Spinal cord injury (SCI) results in neural loss and consequently motor and sensory impairment below the injury. There are currently no effective therapies for the treatment of traumatic SCI in humans. Different kinds of cells including embryonic, fetal, and adult stem cells have been transplanted into animal models of SCI resulting in sensorimotor benefits. Transplantation of human embryonic stem cell (hESC)-or induced pluripotent stem cell (hiPSC)-derived neural cells is nowadays a promising therapy for SCI. This review updates the recent progress in preclinical studies and discusses the advantages and flaws of various neural cell types derived from hESCs and hiPSCs. Before introducing the stem cell replacement strategies in clinical practice, this complex field needs to advance significantly in understanding the lesion itself, the animal model adequacy, and improve cell replacement source. This knowledge will contribute to the successful translation from animals to humans and lead to established guidelines for rigorous safety screening in order to be implemented in clinical practice.

1 Mesangial cells play an active role in the in¯ammatory response to glomerular injury. We have studied in cultured human mesangial cells (CHMC) several eects of 9-cis retinoic acid (9-cRA), an activator of both retinoic acid receptors (RARs) and retinoid X receptors (RXRs). 2 9-cRA inhibited foetal calf serum-induced CHMC proliferation. It also prevented CHMC death induced by the in¯ammatory mediator H 2 O 2 . This preventive eect was not due to any increase in H 2 O 2 catabolism and it persisted even when both catalase and glutathione synthesis were inhibited. Finally, 9-cRA diminished monocyte adhesion to FCS-stimulated CHMC. Interestingly, the retinoid also inhibited in FCS-stimulated cells the protein expression of two mesangial adhesion molecules, ®bronectin and osteopontin, but it did not modify the protein expression of intercellular adhesion molecule-1 and vascular adhesion molecule-1. 3 All major RARs and RXRs isotypes were expressed in CHMC regardless of the presence or absence of 9-cRA. Transcripts to RAR-a, RAR-b and RXR-a increased after incubation with 9-cRA whereas RXR-g was inhibited, suggesting a major role for RARs and RXRs in 9-cRA-antiin¯ammatory eects. 4 9-cRA was toxic only at 50 mM (a concentration 50 ± 5000 times higher than required for the eects above). Cell death occurred by apoptosis, whose onset was associated with a pronounced increase in catalase activity and reduced glutathione content, being more eectively induced by alltrans retinoic acid. Modulation of the oxidant/antioxidant balance failed to inhibit apoptosis. 5 We conclude that mesangial cells might be a target for the treatment of in¯ammatory glomerulopathies with 9-cRA.

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