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Interleukin 21 Receptor Affects Adipogenesis of Human Adipose-Derived Stem/Stromal Cells
Bruna Cristina Falavinha1, María Julia Barisón1, Carmen Lúcia Kuniyoshi Rebelatto2
1Laboratory for Basic Biology of Stem Cells (LABCET), Instituto Carlos Chagas-FIOCRUZ-PR, Curitiba, Paraná 81830-010, Brazil.
Abstract:
Dysfunctions in adipose tissue cells are responsible for several obesity-related metabolic diseases. Understanding the process of adipocyte formation is thus fundamental for understanding these diseases. The adipocyte differentiation of adipose-derived stem/stromal cells (ADSCs) showed a reduction in the mRNA level of the interleukin 21 receptor (IL21R) during this process. Although the receptor has been associated with metabolic diseases, few studies have examined its function in stem cells. In this study, we used confocal immunofluorescence assays to determine that IL21R colocalizes with mitochondrial protein ATP5B, ALDH4A1, and the nucleus of human ADSCs. We demonstrated that silencing and overexpression of IL21R did not affect the cell proliferation and mitochondrial activity of ADSCs. However, IL21R silencing did reduce ADSC adipogenic capacity. Further studies are needed to understand the mechanism involved between IL21R and the adipogenic differentiation process.
Insights
Interleukin 21 receptor (IL21R) plays a crucial role in adipocyte formation. Silencing IL21R in adipose-derived stem cells reduced their ability to differentiate into fat cells, impacting obesity-related diseases.
Area of Science:
- Cell Biology
- Metabolic Diseases
- Stem Cell Research
Background:
- Adipose tissue dysfunction is linked to metabolic diseases.
- Adipocyte differentiation is key to understanding these conditions.
- Interleukin 21 receptor (IL21R) is implicated in metabolic diseases but its role in stem cells is understudied.
Purpose of the Study:
- To investigate the function of IL21R in human adipose-derived stem/stromal cells (ADSCs).
- To determine the effect of IL21R on ADSC adipogenic differentiation.
Main Methods:
- Confocal immunofluorescence assays to assess IL21R localization.
- IL21R gene silencing and overexpression in ADSCs.
- Assessment of cell proliferation, mitochondrial activity, and adipogenic capacity.
Main Results:
- IL21R was found to colocalize with mitochondrial proteins (ATP5B, ALDH4A1) and the nucleus in human ADSCs.
- IL21R modulation did not impact ADSC proliferation or mitochondrial activity.
- Silencing IL21R significantly reduced the adipogenic capacity of ADSCs.
Conclusions:
- IL21R is important for adipogenic differentiation of ADSCs.
- The precise mechanism linking IL21R to adipogenesis requires further investigation.
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