research is required to develop optimized constructs that will facilitate safe, predictable and long-term augmentation in clinical applications.

Keywords: adipogenesis; adipose tissue; adipose-derived stem cells; cell culture; cell-biomaterial interactions; regenerative medicine; scaffolds; tissue engineering.

Figure 1

Overview of the differentiation of human ASC into mature adipocytes. The detectable markers associated with the various stages of differentiation are highlighted (LPL = lipoprotein lipase; α₂Col6 = alpha 2 chain of collagen type VI; FAT = fatty acid translocase; FAS = fatty acid synthase; aP2 = fatty acid binding protein; Glut4 = glucose transporter-4; GPDH = glycerol-3-phosphate dehydrogenase; HSL = hormone sensitive lipase).

Figure 2

Transcriptional events in adipogenic differentiation. The diagram highlights the critical role of multiple transcription factors in adipogenesis. Arrows generally indicate a stimulatory interaction (with the exception of TNFα and leptin). After ligand binding with either endogenous ligands or TZD, PPARγ binds as a heterodimer with retinoid X receptor (RXR) to PPAR response elements (PPRE) in the transcriptional regulatory regions of the target genes. Insulin R., Insulin Receptor.