Delayed olfactory ensheathing cell transplants reduce nociception after dorsal root injury.

Injury to cervical dorsal roots mimics the deafferentation component of brachial plexus injury in humans, with intractable neuropathic pain in the deafferented limb being a common consequence. Such lesions are generally not amenable to surgical repair. The use of olfactory ensheathing cells (OECs) for dorsal root repair, via acute transplantation, has been successful in several studies.

Effects of human OEC-derived cell transplants in rodent spinal cord contusion injury.

Numerous reports indicate that rodent olfactory ensheathing cells (OECs) assist in spinal cord repair and clinical trials have been undertaken using autologous transplantation of human olfactory ensheathing cells (hOECs) as a treatment for spinal cord injury. However, there are few studies investigating the efficacy of hOECs in animal models of spinal cord injury. In this study hOECs were derived from biopsies of human olfactory mucosa, purified by culture in a serum-free medium containing neurotrophin-3, genetically labelled with EGFP, and stored frozen.

Olfactory ensheathing cells reduce duration of autonomic dysreflexia in rats with high spinal cord injury.

Autonomic dysreflexia is a common complication in high spinal cord injury and can result in serious consequences and death. Here we have examined the effect of acute transplantation of olfactory ensheathing cells on cardiovascular functions in rats. After T4 transection, radio-telemetric recording in conscious animals was used to study blood pressure and heart rate at rest and during autonomic dysreflexia for up to 8 weeks post-injury.

Survival and migration of human and rat olfactory ensheathing cells in intact and injured spinal cord.

Increasing evidence indicates the potential of olfactory ensheathing cells (OECs) for treating spinal cord injuries. The present study compared proliferation and migration of adult rat and human OECs transplanted into the spinal cord of athymic (immunodeficient) rats. OECs were purified from the nasal lamina propria and prelabeled with a cytoplasmic dye.

Blockade of vascular smooth muscle cell proliferation and intimal thickening after balloon injury by the sulfated oligosaccharide PI-88: phosphomannopentaose sulfate directly binds FGF-2, blocks cellular signaling, and inhibits proliferation.

Percutaneous transluminal coronary angioplasty is a frequently used interventional technique to reopen arteries that have narrowed because of atherosclerosis. Restenosis, or renarrowing of the artery shortly after angioplasty, is a major limitation to the success of the procedure and is due mainly to smooth muscle cell accumulation in the artery wall at the site of balloon injury. In the present study, we demonstrate that the antiangiogenic sulfated oligosaccharide, PI-88, inhibits primary vascular smooth muscle cell proliferation and reduces intimal thickening 14 days after balloon angioplasty of rat and rabbit arteries.

Expression of heparan sulphate N-deacetylase/N-sulphotransferase by vascular smooth muscle cells.

Heparan sulphate is an important mediator in determining vascular smooth muscle cell (SMC) phenotype. The sulphation pattern of the heparan sulphate chains is critical to their function. We have examined the initial step in the biosynthesis of the sulphated domains mediated by the enzyme heparan sulphate N-deacetylase/N-sulphotransferase (NDST).

Cloning of a differentially expressed tropomyosin isoform from cultured rabbit aortic smooth muscle cells.

The four known tropomyosin genes have highly conserved DNA and amino acid sequences, and at least 18 isoforms are generated by alternative RNA splicing in muscle and non-muscle cells. No rabbit tropomyosin nucleotide sequences are known, although protein sequences for alpha- and beta-tropomyosin expressed by rabbit skeletal muscle have been described. Subtractive hybridisation was used to select for genes differentially expressed in rabbit aortic smooth muscle cells (SMC), during the change in cell phenotype in primary culture that is characterised by a loss of cytoskeletal filaments and contractile proteins.