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Abstract
Our objective is to study the relationship between the regulatory proteins Bcl-2/Bax and mitochondria-mediated apoptosis during the differentiation of adipose-derived stromal cells (ADSCs) into neurons. Immunocytochemistry and western blotting showed that the cells weakly expressed neuron-specific enolase (NSE) in the non-induced group and expressed NSE more strongly in the groups induced for 1 h, 3 h, 5 h and 8 h. NSE expression peaked at 5 h (P < 0.05), although there was no significant difference between 5 and 8 h (P > 0.05). Bcl-2 expression gradually decreased over time in the non-induced group (P < 0.05). However, Bax, caspase-9, Cyt-c and caspase-3 expression gradually increased and peaked at 8 h (P < 0.05). Transmission electron microscopy revealed karyopyknosis, chromatin edge setting, mitochondria swelling and cavitation in cells at 5 h, and the mitochondrial membrane potential decreased over time, as demonstrated by laser scanning confocal microscopy. After a 5 h induction, cells differentiated into typical neurons and expressed Bcl-2, which inhibited apoptosis. Bax showed a strong apoptosis-promoting capacity, leading to changes in the mitochondrial membrane potential and structure, and then triggered the caspase-independent apoptotic response through the mitochondrial pathway. At the same time, Cyt-c was directly or indirectly released from the mitochondria to the cytoplasm to trigger the caspase-dependent apoptotic response through the mitochondrial pathway. Therefore, Bcl-2/Bax play an important role in regulating caspase-dependent and caspase-independent apoptosis mediated by the mitochondrial pathway during the differentiation of ADSCs into neurons.
Highlights
When Zuk et al [1,2] successfully isolated and cultured adipose-derived stromal cells (ADSCs) from adult adipose aspirates and found that they could be induced to differentiate into many types of cells from all three germ layers, neurons and astrocytes, it drew considerable attention for two reasons: these cells are easy to obtain, and they exhibit a strong proliferative capacity and low immunogenicity [3,4,5,6]
When ADSCs differentiate into neurons, the caspase-dependent apoptosis mediated by the mitochondria pathway is the main cause of death in the induction process [18]
The results of our experiments showed that adult ADSCs did not express neuron-specific enolase (NSE), a result that was similar to our previous study [7]
Summary
When Zuk et al [1,2] successfully isolated and cultured adipose-derived stromal cells (ADSCs) from adult adipose aspirates and found that they could be induced to differentiate into many types of cells from all three germ layers, neurons and astrocytes, it drew considerable attention for two reasons: these cells are easy to obtain, and they exhibit a strong proliferative capacity and low immunogenicity [3,4,5,6]. The method of differentiating ADSCs into neurons in vitro has gradually matured Certain disadvantages, such as the small number of target cells and the short cell survival time during the differentiation of ADSCs into neurons, have limited the research and application of ADSC-derived neurons [7,8,9,10,11,12,13,14]. Apoptosis is the main cell death mechanism that occurs when ADSCs differentiate into neurons [15] This differentiation involves mitochondrial swelling, cavitation and other ultrastructural changes, suggesting that changes in mitochondrial morphology and function play important roles in the process [16]. Mitochondrial alterations are one of the main pathways regulating Bcl family proteins and caspase-independent apoptosis [17,18]. The role of the mitochondria during the differentiation of ADSCs into neurons and the relationship between the mitochondria and the Bcl-2/Bax apoptosis regulatory proteins are not clear
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