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12. PP124-SUN ANTIFIBROGENIC AND PROAPOPTOTIC EFFECTS OF BUTYRATE/DHA VIA PGE2 SECRETION ON KELOID FIBROBLASTS IN INFLAMMATORY MODEL

Author

Maeshige, N., primary, Torii, K., additional, Tabuchi, H., additional, Saka, A., additional, Araki, K., additional, Ishikawa, M.A., additional, Imai, M., additional, Koga, Y., additional, Ochi, A., additional, Uemura, M., additional, Miyoshi, M., additional, Hamada, Y., additional, Terashi, H., additional, and Usami, M., additional

Published
2013
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27. Extended V-Y Flap

Author

Terashi, H., primary, Kurata, S., additional, Hashimoto, H., additional, Tadokoro, T., additional, Miura, Y., additional, Sato, H., additional, and Matsuo, Y., additional

Published
1997
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49. Morphometric analysis of spinal motor neuron degeneration in sporadic amyotrophic lateral sclerosis.

Author

Aizawa H, Nagumo S, Hideyama T, Kato H, Kwak S, Terashi H, Suzuki Y, and Kimura T

Subjects
Humans, Male, Female, Middle Aged, Aged, Anterior Horn Cells pathology, Motor Neurons pathology, Motor Neurons metabolism, Amyotrophic Lateral Sclerosis pathology, Amyotrophic Lateral Sclerosis metabolism, DNA-Binding Proteins metabolism, Spinal Cord pathology, Spinal Cord metabolism, Nerve Degeneration pathology
Abstract

Objectives: This study aimed to clarify the relationship between 43-kDa TAR DNA-binding protein (TDP-43) pathology and spinal cord anterior horn motor neuron (AHMN) atrophy in sporadic amyotrophic lateral sclerosis (SALS)., Methods: Eight patients with SALS and 12 controls were included in this study. Formalin-fixed specimens of lumbar spinal cord samples were paraffin-embedded and sectioned at the level of the fourth lumbar spinal cord with a 4 μm thickness. Using a microscope, the long diameters of the neurons with nucleoli were measured in spinal AHMNs stained with an anti-SMI-32 antibody. AHMNs were divided into medial and lateral nuclei for statistical analysis. We also used previously reported data to measure the long diameter of AHMNs with initial TDP-43 pathology, in which TDP-43 was present both in the nucleus and cytoplasm., Results: The long diameter of the lumbar spinal AHMNs in patients with SALS was smaller in the medial nucleus (42.54 ± 9.33 μm, n = 24) and the lateral nucleus (49.41 ± 13.86 μm, n = 129) than in controls (medial nucleus: 55.84 ± 13.49 μm, n = 85, p < 0.001; lateral nucleus: 62.39 ± 13.29 μm, n = 756, p < 0.001, Mann-Whitney U test). All 21 motor neurons with initial TDP-43 pathology were in the lateral nucleus, and their long diameter (67.60 ± 18.3 μm, p = 0.352) was not significantly different from that of controls., Conclusion: Motor neuron atrophy in SALS does not occur during the initial stages of TDP-43 pathology, and TDP-43 pathology is already advanced in the atrophied motor neurons., Competing Interests: Declaration of competing interest None., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Published
2024
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50. Negative features of sporadic amyotrophic lateral sclerosis: Motor neurons of Onuf's nucleus survive in ADAR2-conditional knockout mice.

Author

Hideyama T, Teramoto S, Kato H, Terashi H, Kwak S, and Aizawa H

Subjects
Animals, Mice, DNA-Binding Proteins genetics, DNA-Binding Proteins metabolism, Disease Models, Animal, Receptors, AMPA genetics, Receptors, AMPA metabolism, Mice, Transgenic, Amyotrophic Lateral Sclerosis genetics, Amyotrophic Lateral Sclerosis pathology, Adenosine Deaminase genetics, Adenosine Deaminase deficiency, Adenosine Deaminase metabolism, Motor Neurons pathology, Motor Neurons metabolism, RNA-Binding Proteins genetics, RNA-Binding Proteins metabolism, Mice, Knockout
Abstract

Patients with amyotrophic lateral sclerosis (ALS) do not develop oculomotor disturbances and vesicorectal dysfunction until end-stage disease owing to the survival of certain motor neurons (MNs), including oculomotor neurons and MNs within Onuf's nucleus. In sporadic ALS, adenosine deaminase acting on RNA 2 (ADAR2)-mediated editing of GluA2 mRNA at the Q/R site is compromised in lower MNs. We previously developed genetically modified mice with a conditional knockout of ADAR2 in cholinergic neurons (ADAR2 flox/flox /VAChT-Cre, Fast; AR2). These mice displayed slow and progressive lower motor neuron death with TAR DNA-binding protein 43 (TDP-43) pathology, attributable to insufficient editing at the GluA2 Q/R site due to ADAR2 deficiency. MN death was more common in fast-fatigable MNs owing to differential vulnerability under conditions of ADAR2 deficiency. Although facial and hypoglossal nerves were impaired in AR2 mice, cell death did not occur within the oculomotor nerve nucleus, as observed in patients with sporadic ALS. Since the basis for avoiding cystorectal damage in ALS is unknown, we compared the features of Onuf's nucleus MNs in 12-month-old AR2 mice with those in age-matched wild-type mice. Although the number of MNs was not significantly lower in AR2 mice, the neurons exhibited a shrunken morphology and TDP-43 pathology. Onuf's nucleus MNs could survive in an ADAR2-deficient state and mainly included fast fatigue-resistant (FR) and slow (S) MNs. In summary, FR and S MNs show increased resilience to ADAR2 deficiency, potentially participating in an important neuronal death avoidance mechanism in ALS., Competing Interests: Declaration of competing interest None., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Published
2024
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