On 2016 Apr 07, Angelo Calderone commented:

The paper by Tamura and colleagues has provided the interesting observation that a subpopulation of cardiac resident neural crest-derived stem cells differentiated to an adrenergic phenotype following heterotopic transplantation of the mouse heart. Previous work from this lab (JBC 2005) reported that cardiac resident neural-crest derived stem cells grew as spheres in the presence of EGF and FGF2, expressed nestin, musashi-1 and differentiated to a neuronal phenotype in vitro. Work from our lab has likewise revealed the presence of neural crest-derived stem cells in the rodent heart and expressed nestin (El-Helou et al, 2008, J Molecular Cellular Cardiology). Furthermore, nestin(+)-cells isolated from the scar of the infarcted heart grew as spheres when cultured in EGF/FGF2 and differentiated to a neuronal phenotype in vitro (El-Helou et al, 2008, J Molecular Cellular Cardiology). Furthermore, work from our lab has reported that a subpopulation of nestin(+)-cells in the infarct region expressed neurofilament-M and contributed in part to the reported innervation of the scar (Beguin et al, 2011, J Cellular Physiology; Chabot et al, 2013 Cardiovascular Diabetology). Moreover, we further demonstrated that following isogenic heterotopic transplantation of the rat heart, the superimposition of an ischemic injury to the transplanted heart led to de novo cardiac innervation mediated by the expression of neurofilament-M by nestin(+)-cells (Beguin et al, 2011, J Cellular Physiology). However, we did not further assess whether these nestin(+)-cells that expressed neurofilament-M in the ischemically damaged transplanted heart acquired an adrenergic phenotype. Thus, in the true spirit of scientific research, the paper by Tamura and colleagues should have cited previous work from our lab that recapitulated in part the findings provided in their recent paper published in Cardiovascular Research.

On 2016 Apr 07, Angelo Calderone commented:

The paper by Tamura and colleagues has provided the interesting observation that a subpopulation of cardiac resident neural crest-derived stem cells differentiated to an adrenergic phenotype following heterotopic transplantation of the mouse heart. Previous work from this lab (JBC 2005) reported that cardiac resident neural-crest derived stem cells grew as spheres in the presence of EGF and FGF2, expressed nestin, musashi-1 and differentiated to a neuronal phenotype in vitro. Work from our lab has likewise revealed the presence of neural crest-derived stem cells in the rodent heart and expressed nestin (El-Helou et al, 2008, J Molecular Cellular Cardiology). Furthermore, nestin(+)-cells isolated from the scar of the infarcted heart grew as spheres when cultured in EGF/FGF2 and differentiated to a neuronal phenotype in vitro (El-Helou et al, 2008, J Molecular Cellular Cardiology). Furthermore, work from our lab has reported that a subpopulation of nestin(+)-cells in the infarct region expressed neurofilament-M and contributed in part to the reported innervation of the scar (Beguin et al, 2011, J Cellular Physiology; Chabot et al, 2013 Cardiovascular Diabetology). Moreover, we further demonstrated that following isogenic heterotopic transplantation of the rat heart, the superimposition of an ischemic injury to the transplanted heart led to de novo cardiac innervation mediated by the expression of neurofilament-M by nestin(+)-cells (Beguin et al, 2011, J Cellular Physiology). However, we did not further assess whether these nestin(+)-cells that expressed neurofilament-M in the ischemically damaged transplanted heart acquired an adrenergic phenotype. Thus, in the true spirit of scientific research, the paper by Tamura and colleagues should have cited previous work from our lab that recapitulated in part the findings provided in their recent paper published in Cardiovascular Research.