MRNA Profile Analysis By Genechip After Acute Spinal Cord Injury In Rats

Spinal cord injury (SCI) is a devastating and common neurological disorder that has profound influences on mordern society. Spinal cord injury may be divided both primary and secondary mechanisms of injury. The primary injury, in large part, determines a given patient's neurologic grade on admission and thereby is the strongest prognostic indicator. However secondary mechanisms of injury can exacerbate damage and limit restorative processes, and hence, contribute to overall morbidity and mortality. Nowadays, researches of therapy after SCI mainly focused on two fields. One way is to stop or relive secondary injury, another way is to promote the regeneration of neuron or transplantation and replace of nerve tissues. Secondary mechanisms of injury encompass an array of perturbances and include neurogenic shock, vacular insults such as hemorrhage and ischemia-reperfusion, excitotoxicity, calcium-mediated secondary injury and fluid -electrolyte disturbances, immunologic injury, apoptosis, disturbances in mitochondrial function, and other miscellaneous processes. Comprehension of secondary mechanisms of injury serves as a basis for the development and application of targeted pharmacological strategies to confer neuroprotection and restoration while mitigating ongoing neural injury.Concerted expression of thousands of genes in a controlled manner is essential for proper CNS function. Traumatic injury to the spinal cords leads to the altered expression of several families of genes with significant functional consequences. To identify the specific molecular pathways altered as a function of time after SCI, which would facilitate the development of strategies for favorable manipulation of the beneficial pathways and inhibition of toxic pathways, we analyzed the changes of mRNA profile after traumatic injury to rat spinal cord using cDNA microarray. SCI was induced at T8 level by dropping a 10-g weight from a height of 50mm.-?-The cDNA microarray kits we used were products of Clotech Ltd, which comprise 1176 known genes of rat, including 23 groups of genes encoding different preteins, such as stress response proteins, inflammation proteins, ion channels and transport proteins, extracellular cell signalling and communication proteins, oncogenes, immune system proteins, intracellular transducers and so on, which can make it possible to study the mechanisms after SCI in a comprehensive way. Results reveal that expression levels of 81 genes have changed after SCI, which includes some cell surface antigens, immune system proteins, transcription factors, stress response proteins, ion channel transportation proteins, translation proteins, excellular and intracellular signal transducer, growing factors, cytokine and receptors and so on. Some of the differentiated expressed genes, such as Immediately early genes (c-fos, c-jun), cytokines (IL-lp, IL-6, TNF-ce), heat shock proteins and so on, have been consistent with literatures. Noticeably, some genes have been found to be corelated with pathophysiologic processes of ASCI for the first time.Using Northern blotting, the changes observed by genechip were confirmed for 4 genes (p -NGF, FGF-10, IGFBP3 and somatostatin).