The Use of Antisense-Mediated Inhibition to Delineate The Role of Inflammatory Agents in The Pathophysiology of Spinal Cord Injury
Injuries to the central nervous system (CNS) usually lead to a potent and acute inflammatory response[1]. During this period, glia and immune cells respond to chemical cues associated with the debris of lysed neurons, disrupted axons, and a broken blood-brain-barrier by releasing a battery of cytoki...
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| Format: | Article |
| Language: | English |
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Wiley
2002-01-01
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| Series: | The Scientific World Journal |
| Online Access: | http://dx.doi.org/10.1100/tsw.2002.63 |
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| author | Damien D. Pearse Francisco C. Pereira Katina Chatzipanteli Francisco W. Dalton Dietrich Mary Bartlett Bunge |
| author_facet | Damien D. Pearse Francisco C. Pereira Katina Chatzipanteli Francisco W. Dalton Dietrich Mary Bartlett Bunge |
| author_sort | Damien D. Pearse |
| collection | DOAJ |
| description | Injuries to the central nervous system (CNS) usually lead to a potent and acute inflammatory response[1]. During this period, glia and immune cells respond to chemical cues associated with the debris of lysed neurons, disrupted axons, and a broken blood-brain-barrier by releasing a battery of cytokines including tumor necrosis factor-α (TNF-α) and, interleukin-β (IL-1β) as well as reactive oxygen species such as nitric oxide (NO-)[2]. The secretion of these factors may be primarily responsible for secondary damage to surrounding uninjured tissue that potentiates the initial injury[3]. Antisense oligonucleotides (ASOs) are designed to hybridize to specific regions of specific mRNAs. Hybridization of the oligonucleotide to the mRNA then interferes with the normal processing of that mRNA at the ribosome or targets the RNA duplex for cleavage by the RNA digestive enzyme, ribonuclease H, resulting in greatly reduced expression of the coded protein. This effectively reduces the amount of corresponding translated protein product and experiments can be designed to examine the requirement of particular inflammatory agents in eliciting specific deleterious responses after injury, e.g., cell death. |
| format | Article |
| id | doaj-art-731849876c374c6485db88b727f25af2 |
| institution | Kabale University |
| issn | 1537-744X |
| language | English |
| publishDate | 2002-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | The Scientific World Journal |
| spelling | doaj-art-731849876c374c6485db88b727f25af22025-02-03T05:54:28ZengWileyThe Scientific World Journal1537-744X2002-01-01213313510.1100/tsw.2002.63The Use of Antisense-Mediated Inhibition to Delineate The Role of Inflammatory Agents in The Pathophysiology of Spinal Cord InjuryDamien D. Pearse0Francisco C. Pereira1Katina Chatzipanteli2Francisco W. Dalton Dietrich3Mary Bartlett Bunge4The Miami Project to Cure Paralysis, Department of Cell Biology and Anatomy, University of Miami School of Medicine, Miami, FL, USADepartment of Anatomy, University of Sao Paulo, BrazilThe Miami Project to Cure Paralysis, Department of Cell Biology and Anatomy, University of Miami School of Medicine, Miami, FL, USAThe Miami Project to Cure Paralysis, Department of Cell Biology and Anatomy, University of Miami School of Medicine, Miami, FL, USAThe Miami Project to Cure Paralysis, Department of Cell Biology and Anatomy, University of Miami School of Medicine, Miami, FL, USAInjuries to the central nervous system (CNS) usually lead to a potent and acute inflammatory response[1]. During this period, glia and immune cells respond to chemical cues associated with the debris of lysed neurons, disrupted axons, and a broken blood-brain-barrier by releasing a battery of cytokines including tumor necrosis factor-α (TNF-α) and, interleukin-β (IL-1β) as well as reactive oxygen species such as nitric oxide (NO-)[2]. The secretion of these factors may be primarily responsible for secondary damage to surrounding uninjured tissue that potentiates the initial injury[3]. Antisense oligonucleotides (ASOs) are designed to hybridize to specific regions of specific mRNAs. Hybridization of the oligonucleotide to the mRNA then interferes with the normal processing of that mRNA at the ribosome or targets the RNA duplex for cleavage by the RNA digestive enzyme, ribonuclease H, resulting in greatly reduced expression of the coded protein. This effectively reduces the amount of corresponding translated protein product and experiments can be designed to examine the requirement of particular inflammatory agents in eliciting specific deleterious responses after injury, e.g., cell death.http://dx.doi.org/10.1100/tsw.2002.63 |
| spellingShingle | Damien D. Pearse Francisco C. Pereira Katina Chatzipanteli Francisco W. Dalton Dietrich Mary Bartlett Bunge The Use of Antisense-Mediated Inhibition to Delineate The Role of Inflammatory Agents in The Pathophysiology of Spinal Cord Injury The Scientific World Journal |
| title | The Use of Antisense-Mediated Inhibition to Delineate The Role of Inflammatory Agents in The Pathophysiology of Spinal Cord Injury |
| title_full | The Use of Antisense-Mediated Inhibition to Delineate The Role of Inflammatory Agents in The Pathophysiology of Spinal Cord Injury |
| title_fullStr | The Use of Antisense-Mediated Inhibition to Delineate The Role of Inflammatory Agents in The Pathophysiology of Spinal Cord Injury |
| title_full_unstemmed | The Use of Antisense-Mediated Inhibition to Delineate The Role of Inflammatory Agents in The Pathophysiology of Spinal Cord Injury |
| title_short | The Use of Antisense-Mediated Inhibition to Delineate The Role of Inflammatory Agents in The Pathophysiology of Spinal Cord Injury |
| title_sort | use of antisense mediated inhibition to delineate the role of inflammatory agents in the pathophysiology of spinal cord injury |
| url | http://dx.doi.org/10.1100/tsw.2002.63 |
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