An in vitro expansion score for tissue-engineering applications with human bone marrow-derived mesenchymal stem cells.

Human bone marrow-derived mesenchymal stem cells (MSCs) have limited growth potential in vitro and cease to divide due to replicative senescence, which from a tissue-engineering perspective has practical implications, such as defining the correct starting points for differentiation and transplantation. Time spent in culture before the loss of required differentiation potential is different and reflects patient variability, which is a problem for cell expansion. This study aimed to develop a score set which can be used to quantify the senescent state of MSCs and predict whether cells preserve their ability to differentiate to osteogenic, adipogenic and chondrogenic phenotypes, based on colony-forming unit (CFU) assay, population doubling time (PDT), senescence-associated β-galactosidase (SA-β-Gal) activity, cell size, telomere length and gene expression of MSCs cultured in vitro over 11 passages.

Necessity for re-vascularization after spinal cord injury and the search for potential therapeutic options.

Disruption of the blood-spinal cord barrier (BSCB) and microvascular changes leading to reduction of blood supply represent hallmarks of spinal cord secondary injury causing further deterioration of the traumatized patient. Injury to the blood vessels starts with prominent hemorrhage and generation of inflammation. Furthermore, spinal cord ischemia and extravasation of blood components contribute to edema formation resulting in death of neural cells.

Traumatic spinal cord injury alters angiogenic factors and TGF-beta1 that may affect vascular recovery.

Traumatic spinal cord injury (SCI) disrupts the blood-spinal cord barrier and reduces the blood supply caused by microvascular changes. Vessel regression and neovascularization have been observed in the course of secondary injury contributing to microvascular remodeling after trauma. Spatio-temporal distribution of blood vessels and modulation of gene expression of several angiogenic factors have been investigated in rats after spinal cord compression injury.

CD133 expressing pericytes and relationship to SDF-1 and CXCR4 in spinal cord injury.

Compression injury to the spinal cord (SC) results in vascular changes affecting the severity of the primary damage of the spinal cord. The recruitment of bone marrow (BM)-derived cells contribute to revascularization and tissue regeneration in a wide range of ischemic pathologies. Involvement of these cells in the vascular repair process has been investigated in an animal model of spinal cord injury (SCI).

Normal-appearing white matter in multiple sclerosis is in a subtle balance between inflammation and neuroprotection.

Multiple sclerosis is a chronic inflammatory disease of the CNS. Although progressive axonal injury and diffuse inflammatory damage has been shown in the chronic phase of the disease, little is known about the molecular mechanisms underlying these pathological processes. In order to identify these mechanisms, we have studied the gene expression profile in non-lesion containing tissue, the so-called normal-appearing white matter (NAWM).

Molecular changes in normal appearing white matter in multiple sclerosis are characteristic of neuroprotective mechanisms against hypoxic insult.

Multiple sclerosis is a chronic inflammatory disease of the CNS leading to focal destruction of myelin, still the earliest changes that lead to lesion formation are not known. We have studied the gene-expression pattern of 12 samples of normal appearing white matter from 10 post-mortem MS brains. Microarray analysis revealed upregulation of genes involved in maintenance of cellular homeostasis, and in neural protective mechanisms known to be induced upon ischemic preconditioning.