Transcriptional profiling of spinal cord injury‐induced central neuropathic pain

Nešić, Olivera; Lee, Julieann; Johnson, Kathia M.; Ye, Zaiming; Xu, Guo Ying; Unabia, Geda; Wood, Thomas G.; McAdoo, David J.; Westlund, Karin N.; Hulsebosch, Claire E.; Perez‐Polo, J. Regino

doi:10.1111/j.1471-4159.2005.03462.x

Cited by 144 publications

(144 citation statements)

References 84 publications

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“…In pathological conditions of spinal cord injury, a biphasic change in AQP4 expression levels was demonstrated in astrocytes, revealing early down-regulation and subsequent up-regulation of the protein (Nesic et al 2006). AQP4 up-regulation associated with activated astroglial cells suggests strong implications for AQP4 in the development of neuropathies like cell swelling or persistent pain progression (Nesic et al 2005;Nagelhus et al 2013).…”

Section: Discussionmentioning

confidence: 99%

Immunolocalization of Water Channel Proteins AQP1 and AQP4 in Rat Spinal Cord

Oklinski

Lim

Choi

et al. 2014

J Histochem Cytochem.

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SummaryAquaporin (AQP) is a water-selective channel protein. In the brain, AQPs play critical roles in the production of cerebrospinal fluid and in edema formation. In contrast, the expression and role of AQPs in spinal cord are unclear. We aimed to investigate the localization of AQP1 and AQP4 in normal rat spinal cord compared with the expression of marker proteins for astrocytes, neurons, and endothelial cells. Immunohistochemistry demonstrated that AQP1 and AQP4 are expressed along all levels of the spinal cord from the cervical to lumbar levels. AQP1 immunolabeling was observed in the dorsal horns in the gray matter, whereas the labeling was weak and mainly seen close to glia limitans in the white matter. AQP1 was co-labeled with marker proteins for unmyelinated neuronal fibers (peripherin) and endothelial cells (RECA-1) of blood vessels that had penetrated through the glia limitans. In contrast, AQP1 did not colocalize with GFAP, an astrocyte marker, at any level of the spinal cord. AQP4 was exclusively localized at the astrocytes, but AQP4 expression in spinal cord exhibited a less polarized and more spatial distribution than that of brain astrocytes. The observed characteristic localization and expression patterns of AQP1 and AQP4 could provide insights toward gaining an understanding of the role of AQPs in the spinal cord. (J Histochem Cytochem 62:598-611, 2014)

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Section: Discussionmentioning

confidence: 99%

Immunolocalization of Water Channel Proteins AQP1 and AQP4 in Rat Spinal Cord

Oklinski

Lim

Choi

et al. 2014

J Histochem Cytochem.

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“…The GFAP expression increased and reached its maximum level after 3 days, and then decreased to the control level over the remainder of the 2-week experiment. Data from a mammalian CNS injury showed that mouse GFAP expression increased significantly after SCI, reaching a peak at 4 weeks and persisting for months [43][44][45][46]. The effect of reactive astrocytes in mammalian CNS after injury seems to be two-fold: reactive astrocytes play a beneficial role, such as the promotion of synaptic regeneration in the acute stage after CNS injury, but later act as inhibitors of CNS regeneration [47].…”

Section: Discussionmentioning

confidence: 99%

The molecular cloning of glial fibrillary acidic protein in Gekko japonicus and its expression changes after spinal cord transection

Gao

Wang

Liu

et al. 2010

Cellular and Molecular Biology Letters

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The glial fibrillary acidic protein (GFAP) is an astrocyte-specific member of the class III intermediate filament proteins. It is generally used as a specific marker of astrocytes in the central nervous system (CNS). We isolated a GFAP cDNA from the brain and spinal cord cDNA library of Gekko japonicus, and prepared polyclonal antibodies against gecko GFAP to provide useful tools for further immunochemistry studies. Both the real-time quantitative PCR and western blot results revealed that the expression of GFAP in the spinal cord after transection increased, reaching its maximum level after 3 days, and then gradually decreased over the rest of the 2 weeks of the experiment. Immunohistochemical analyses demonstrated that the increase in GFAP-positive labeling was restricted to the white matter rather than the gray matter. In particular, a slight increase in the number of GFAP positive star-shaped astrocytes was detected in the ventral and lateral regions of the white matter. Our results indicate that reactive astrogliosis in the gecko spinal cord took place primarily in the white matter during a short time interval, suggesting that the specific astrogliosis evaluated by GFAP expression might be advantageous in spinal cord regeneration.

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“…In addition, we and others have studied the changes in gene expression levels in the dorsal root ganglia and in the spinal cord after nerve injury. [41][42][43][44][45][46][47][48][49][50][51][52][53][54][55][56][57][58][59] When the human genome is mapped for genes controlling CPSP, these comparative studies will facilitate identifying conserved loci for CPSP in mice and humans. This knowledge will become important when developing novel analgesics in mice, which share CPSP genetic ''architecture'' similar to that in humans.…”

Section: Pain Genetics: Ongoing Studiesmentioning

confidence: 99%

Genetics of chronic post-surgical pain: a crucial step toward personal pain medicine

Clarke

Katz

Flor

et al. 2014

Can J Anesth/J Can Anesth

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Purpose Most patients who undergo surgery or experience a traumatic injury suffer from acute pain that subsides once tissues heal. Nevertheless, the pain remains in 15-30% of patients, sometimes for life, and this chronic post-surgical pain (CPSP) can result in suffering, depression, anxiety, sleep disturbance, physical incapacitation, and an economic burden. The incorporation of genetic knowledge is expected to lead to the development of more effective means to prevent and manage CPSP using tools of personalized pain medicine. The purpose of this review article is to provide an update on the current state of CPSP genetics and its future potential.Principle findings The large variability in CPSP amongst patients undergoing similar surgery suggests that individual factors are significant contributors to CPSP, raising the possibility that CPSP is influenced by genetic determinants. Heritability estimates suggest that about half of the variance in CPSP levels is attributable to genetic variation. These estimates suggest that identifying the genetic underpinnings of CPSP may lead to significant improvements in treatment. Analyzing patients' DNA sequences, blood and salivary pain biomarkers, as well as their analgesic responses to medications will facilitate developing insights into CPSP pathophysiology and inform predictive algorithms to determine a patient's likelihood of developing CPSP even prior to surgery. These algorithms could facilitate effective treatment regimens that will protect against the transition to chronicity in traumatically injured patients or those scheduled for surgery and lead to better therapy for patients who have already developed CPSP.Author contributions Hance Clarke, Joel Katz, Herta Flor, Marcella Rietschel, and Scott Diehl are co-authors of the manuscript and are responsible for revising some of the manuscript. Ze'ev Seltzer is the lead author responsible for revising the manuscript.

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Transcriptional profiling of spinal cord injury‐induced central neuropathic pain

Cited by 144 publications

References 84 publications

Immunolocalization of Water Channel Proteins AQP1 and AQP4 in Rat Spinal Cord

Immunolocalization of Water Channel Proteins AQP1 and AQP4 in Rat Spinal Cord

The molecular cloning of glial fibrillary acidic protein in Gekko japonicus and its expression changes after spinal cord transection

Genetics of chronic post-surgical pain: a crucial step toward personal pain medicine

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