scholarly journals Coupled Control of Distal Axon Integrity and Somal Responses to Axonal Damage by the Palmitoyl Acyltransferase ZDHHC17

Cell Reports ◽  
2020 ◽  
Vol 33 (7) ◽  
pp. 108365 ◽  
Author(s):  
Jingwen Niu ◽  
Shaun S. Sanders ◽  
Hey-Kyeong Jeong ◽  
Sabrina M. Holland ◽  
Yue Sun ◽  
...  
Keyword(s):  
Axonal Damage ◽  
Palmitoyl Acyltransferase

scholarly journals The Adverse Pial Arteriolar and Axonal Consequences of Traumatic Brain Injury Complicated by Hypoxia and Their Therapeutic Modulation with Hypothermia in Rat

2009 ◽  
Vol 30 (3) ◽  
pp. 628-637 ◽  
Author(s):  
Guoyi Gao ◽  
Yasutaka Oda ◽  
Enoch P Wei ◽  
John T Povlishock
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Amyloid Precursor Protein ◽  
Vascular Reactivity ◽  
Axonal Damage ◽  
Precursor Protein ◽  
Moderate Hypothermia ◽  
Vascular Protection ◽  
Impact Acceleration ◽  
Cerebral Vascular

This study examined the effect of posttraumatic hypoxia on cerebral vascular responsivity and axonal damage, while also exploring hypothermia's potential to attenuate these responses. Rats were subjected to impact acceleration injury (IAI) and equipped with cranial windows to assess vascular reactivity to topical acetylcholine, with postmortem analyses using antibodies to amyloid precursor protein to assess axonal damage. Animals were subjected to hypoxia alone, IAI and hypoxia, IAI and hypoxia before induction of moderate hypothermia (33°C), IAI and hypoxia induced during hypothermic intervention, and IAI and hypoxia initiated after hypothermia. Hypoxia alone had no impact on vascular reactivity or axonal damage. Acceleration injury and posttraumatic hypoxia resulted in dramatic axonal damage and altered vascular reactivity. When IAI and hypoxia were followed by hypothermic intervention, no axonal or vascular protection ensued. However, when IAI was followed by hypoxia induced during hypothermia, axonal and vascular protection followed. When this same hypoxic insult followed the use of hypothermia, no benefit ensued. These studies show that early hypoxia and delayed hypoxia exert damaging axonal and vascular consequences. Although this damage is attenuated by hypothermia, this follows only when hypoxia occurs during hypothermia, with no benefit found if the hypoxic insult proceeds or follows hypothermia.

scholarly journals Main Role of Antibodies in Demyelination and Axonal Damage in Multiple Sclerosis

2021 ◽  
Author(s):  
Ursula Muñoz ◽  
Cristina Sebal ◽  
Esther Escudero ◽  
Margaret Esiri ◽  
John Tzartos ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Axonal Damage ◽  
Main Role

scholarly journals Axonal damage in spinal cord is associated with gray matter atrophy in sensorimotor cortex in experimental autoimmune encephalomyelitis

2019 ◽  
Vol 26 (3) ◽  
pp. 294-303 ◽  
Author(s):  
Cassandra E Meyer ◽  
Josephine L Gao ◽  
James Ying-Jie Cheng ◽  
Mandavi R Oberoi ◽  
Hadley Johnsonbaugh ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Gray Matter ◽  
Sensorimotor Cortex ◽  
Axonal Damage ◽  
Strongly Correlated ◽  
Autoimmune Encephalomyelitis ◽  
Normal Controls ◽  
Experimental Autoimmune

Background: Gray matter (GM) atrophy in brain is one of the best predictors of long-term disability in multiple sclerosis (MS), and recent findings have revealed that localized GM atrophy is associated with clinical disabilities. GM atrophy associated with each disability mapped to a distinct brain region, revealing a disability-specific atlas (DSA) of GM loss. Objective: To uncover the mechanisms underlying the development of localized GM atrophy. Methods: We used voxel-based morphometry (VBM) to evaluate localized GM atrophy and Clear Lipid-exchanged Acrylamide-hybridized Rigid Imaging-compatible Tissue-hYdrogel (CLARITY) to evaluate specific pathologies in mice with experimental autoimmune encephalomyelitis (EAE). Results: We observed extensive GM atrophy throughout the cerebral cortex, with additional foci in the thalamus and caudoputamen, in mice with EAE compared to normal controls. Next, we generated pathology-specific atlases (PSAs), voxelwise mappings of the correlation between specific pathologies and localized GM atrophy. Interestingly, axonal damage (end-bulbs and ovoids) in the spinal cord strongly correlated with GM atrophy in the sensorimotor cortex of the brain. Conclusion: The combination of VBM with CLARITY in EAE can localize GM atrophy in brain that is associated with a specific pathology in spinal cord, revealing a PSA of GM loss.

scholarly journals Dysfunction of the blood-brain barrier in postoperative delirium patients, referring to the axonal damage biomarker phosphorylated neurofilament heavy subunit

PLoS ONE ◽  
2019 ◽  
Vol 14 (10) ◽  
pp. e0222721 ◽  
Author(s):  
Kazuhito Mietani ◽  
Masahiko Sumitani ◽  
Toru Ogata ◽  
Nobutake Shimojo ◽  
Reo Inoue ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Postoperative Delirium ◽  
Axonal Damage ◽  
Brain Barrier ◽  
Blood Brain

scholarly journals Palmitoylation of Cytoskeleton Associated Protein 4 by DHHC2 Regulates Antiproliferative Factor-mediated Signaling

2009 ◽  
Vol 20 (5) ◽  
pp. 1454-1463 ◽  
Author(s):  
Sonia L. Planey ◽  
Susan K. Keay ◽  
Chen-Ou Zhang ◽  
David A. Zacharias
Keyword(s):  
Epithelial Cells ◽  
Cellular Proliferation ◽  
Phosphorylated Protein ◽  
Normal Bladder ◽  
High Affinity Receptor ◽  
Palmitoyl Acyltransferase ◽  
Cellular Behaviors ◽  
Affinity Receptor ◽  
Induced Changes

Previously, we identified cytoskeleton-associated protein 4 (CKAP4) as a major substrate of the palmitoyl acyltransferase, DHHC2, using a novel proteomic method called palmitoyl-cysteine identification, capture and analysis (PICA). CKAP4 is a reversibly palmitoylated and phosphorylated protein that links the ER to the cytoskeleton. It is also a high-affinity receptor for antiproliferative factor (APF), a small sialoglycopeptide secreted from bladder epithelial cells of patients with interstitial cystitis (IC). The role of DHHC2-mediated palmitoylation of CKAP4 in the antiproliferative response of HeLa and normal bladder epithelial cells to APF was investigated. Our data show that siRNA-mediated knockdown of DHHC2 and consequent suppression of CKAP4 palmitoylation inhibited the ability of APF to regulate cellular proliferation and blocked APF-induced changes in the expression of E-cadherin, vimentin, and ZO-1 (genes known to play a role in cellular proliferation and tumorigenesis). Immunocytochemistry revealed that CKAP4 palmitoylation by DHHC2 is required for its trafficking from the ER to the plasma membrane and for its nuclear localization. These data suggest an important role for DHHC2-mediated palmitoylation of CKAP4 in IC and in opposing cancer-related cellular behaviors and support the idea that DHHC2 is a tumor suppressor.

Imaging of axonal damage in vivo in Rasmussen's syndrome

Brain ◽  
1995 ◽  
Vol 118 (3) ◽  
pp. 753-758 ◽  
Author(s):  
Fernando Cendes ◽  
Frederick Andermann ◽  
Kenneth Silver ◽  
Douglas L. Arnold
Keyword(s):  
Axonal Damage ◽  
Rasmussen’S Syndrome

Axonal damage and behavioral deficits in rats with repetitive exposure of the brain to laser-induced shock waves: Effects of inter-exposure time

2021 ◽  
Vol 749 ◽  
pp. 135722
Author(s):  
Kosuke Miyai ◽  
Satoko Kawauchi ◽  
Tamaki Kato ◽  
Tetsuo Yamamoto ◽  
Yasuo Mukai ◽  
...  
Keyword(s):  
Shock Waves ◽  
Exposure Time ◽  
Axonal Damage ◽  
Behavioral Deficits ◽  
Repetitive Exposure ◽  
The Brain

Putting Magnetic Resonance Spectroscopy Studies in Context: Axonal Damage and Disability in Multiple Sclerosis

1998 ◽  
Vol 18 (03) ◽  
pp. 327-336 ◽  
Author(s):  
P. Matthews ◽  
N. De Stefano ◽  
S. Narayanan ◽  
G. Francis ◽  
J. Wolinsky ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Magnetic Resonance ◽  
Magnetic Resonance Spectroscopy ◽  
Axonal Damage ◽  
Resonance Spectroscopy ◽  
Spectroscopy Studies
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