Endogenous Adipocyte Precursor Cells for Regenerative Soft-Tissue Engineering

Toriyama, Kazuhiro; Kawaguchi, Nobuko; Kitoh, Junzou; Tajima, Rie; Inou, Kazuhiko; Kitagawa, Yasuo; Torii, Shuhei

doi:10.1089/107632702753503144

Cited by 71 publications

(42 citation statements)

References 20 publications

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“…31 Angiogenesis and adipogenesis are closely related during fetal development 35 and in adult neoadipogenesis. 3,36,37 From our results, one could argue that macrophages only play a direct role in angiogenesis in the tissue engineering model and that the perceived neoadipogenesis is simply a result of increased angiogenesis, without further involvement of macrophages. There are, however, arguments for macrophages playing a role in the adipogenesis process as well.…”

Section: Debels Et Almentioning

confidence: 77%

Macrophages Play a Key Role in Angiogenesis and Adipogenesis in a Mouse Tissue Engineering Model

Debels

Galea

Han

et al. 2013

Tissue Engineering Part A

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We have previously described a mouse adipose tissue engineering model using a silicon chamber enclosing the superficial epigastric pedicle in a Matrigel based environment. We have shown that when Zymosan, a sterile inflammatory agent, is added to the chamber, angiogenesis and adipogenesis are significantly improved. As Zymosan interacts with toll-like receptors on macrophages, the role of macrophages in new tissue development in the tissue engineering chamber was assessed. Morphological and histological results showed that macrophages were presenting in high numbers at 2 weeks but had decreased significantly by 4 and 6 weeks in the chamber. Numerous immature new blood vessels had formed by 2 weeks, becoming more mature at 4 and 6 weeks. Immature adipocytes were visualized at 4 weeks and mature cells, at 6 weeks. To investigate the functional role of macrophages in the tissue engineering process, we knocked out the local macrophage population by inserting Clodronate liposomes in this chamber. This study shows for the first time that when macrophages are depleted, there is minimal new vascular and adipose tissue development. We propose a new theory for tissue engineering in which macrophages play a central role in both neovascularisation and adipogenesis.

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Section: Debels Et Almentioning

confidence: 77%

Macrophages Play a Key Role in Angiogenesis and Adipogenesis in a Mouse Tissue Engineering Model

Debels

Galea

Han

et al. 2013

Tissue Engineering Part A

View full text Add to dashboard Cite

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“…Many of these same proteins have been detected in the proteome of mature 3T3-L1 adipocytes (38,39). The mature adipocyte contains an increased number of mitochondria in comparison to fibroblastic cells (40). Recent studies link mitochondrial biogenesis to the etiology of diabetes, and it is postulated that the thiazolidinediones, oral antidiabetic drugs and peroxisome proliferator-activated receptor ␥ ligands, may act in part by regulating mitochondrial formation especially in brown adipose tissue (39,41).…”

Section: Resultsmentioning

confidence: 99%

Proteomic Analysis of Primary Cultures of Human Adipose-derived Stem Cells

DeLany

Floyd

Zvonic

et al. 2005

Molecular & Cellular Proteomics

132

128

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Adipogenesis plays a critical role in energy metabolism and is a contributing factor to the obesity epidemic. This study examined the proteome of primary cultures of human adipose-derived adult stem (ADAS) cells as an in vitro model of adipogenesis. Protein lysates obtained from four individual donors were compared before and after adipocyte differentiation by two-dimensional gel electrophoresis and tandem mass spectroscopy. Over 170 individual protein features in the undifferentiated adipose-derived adult stem cells were identified. Following adipogenesis, over 40 proteins were up-regulated by >2-fold, whereas 13 showed a >3-fold reduction. The majority of the modulated proteins belonged to the following functional categories: cytoskeleton, metabolic, redox, protein degradation, and heat shock protein/chaperones. Additional immunoblot analysis documented the induction of four individual heat shock proteins and confirmed the presence of the heat shock protein 27 phosphoserine 82 isoform, as predicted by the proteomic analysis, as well as the crystallin ␣ phosphorylated isoforms. These findings suggest that the heat shock protein family proteome warrants further investigation with respect to the etiology of obesity and type 2 diabetes. Molecular & Cellular Proteomics 4:731-740, 2005.Obesity is a health problem of epidemic proportions. It is estimated that in 2000 over 60% of adults are overweight (BMI 1 Ͼ 25) and that 30% are obese (BMI Ͼ 30); this compares to levels of 46 and 14%, respectively, in 1980. Obesity and increased adiposity are associated clinically with the onset of insulin resistance, dysfunctional glucose sensing and utilization, hypertension, and hypertriglyceridemia, all contributing to the pathologic sequelae of type 2 diabetes. Paradoxically type 2 diabetes also occurs in patients with inherited or acquired forms of lipodystrophy or loss of adipose tissue depots (1, 2). Lipodystrophy occurs through defects in genes associated with triglyceride metabolism or as a consequence of antiretroviral therapy in human immunodeficiency viruspositive patients (1, 2). Animal models confirm these clinical observations; multiple strains of transgenic mice with a lipodystrophic phenotype exhibit type 2 diabetes (3-5). Diabetes in these animals responds not to insulin therapy but to transplantation of subcutaneous adipose tissue or to leptin treatment (3-5). These clinical and experimental observations have led to the hypothesis that a failure in adipocyte differentiation is a critical etiologic factor leading to type 2 diabetes (6 -8). Danforth (6) and others postulate that in obese individuals adipose tissue depots have already committed all of their stem cell reserves to the adipocyte lineage and have lost their capacity to create new adipocytic cells (6 -8). In the face of excess energy balance, both obese and lipodystrophic individuals deposit triglycerides in ectopic sites, such as muscle and liver, thereby contributing to the metabolic dysfunction associated with type 2 diabetes (increased hepatic glucon...

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“…The rationale for selecting bFGF over VEGF is primarily because that bFGF promotes both angiogenesis and adipogenesis. 33,39,40 In addition, bFGF and VEGF promote different phases of engineered angiogenesis.45…”

Section: Methodsmentioning

confidence: 99%