Adipose-derived stem cells (ASCs) are being explored as a potential therapy for type 2 diabetes (T2D) due to their regenerative properties. However, recent findings suggest that the adrenergic α2 receptor (Adra2α) may be important in regulating ASC function in diabetic conditions.
A study published in Stem Cell Research & Therapy investigated the effects of Adra2α on ASC behavior and its impact on T2D treatment. Researchers found that ASCs from T2D mice exhibited higher Adra2α expression compared to healthy controls, potentially limiting their therapeutic effectiveness.
To examine this further, the study utilized clonidine (an Adra2α agonist) and siRNA-mediated knockdown of Adra2α in ASCs. Activation of Adra2α with clonidine led to a reduction in ASC proliferation, migration, and secretion of key growth factors, including hepatocyte growth factor (HGF), transforming growth factor β1 (TGF-β1), and vascular endothelial growth factor (VEGF). Conversely, knocking down Adra2α expression enhanced these functions.
When transplanted into T2D mice, ASCs with suppressed Adra2α expression demonstrated improved therapeutic effects. Mice receiving these modified ASCs showed better glucose regulation, increased insulin sensitivity, reduced fat accumulation in adipose and liver tissues, lower systemic inflammation, and higher pancreatic β-cell mass compared to controls.
These results suggest that Adra2α plays a significant role in regulating ASC function in diabetes. Suppressing Adra2α expression could enhance ASC-based therapies by improving their regenerative potential.
