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Tytuł:
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Involvement of Autophagy in Rat Tail Static Compression-Induced Intervertebral Disc Degeneration and Notochordal Cell Disappearance.
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Autorzy:
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Yurube T; Department of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
Hirata H; Department of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
Ito M; Department of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
Terashima Y; Department of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
Kakiuchi Y; Department of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
Kuroda R; Department of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
Kakutani K; Department of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
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Źródło:
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International journal of molecular sciences [Int J Mol Sci] 2021 May 26; Vol. 22 (11). Date of Electronic Publication: 2021 May 26.
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Typ publikacji:
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Journal Article
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Język:
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English
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Imprint Name(s):
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Original Publication: Basel, Switzerland : MDPI, [2000-
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MeSH Terms:
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Autophagy*
Annulus Fibrosus/*metabolism
Intervertebral Disc Degeneration/*metabolism
Nucleus Pulposus/*metabolism
Animals ; Annulus Fibrosus/pathology ; Humans ; Intervertebral Disc Degeneration/pathology ; Male ; Nucleus Pulposus/pathology ; Rats ; Rats, Sprague-Dawley
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References:
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Grant Information:
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JP26893151 Japan Society for the Promotion of Science; JP15H03033 Japan Society for the Promotion of Science; JP15K10406 Japan Society for the Promotion of Science; JP16K20051 Japan Society for the Promotion of Science; 312 Japan Orthopaedics and Traumatology Foundation
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Contributed Indexing:
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Keywords: animal model; apoptosis; autophagy; intervertebral disc degeneration; low back pain; notochordal cells; nucleus pulposus; nutrient deprivation; spine; static compression loading
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Entry Date(s):
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Date Created: 20210602 Date Completed: 20210617 Latest Revision: 20210617
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Update Code:
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20240104
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PubMed Central ID:
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PMC8199019
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DOI:
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10.3390/ijms22115648
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PMID:
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34073333
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The intervertebral disc is the largest avascular low-nutrient organ in the body. Thus, resident cells may utilize autophagy, a stress-response survival mechanism, by self-digesting and recycling damaged components. Our objective was to elucidate the involvement of autophagy in rat experimental disc degeneration. In vitro, the comparison between human and rat disc nucleus pulposus (NP) and annulus fibrosus (AF) cells found increased autophagic flux under serum deprivation rather in humans than in rats and in NP cells than in AF cells of rats ( n = 6). In vivo, time-course Western blotting showed more distinct basal autophagy in rat tail disc NP tissues than in AF tissues; however, both decreased under sustained static compression ( n = 24). Then, immunohistochemistry displayed abundant autophagy-related protein expression in large vacuolated disc NP notochordal cells of sham rats. Under temporary static compression ( n = 18), multi-color immunofluorescence further identified rapidly decreased brachyury-positive notochordal cells with robust expression of autophagic microtubule-associated protein 1 light chain 3 (LC3) and transiently increased brachyury-negative non-notochordal cells with weaker LC3 expression. Notably, terminal deoxynucleotidyl transferase dUTP nick end labeling-positive apoptotic death was predominant in brachyury-negative non-notochordal cells. Based on the observed notochordal cell autophagy impairment and non-notochordal cell apoptosis induction under unphysiological mechanical loading, further investigation is warranted to clarify possible autophagy-induced protection against notochordal cell disappearance, the earliest sign of disc degeneration, through limiting apoptosis.
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