Smooth Muscle Cells: To Be or Not To Be? Response to Nguyen et al
The conversion of contractile vascular smooth muscle cells (SMCs) to a synthetic or proliferative phenotype is thought to play a major role in vascular diseases such as atherosclerosis and restenosis.1-3 Our recent work presents evidence that challenges this widely accepted dogma. Our findings suggest that multipotent vascular stem cells (MVSCs) rather than SMCs are a major contributor to vascular remodeling.4 The experimental results demonstrate that the major population of the traditionally defined "proliferative/synthetic SMCs" is derived from the differentiation of MVSCs rather than the de-differentiation of mature SMCs. Both In vitro and in vivo results suggest that vascular disease is a stem cell disease, which raises the question on the previous dogma: Is vascular disease a SMC disease?
In this issue of Circulation Research, a group of leaders in the area of SMC biology wrote a commentary on this work.5 They present evidence in the literature that seems to support the SMC de-differentiation hypothesis. However, in many previous studies, it was incorrectly assumed that the vascular cells in the primary SMC culture and in injured blood vessels were mostly derived from SMCs. Thus, the previous experimental findings on vascular cells were often attributed to SMCs, which resulted in data misinterpretation and the overstatement on the roles of SMCs. While we agree that further investigations are needed to determine the relative contribution of MVSCs and SMCs to vascular remodeling in various animal models, we respectfully disagree on some of the arguments in the commentary. [Extract]
- Accepted October 18, 2012.
- Copyright © 2012, American Heart Association