Polyamine and aminoguanidine treatments to promote structural and functional recovery in the adult mammalian brain after injury: A brief literature review and preliminary data about their combined administration

Biphasic Role of Tgf-β Signaling during Müller Glia Reprogramming and Retinal Regeneration in Zebrafish

“…In an injured mammalian retina, the MG cells often fail to elicit an adequate regenerative response to restore vision. It is believed that mammalian retina mounts an inhibitory environment through various cytokines and growth factors to prevent the growth of new nervous tissue (Liu et al, 2008;Schimchowitsch and Cassel, 2006). In zebrafish, the scenario is the opposite, where the vision is restored after an acute injury through retinal regeneration.…”

The effects of erythropoietin on RhoA/Rho-associated kinase expression in rat retinal explants cultured with glutamate

“…Three types of molecules derived from myelin which can suppress axon growth have been identified thus far: Nogo-A, myelin-associated glycoprotein (MAG) and oligodendrocyte-myelin glycoprotein (Omgp) (1). Previous studies indicate that Nogo-A, MAG and Omgp may activate Rho by common or different pathways and subsequently cause growth cone collapse (33,34).…”

Regulation of axonal regeneration following the central nervous system injury in adult mammalian

“…In addition, a recent study indicated that some key proteins, such as Rho and PKC, were implicated in NgR-mediated signaling cascades, and elucidated the implications of cAMP and Arginase I in overcoming the growth-inhibitory influence of myelin. This suggests that their association might be a potent way to enable the functional-relevant regeneration in adult mammalian CNS [2] .…”

“…Investigation in this field is beginning to blossom. Some researchers blocked Nogo-A Similarly, MAG has been targeted to antagonize the known receptors and to inhibit the intracellular signal transduction of these inhibitory molecules [2] . In addition, a recent study indicated that some key proteins, such as Rho and PKC, were implicated in NgR-mediated signaling cascades, and elucidated the implications of cAMP and Arginase I in overcoming the growth-inhibitory influence of myelin.…”

“…It is now known that the failure of adult axons to regenerate is not exclusively due to neurons' intrinsic and irreversible lack of regenerative ability, but is largely attributable to the presence of an inhibitory cellular environment [2] . Thus, adult neurons are not only able to sprout new axonal or dendritic branches in response to various changes of their environment, but also have a genuine endogenous ability to regenerate after lesion formation.…”