Spinal Cord Injury: Hope To Improve Healing
The spinal cord often tragic consequences, about half of people suffering such an injury following an accident are paraplegic and have to undergo costly and lengthy hospitalization rehabilitation sessions. U.S. researchers have made a discovery that opens the way for new treatments. A protein called SUR1 (sulfonylurea receptor 1) plays a crucial role in the aggravation of an injury to the spinal cord according to this new study published in Science Translational Medicine
Paradox: a protective mechanism aggravates injury:
A sharp blow to the spine can break or dislocate the vertebrae, which then crush and destroy the axons, extensions of these nerve cells which pass into the spinal cord the signals between the brain and rest of body. Even if the spinal cord is not self-destruct after a serious injury, the paradox is that in attempting to protect herself is even more damaging its own cells.
Encoded by the gene ABCC8 activated after injury, the SUR1 protein is part of defense mechanism that protects cells from death due to excessive calcium entry. Sur1 also allows the introduction of sodium, which helps reduce the amount of calcium entering cells. In a serious injury, however, this protective mechanism goes awry and the SUR1 protein is hyperactivated, leading to a uncontrolled entry of sodium which is fatal to cells.
Acting quickly after spinal cord
Marc Simard and colleagues at the University of Maryland at Baltimore have discovered after studying the tissue injury of the spinal cord in humans and rodents that the same mechanism of cell death and cell destruction involving SUR1 is involved both in humans than in mice or rats. By suppressing the expression of the gene ABCC8, researchers have managed to stop in mice the process of self-destruction and to improve long-term recovery from spinal cord injuries. They showed in rats that if they stop short of ABCC8 expression using an oligonucleotide, a small sequence of DNA single strand-specific gene, the lesions after spinal cord injuries are much more limited ( 75% of lesions less).
The study indicates that treatment with this oligonucleotide as quickly as possible after spinal cord injury patients may reduce tissue destruction that follows and improve their long-term restoration. The researchers also show that a drug inhibitor of SUR1 (glibenclamide) has also yielded promising results.
References:
Brief ABCC8 Prevents Suppression of Self-destruction of Spinal Cord After Trauma. J. Marc Simard, S. Kyoon Woo, Michael D. Norenberg, Cigdem Tosun, Zheng Chen, Svetlana Ivanova, Orest Tsymbalyuk, Joseph Bryan, Douglas Landsman & Volodymyr Gerzanich. Science Translational Medicine.
Link: http://stm.sciencemag.org/content/2/28/28ra29.abstract
The spinal cord often tragic consequences, about half of people suffering such an injury following an accident are paraplegic and have to undergo costly and lengthy hospitalization rehabilitation sessions. U.S. researchers have made a discovery that opens the way for new treatments. A protein called SUR1 (sulfonylurea receptor 1) plays a crucial role in the aggravation of an injury to the spinal cord according to this new study published in Science Translational Medicine
Paradox: a protective mechanism aggravates injury:
A sharp blow to the spine can break or dislocate the vertebrae, which then crush and destroy the axons, extensions of these nerve cells which pass into the spinal cord the signals between the brain and rest of body. Even if the spinal cord is not self-destruct after a serious injury, the paradox is that in attempting to protect herself is even more damaging its own cells.
Encoded by the gene ABCC8 activated after injury, the SUR1 protein is part of defense mechanism that protects cells from death due to excessive calcium entry. Sur1 also allows the introduction of sodium, which helps reduce the amount of calcium entering cells. In a serious injury, however, this protective mechanism goes awry and the SUR1 protein is hyperactivated, leading to a uncontrolled entry of sodium which is fatal to cells.
Acting quickly after spinal cord
Marc Simard and colleagues at the University of Maryland at Baltimore have discovered after studying the tissue injury of the spinal cord in humans and rodents that the same mechanism of cell death and cell destruction involving SUR1 is involved both in humans than in mice or rats. By suppressing the expression of the gene ABCC8, researchers have managed to stop in mice the process of self-destruction and to improve long-term recovery from spinal cord injuries. They showed in rats that if they stop short of ABCC8 expression using an oligonucleotide, a small sequence of DNA single strand-specific gene, the lesions after spinal cord injuries are much more limited ( 75% of lesions less).
The study indicates that treatment with this oligonucleotide as quickly as possible after spinal cord injury patients may reduce tissue destruction that follows and improve their long-term restoration. The researchers also show that a drug inhibitor of SUR1 (glibenclamide) has also yielded promising results.
References:
Brief ABCC8 Prevents Suppression of Self-destruction of Spinal Cord After Trauma. J. Marc Simard, S. Kyoon Woo, Michael D. Norenberg, Cigdem Tosun, Zheng Chen, Svetlana Ivanova, Orest Tsymbalyuk, Joseph Bryan, Douglas Landsman & Volodymyr Gerzanich. Science Translational Medicine.
Link: http://stm.sciencemag.org/content/2/28/28ra29.abstract
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