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Attenuation of Robust Glial Scar Formation Facilitates Functional Recovery in Animal Models of Chronic Nerve Compression Injury.

Abstract Late surgery for chronic nerve compression injuries usually improves sensation but rarely reverses motor atrophy. We hypothesized that a persistent glial scar after chronic nerve compression injury might account for poor motor recovery and that degradation of the glial scar as an adjunct to surgical decompression would improve functional recovery.
PMID
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Mayor MeshTerms
Keywords
Journal Title the journal of bone and joint surgery. american volume
Publication Year Start




PMID- 29257018
OWN - NLM
STAT- MEDLINE
DCOM- 20171227
LR  - 20171227
IS  - 1535-1386 (Electronic)
IS  - 0021-9355 (Linking)
VI  - 99
IP  - 24
DP  - 2017 Dec 20
TI  - Attenuation of Robust Glial Scar Formation Facilitates Functional Recovery in
      Animal Models of Chronic Nerve Compression Injury.
PG  - e132
LID - 10.2106/JBJS.17.00396 [doi]
AB  - BACKGROUND: Late surgery for chronic nerve compression injuries usually improves 
      sensation but rarely reverses motor atrophy. We hypothesized that a persistent
      glial scar after chronic nerve compression injury might account for poor motor
      recovery and that degradation of the glial scar as an adjunct to surgical
      decompression would improve functional recovery. METHODS: A previously described 
      model of chronic nerve compression injury was created in C57BL/6 mice and
      Sprague-Dawley rats, and the nerves were harvested early or late after
      electrophysiological confirmation of the injury. Western blot, polymerase chain
      reaction, and quantitative immunohistochemical analyses were performed to
      determine levels of chondroitin sulfate proteoglycans and extracellular matrix
      molecules. Subsets of mice were treated either with surgical decompression alone 
      or with decompression coupled with intraepineurial injection of a low dose (0.1
      mugmuL) or a high dose (0.2 mug/muL) of chondroitinase ABC at 6 weeks after
      injury. RESULTS: Aggrecan showed the greatest change in mRNA and protein levels
      at the early and late time points following creation of the chronic nerve
      compression injury. Quantitative immunohistochemical analysis revealed early
      aggrecan upregulation localized primarily to the endoneurium and late
      upregulation localized to the perineurium and epineurium (p < 0.0105).
      Quantitative immunohistochemical analysis for collagen IV, laminin-alpha2, and
      fibronectin also showed early upregulation with perineurial scarring.
      Quantitative immunohistochemical analysis and Western blot analysis for aggrecan 
      demonstrated a marked increase in the endoneurium at the early time points and
      upregulation of expression in the epineurium and perineurium at the late time
      points. Decompression along with intraepineurial injection of high-dose
      chondroitinase ABC at 6 weeks after creation of the compression injury resulted
      in marked attenuation of decorin and aggrecan expression with functional
      improvement in nerve conduction velocity. CONCLUSIONS: Significant upregulation
      of chondroitin sulfate proteoglycans and other extracellular matrix components
      contributes to the pathogenesis of compression neuropathies in murine models. The
      administration of chondroitinase ABC degrades these chondroitin sulfate
      proteoglycans and improves functional recovery after chronic nerve compression
      injury; thus, it can be considered as a possible therapeutic adjunct.
FAU - Zhu, Diana
AU  - Zhu D
AD  - Peripheral Nerve Research Laboratory, Department of Orthopaedic Surgery,
      University of California, Irvine, Irvine, California.
FAU - Tapadia, Minal D
AU  - Tapadia MD
AD  - Peripheral Nerve Research Laboratory, Department of Orthopaedic Surgery,
      University of California, Irvine, Irvine, California.
FAU - Palispis, Winnie
AU  - Palispis W
AD  - Peripheral Nerve Research Laboratory, Department of Orthopaedic Surgery,
      University of California, Irvine, Irvine, California.
FAU - Luu, Michele
AU  - Luu M
AD  - Peripheral Nerve Research Laboratory, Department of Orthopaedic Surgery,
      University of California, Irvine, Irvine, California.
FAU - Wang, Weiping
AU  - Wang W
AD  - Peripheral Nerve Research Laboratory, Department of Orthopaedic Surgery,
      University of California, Irvine, Irvine, California.
FAU - Gupta, Ranjan
AU  - Gupta R
AD  - Peripheral Nerve Research Laboratory, Department of Orthopaedic Surgery,
      University of California, Irvine, Irvine, California.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Bone Joint Surg Am
JT  - The Journal of bone and joint surgery. American volume
JID - 0014030
RN  - 0 (Aggrecans)
RN  - 0 (RNA, Messenger)
RN  - EC 4.2.2.20 (Chondroitin ABC Lyase)
SB  - AIM
SB  - IM
MH  - Aggrecans/pharmacology
MH  - Analysis of Variance
MH  - Animals
MH  - Blotting, Western
MH  - Chondroitin ABC Lyase/*pharmacology
MH  - Chronic Disease
MH  - Cicatrix/*prevention & control
MH  - Decompression, Surgical/*methods
MH  - Disease Models, Animal
MH  - Injections, Intralesional
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Nerve Compression Syndromes/*drug therapy/pathology/surgery
MH  - Neural Conduction/drug effects
MH  - Peripheral Nerve Injuries/*drug therapy/*pathology/surgery
MH  - RNA, Messenger/drug effects
MH  - Random Allocation
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Real-Time Polymerase Chain Reaction/methods
MH  - Recovery of Function/physiology
MH  - Sensitivity and Specificity
EDAT- 2017/12/20 06:00
MHDA- 2017/12/28 06:00
CRDT- 2017/12/20 06:00
PHST- 2017/12/20 06:00 [entrez]
PHST- 2017/12/20 06:00 [pubmed]
PHST- 2017/12/28 06:00 [medline]
AID - 10.2106/JBJS.17.00396 [doi]
AID - 00004623-201712200-00009 [pii]
PST - ppublish
SO  - J Bone Joint Surg Am. 2017 Dec 20;99(24):e132. doi: 10.2106/JBJS.17.00396.