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Reviewer #1: The authorstried to show the involvement of mir-145 for CD-137 induced migration ofvascular smooth muscle cells. The concept is too complex and data qualityis not good. Composition of manuscript is not good. Manuscript included the manyof type-miss, mixed with some non-english characters.
1) Authors mentioned CD-137 down-regulate mir145, which leaded to down regulation of NFATc1 but In Fig 2A the expression ofNFATc1 with CD137 is very small. Data quality is not generally good, thus, I donot recommend the manuscript for publication.
Reviewer #2: Yan et alshowed that CD137 accelerated neointima formation and VSMCs proliferation andmigration in vivo and in vitro. Mechanistically, miR145 was downregulated andresulted in increased NFATc1 expression in VSMCs upon treatment with agonisticCD137 antibody. To investigate why VSMCs phenotype transformed, the authorsshowed that overexpression of miR145 or NFATc1 deficiency could rescue the VSMCtransformation led by CD137. This is a well design and performed manuscript.There will be interesting for the readers of JMCC. However, this manuscript canbe strengthened with the following revision:
Major comments
Reviewer #3: The study byYan et al. showed that CD137, a protein belonging to the TNF superfamily,induces vascular smooth muscle cell dedifferentiation through down regulatingmiR-145 and up-regulating NFATc1. Previously many reports showed that miR-145could modulate the fate of smooth muscle cells In this study, the authorsshowed that miR-145 targets NFATc1 mRNA to reduces its expression, which is anovel finding. In general, the study design is logic and the data aresupporting the hypothesis. However, there are multiple issues with the study:
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