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      Expression of Hyaluronidase-4 in a Rat Spinal Cord Hemisection Model

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      https://www.riss.kr/link?id=A105944921

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      다국어 초록 (Multilingual Abstract)

      Study Design: Examination of hyaluronidase-4 (Hyal-4) expression in a rat spinal cord hemisection model. Purpose: To determine the status of Hyal-4 expression after hemisection of the spinal cord, and the relationship between its expression and that o...

      Study Design: Examination of hyaluronidase-4 (Hyal-4) expression in a rat spinal cord hemisection model.
      Purpose: To determine the status of Hyal-4 expression after hemisection of the spinal cord, and the relationship between its expression and that of chondroitin sulfate proteoglycans (CSPGs).
      Overview of Literature: CSPGs are expressed at the site of spinal cord injury and inhibit axon regeneration. Administration of exogenous chrondroitinase ABC (ChABC), derived from bacteria, digested CSPGs and promoted axonal regrowth. Using a rat hemisection model, we have demonstrated peak CSPGs levels at by 3 weeks after injury but then decreased spontaneously. Could there be an endogenous enzyme similar to ChABC in the spinal cord? It has been suggested that Hyal-4 is involved in CSPG degradation.
      Methods: A rat hemisection model was prepared and spinal cord frozen sections were prepared at 4 days and 1, 2, 3, 4, 5, and 6 weeks post-cordotomy and stained for CSPGs and Hyal-4 and subjected to Western blotting.
      Results: CSPGs appeared at the injury site at 4 days after hemisection, reached a peak after 3 weeks, and then decreased. Hyal-4 was observed around the injury site from 4 days after cordotomy and increased until after 5–6 weeks. Double staining showed Hyal-4 around CSPGs. Western blotting identified a band corresponding to Hyal-4 from 4 days after hemisection.
      Conclusions: Hyal-4 was expressed in a rat hemisection model in areas surrounding CSPGs, and as its peak was delayed compared with that of CSPGs. These results suggest the involvement of Hyal-4 in the digestion of CSPGs.

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      참고문헌 (Reference)

      1 Csoka AB, "The six hyaluronidaselike genes in the human and mouse genomes" 20 : 499-508, 2001

      2 Fawcett JW, "The glial scar and central nervous system repair" 49 : 377-391, 1999

      3 McKeon RJ, "The chondroitin sulfate proteoglycans neurocan and phosphacan are expressed by reactive astrocytes in the chronic CNS glial scar" 19 : 10778-10788, 1999

      4 Iseda T, "Single, high-dose intraspinal injection of chondroitinase reduces glycosaminoglycans in injured spinal cord and promotes corticospinal axonal regrowth after hemisection but not contusion" 25 : 334-349, 2008

      5 Silver J, "Regeneration beyond the glial scar" 5 : 146-156, 2004

      6 McKeon RJ, "Reduction of neurite outgrowth in a model of glial scarring following CNS injury is correlated with the expression of inhibitory molecules on reactive astrocytes" 11 : 3398-3411, 1991

      7 Yamagata T, "Purification and properties of bacterial chondroitinases and chondrosulfatases" 243 : 1523-1535, 1968

      8 Pasterkamp RJ, "Peripheral nerve injury fails to induce growth of lesioned ascending dorsal column axons into spinal cord scar tissue expressing the axon repellent Semaphorin3A" 13 : 457-471, 2001

      9 Chen MS, "Nogo-A is a myelin-associated neurite outgrowth inhibitor and an antigen for monoclonal antibody IN-1" 403 : 434-439, 2000

      10 Kim JE, "Nogo-66 receptor prevents raphespinal and rubrospinal axon regeneration and limits functional recovery from spinal cord injury" 44 : 439-451, 2004

      1 Csoka AB, "The six hyaluronidaselike genes in the human and mouse genomes" 20 : 499-508, 2001

      2 Fawcett JW, "The glial scar and central nervous system repair" 49 : 377-391, 1999

      3 McKeon RJ, "The chondroitin sulfate proteoglycans neurocan and phosphacan are expressed by reactive astrocytes in the chronic CNS glial scar" 19 : 10778-10788, 1999

      4 Iseda T, "Single, high-dose intraspinal injection of chondroitinase reduces glycosaminoglycans in injured spinal cord and promotes corticospinal axonal regrowth after hemisection but not contusion" 25 : 334-349, 2008

      5 Silver J, "Regeneration beyond the glial scar" 5 : 146-156, 2004

      6 McKeon RJ, "Reduction of neurite outgrowth in a model of glial scarring following CNS injury is correlated with the expression of inhibitory molecules on reactive astrocytes" 11 : 3398-3411, 1991

      7 Yamagata T, "Purification and properties of bacterial chondroitinases and chondrosulfatases" 243 : 1523-1535, 1968

      8 Pasterkamp RJ, "Peripheral nerve injury fails to induce growth of lesioned ascending dorsal column axons into spinal cord scar tissue expressing the axon repellent Semaphorin3A" 13 : 457-471, 2001

      9 Chen MS, "Nogo-A is a myelin-associated neurite outgrowth inhibitor and an antigen for monoclonal antibody IN-1" 403 : 434-439, 2000

      10 Kim JE, "Nogo-66 receptor prevents raphespinal and rubrospinal axon regeneration and limits functional recovery from spinal cord injury" 44 : 439-451, 2004

      11 Asher RA, "Neurocan is upregulated in injured brain and in cytokinetreated astrocytes" 20 : 2427-2438, 2000

      12 McKeon RJ, "Injury-induced proteoglycans inhibit the potential for laminin-mediated axon growth on astrocytic scars" 136 : 32-43, 1995

      13 Silver J, "Immunocytochemical demonstration of early appearing astroglial structures that form boundaries and pathways along axon tracts in the fetal brain" 328 : 415-436, 1993

      14 Kaneiwa T, "Identification of human hyaluronidase-4 as a novel chondroitin sulfate hydrolase that preferentially cleaves the galactosaminidic linkage in the trisulfated tetrasaccharide sequence" 20 : 300-309, 2010

      15 Meyer K, "Hyaluronidases of bacterial and animal origin" 73 : 309-326, 1941

      16 Csoka AB, "Expression analysis of six paralogous human hyaluronidase genes clustered on chromosomes 3p21 and 7q31" 60 : 356-361, 1999

      17 Haas CA, "Entorhinal cortex lesion in adult rats induces the expression of the neuronal chondroitin sulfate proteoglycan neurocan in reactive astrocytes" 19 : 9953-9963, 1999

      18 Stern R, "Devising a pathway for hyaluronan catabolism: are we there yet?" 13 : 105R-115R, 2003

      19 Okada S, "Conditional ablation of Stat3 or Socs3 discloses a dual role for reactive astrocytes after spinal cord injury" 12 : 829-834, 2006

      20 Barritt AW, "Chondroitinase ABC promotes sprouting of intact and injured spinal systems after spinal cord injury" 26 : 10856-10867, 2006

      21 Bradbury EJ, "Chondroitinase ABC promotes functional recovery after spinal cord injury" 416 : 636-640, 2002

      22 Ikegami T, "Chondroitinase ABC combined with neural stem/progenitor cell transplantation enhances graft cell migration and outgrowth of growth-associated protein-43-positive fibers after rat spinal cord injury" 22 : 3036-3046, 2005

      23 Brittis PA, "Chondroitin sulfate as a regulator of neuronal patterning in the retina" 255 : 733-736, 1992

      24 Fitch MT, "Cellular and molecular mechanisms of glial scarring and progressive cavitation: in vivo and in vitro analysis of inflammation-induced secondary injury after CNS trauma" 19 : 8182-8198, 1999

      25 Yick LW, "Axonal regeneration of Clarke’s neurons beyond the spinal cord injury scar after treatment with chondroitinase ABC" 182 : 160-168, 2003

      26 Kaneko S, "A selective Sema3A inhibitor enhances regenerative responses and functional recovery of the injured spinal cord" 12 : 1380-1389, 2006

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