Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.4.37 (CNPase)
 539 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The implication of insulin-like growth factor I (IGF-I) in the myelination and the repair of myelin that occur after a demyelinating process was evaluated in organotypic cultures of embryonic nerve tissue. The amount of myelin of mouse spinal cord explants exposed to media supplemented with IGF-I beginning on the first day of explantation was recorded by light-microscopic examination and quantitation of the 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNPase) activity. After 9 days in vitro (DIV), the cultures treated with medium supplemented with 0.1-1 microgram/ml IGF-I showed a greater amount of myelin and an increase over the controls in CNPase activity between 50 and 80% at 16 DIV and 100% at 21 DIV. Total demyelination with a concomitant reduction of about 80% in the CNPase activity resulted when anti-white matter antiserum and complement were added to the nutrient medium of fully myelinated cultures. This effect was partially reverted when IGF-I was included in the demyelinating medium. The higher inhibition, about 50%, was obtained with concentrations of IGF-I between 0.1 and 0.5 micrograms/ml. To study the effect of IGF-I on remyelination, well-myelinated cultures were completely demyelinated, maintained in that state for 2 or 15 DIV and after that allowed to remyelinate for 14 days. Cultures exposed to medium supplemented with 0.01-0.1 microgram/ml IGF-I showed a degree of remyelination similar to that of the normal nutrient medium-fed cultures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin-like growth factor I increases myelination and inhibits demyelination in cultured organotypic nerve tissue. 749

The central nervous system has limited capacity for regeneration after traumatic injury. Transplantation of neural stem/progenitor cells (NPCs) has been proposed as a potential therapeutic approach while insulin-like growth factor I (IGF-I) has neuroprotective properties following various experimental insults to the nervous system. We have previously shown that NPCs transduced with a lentiviral vector for IGF-I overexpression have an enhanced ability to give rise to neurons in vitro but also in vivo, upon transplantation in a mouse model of temporal lobe epilepsy. Here we studied the regenerative potential of NPCs, IGF-I-transduced or not, in a mouse model of hippocampal mechanical injury. NPC transplantation, with or without IGF-I transduction, rescued the injury-induced spatial learning deficits as revealed in the Morris Water Maze. Moreover, it had beneficial effects on the host tissue by reducing astroglial activation and microglial/macrophage accumulation while enhancing generation of endogenous oligodendrocyte precursor cells. One or two months after transplantation the grafted NPCs had migrated towards the lesion site and in the neighboring myelin-rich regions. Transplanted cells differentiated toward the oligodendroglial, but not the neuronal or astrocytic lineages, expressing the early and late oligodendrocyte markers NG2, Olig2, and CNPase. The newly generated oligodendrocytes reached maturity and formed myelin internodes. Our current and previous observations illustrate the high plasticity of transplanted NPCs which can acquire injury-dependent phenotypes within the host CNS, supporting the fact that reciprocal interactions between transplanted cells and the host tissue are an important factor to be considered when designing prospective cell-based therapies for CNS degenerative conditions.
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PMID:Neural stem/progenitor cells differentiate into oligodendrocytes, reduce inflammation, and ameliorate learning deficits after transplantation in a mouse model of traumatic brain injury. 2671 14