#1: Effects of molecule X in spinal cord injury. We found that molecule X, regulates the expression of several proteases and induces lesion remodeling, but the survival rate and distribution of transplanted neural stem cells are unchanged, which led us to abandon this research theme.
#2 The characterization of the gene expression profile of lesion scar-forming reactive astrocytes has been reported by another Japanese research group (Hara M. et al., Nature Medicine, 2017 Jul;23(7):818-828) before we could complete our own study.
#3: We found that the transcription factor STAT3 regulates the dynamics of reactive astrocytes in vitro and glial scar formation in vivo. We have shown that regulation of the GTPase RhoA by STAT3 modulates glial scar formation in vivo. This study is published in the Journal of Cell Biology (Renault-Mihara et al., 2017, PMID: 28642362).
#4: Central nervous system healing mechanisms. Two different experimental models were used to characterize novel markers of pathological nerve scars. This marker is not seen in simulated animals. Interestingly, this marker is also expressed in wild-type mice in the chronic phase of spinal cord injury, which may indicate that this marker is useful in the study of the incomplete healing that characterizes neural tissue. By comparing gene expression levels in these different models, we are trying to identify candidate genes responsible for the emergence of this marker. Our hypothesis is that these genes may be associated with incomplete healing in the central nervous system. This study is still in progress.