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Article: Expression of the Trp2 allele of COL9A2 is associated with alterations in the mechanical properties of human intervertebral discs

TitleExpression of the Trp2 allele of COL9A2 is associated with alterations in the mechanical properties of human intervertebral discs
Authors
KeywordsBiomechanics
COL9A2
Collagen
Degeneration
Intervertebral disc
Nucleus pulposus
Polymorphism
Trp2
Issue Date2007
PublisherLippincott, Williams & Wilkins. The Journal's web site is located at http://www.spinejournal.com
Citation
Spine, 2007, v. 32 n. 25, p. 2820-2826 How to Cite?
AbstractSTUDY DESIGN. Biomechanical study into the association between genetic polymorphism in COL9A2 and mechanical properties of human nucleus pulposus. OBJECTIVE. To examine whether there is an association between genetic polymorphism in a structural gene, and alterations in the mechanical properties of the intervertebral discs that may predispose to disc degeneration. SUMMARY OF BACKGROUND DATA. Genetic studies have demonstrated that a polymorphism (Trp2 allele) in COL9A2 coding for α2 chain of collagen IX predisposes the individual to disc degeneration. The mechanism of this predisposition is not known. METHODS. Blood and whole disc samples were retrieved from adolescents and young adults during scoliosis surgery, degenerated discs were retrieved from patients with back pain during anterior spinal fusion. Anulus fibrosus and nucleus pulposus from a set of the scoliosis discs were used to perform immunohistochemistry to demonstrate the presence of collagen IX in the scoliosis discs. For the remaining samples, DNA was extracted from blood to determine the Trp2 status by sequencing. Nondegenerated (Trp2-), nondegenerated (Trp2+), and degenerated (Trp2-) nucleus pulposus samples were tested in confined compression. Swelling pressure and compressive modulus were measured and compared between groups. RESULTS. Positive staining of collagen IX was detected in both anulus fibrosus and nucleus pulposus sections confirming its presence in the scoliosis discs. The mean swelling pressure and compressive modulus values of 6 nondegenerated (Trp2+) samples (swelling pressure = 0.0019 MPa, compressive modulus = 0.97 MPa) were significantly lower (P < 0.05) than those of the 6 nondegenerated (Trp2-) samples (swelling pressure = 0.015 MPa; compressive modulus = 1.89 MPa). CONCLUSION. This is the first study to demonstrate an association between the Trp2 allele and disc mechanics, thus relating genetic variations and debilitating mechanical alterations that may ultimately result in intervertebral disc degeneration. © 2007 Lippincott Williams & Wilkins, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/68183
ISSN
2023 Impact Factor: 2.6
2023 SCImago Journal Rankings: 1.221
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorAladin, DMKen_HK
dc.contributor.authorCheung, KMCen_HK
dc.contributor.authorChan, Den_HK
dc.contributor.authorYee, AFYen_HK
dc.contributor.authorJim, JJTen_HK
dc.contributor.authorLuk, KDKen_HK
dc.contributor.authorLu, WWen_HK
dc.date.accessioned2010-09-06T06:02:09Z-
dc.date.available2010-09-06T06:02:09Z-
dc.date.issued2007en_HK
dc.identifier.citationSpine, 2007, v. 32 n. 25, p. 2820-2826en_HK
dc.identifier.issn0362-2436en_HK
dc.identifier.urihttp://hdl.handle.net/10722/68183-
dc.description.abstractSTUDY DESIGN. Biomechanical study into the association between genetic polymorphism in COL9A2 and mechanical properties of human nucleus pulposus. OBJECTIVE. To examine whether there is an association between genetic polymorphism in a structural gene, and alterations in the mechanical properties of the intervertebral discs that may predispose to disc degeneration. SUMMARY OF BACKGROUND DATA. Genetic studies have demonstrated that a polymorphism (Trp2 allele) in COL9A2 coding for α2 chain of collagen IX predisposes the individual to disc degeneration. The mechanism of this predisposition is not known. METHODS. Blood and whole disc samples were retrieved from adolescents and young adults during scoliosis surgery, degenerated discs were retrieved from patients with back pain during anterior spinal fusion. Anulus fibrosus and nucleus pulposus from a set of the scoliosis discs were used to perform immunohistochemistry to demonstrate the presence of collagen IX in the scoliosis discs. For the remaining samples, DNA was extracted from blood to determine the Trp2 status by sequencing. Nondegenerated (Trp2-), nondegenerated (Trp2+), and degenerated (Trp2-) nucleus pulposus samples were tested in confined compression. Swelling pressure and compressive modulus were measured and compared between groups. RESULTS. Positive staining of collagen IX was detected in both anulus fibrosus and nucleus pulposus sections confirming its presence in the scoliosis discs. The mean swelling pressure and compressive modulus values of 6 nondegenerated (Trp2+) samples (swelling pressure = 0.0019 MPa, compressive modulus = 0.97 MPa) were significantly lower (P < 0.05) than those of the 6 nondegenerated (Trp2-) samples (swelling pressure = 0.015 MPa; compressive modulus = 1.89 MPa). CONCLUSION. This is the first study to demonstrate an association between the Trp2 allele and disc mechanics, thus relating genetic variations and debilitating mechanical alterations that may ultimately result in intervertebral disc degeneration. © 2007 Lippincott Williams & Wilkins, Inc.en_HK
dc.languageengen_HK
dc.publisherLippincott, Williams & Wilkins. The Journal's web site is located at http://www.spinejournal.comen_HK
dc.relation.ispartofSpineen_HK
dc.subjectBiomechanicsen_HK
dc.subjectCOL9A2en_HK
dc.subjectCollagenen_HK
dc.subjectDegenerationen_HK
dc.subjectIntervertebral discen_HK
dc.subjectNucleus pulposusen_HK
dc.subjectPolymorphismen_HK
dc.subjectTrp2en_HK
dc.subject.meshAdolescenten_HK
dc.subject.meshAdulten_HK
dc.subject.meshBiomechanicsen_HK
dc.subject.meshCollagen Type IX - analysis - geneticsen_HK
dc.subject.meshCompressive Strengthen_HK
dc.subject.meshGenetic Predisposition to Diseaseen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshIntervertebral Disc - chemistry - physiopathologyen_HK
dc.subject.meshLow Back Pain - genetics - metabolism - physiopathologyen_HK
dc.subject.meshPolymorphism, Geneticen_HK
dc.subject.meshPressureen_HK
dc.subject.meshRisk Factorsen_HK
dc.subject.meshScoliosis - genetics - metabolism - physiopathologyen_HK
dc.subject.meshSpinal Diseases - complications - genetics - metabolism - physiopathologyen_HK
dc.titleExpression of the Trp2 allele of COL9A2 is associated with alterations in the mechanical properties of human intervertebral discsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0887-9869&volume=32&issue=25&spage=2820&epage=2826&date=2007&atitle=Expression+of+the+Trp2+allele+of+COL9A2+is+associated+with+alterations+in+the+mechanical+properties+of+human+intervertebral+discsen_HK
dc.identifier.emailCheung, KMC:cheungmc@hku.hken_HK
dc.identifier.emailChan, D:chand@hkucc.hku.hken_HK
dc.identifier.emailLuk, KDK:hcm21000@hku.hken_HK
dc.identifier.emailLu, WW:wwlu@hku.hken_HK
dc.identifier.authorityCheung, KMC=rp00387en_HK
dc.identifier.authorityChan, D=rp00540en_HK
dc.identifier.authorityLuk, KDK=rp00333en_HK
dc.identifier.authorityLu, WW=rp00411en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1097/BRS.0b013e31815b75c5en_HK
dc.identifier.pmid18246003-
dc.identifier.scopuseid_2-s2.0-39049156861en_HK
dc.identifier.hkuros145953en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-39049156861&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume32en_HK
dc.identifier.issue25en_HK
dc.identifier.spage2820en_HK
dc.identifier.epage2826en_HK
dc.identifier.isiWOS:000251442600006-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridAladin, DMK=23491673700en_HK
dc.identifier.scopusauthoridCheung, KMC=7402406754en_HK
dc.identifier.scopusauthoridChan, D=7402216545en_HK
dc.identifier.scopusauthoridYee, AFY=23494406200en_HK
dc.identifier.scopusauthoridJim, JJT=10341020300en_HK
dc.identifier.scopusauthoridLuk, KDK=7201921573en_HK
dc.identifier.scopusauthoridLu, WW=7404215221en_HK
dc.identifier.issnl0362-2436-

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