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Article: CK8 phosphorylation induced by compressive loads underlies the downregulation of CK8 in human disc degeneration by activating protein kinase C

TitleCK8 phosphorylation induced by compressive loads underlies the downregulation of CK8 in human disc degeneration by activating protein kinase C
Authors
Issue Date2013
Citation
Lab Invest, 2013, v. 93 n. 12, p. 1323-30 How to Cite?
AbstractCytokeratin 8 (CK8) is a member of the cytokeratins family with multiple functions on the basis of its unique structural hallmark. The aberrant expression of CK8 and its phosphorylation are pertinent with various diseases. We have previously shown that CK8 exists in normal human nucleus pulposus (NP) cells and decreases as the intervertebral disc degenerates. However, the underlying molecular regulatory machinery of CK8 in intervertebral disc degeneration (IDD) has not been clarified. Here, we collected NP samples from patients with idiopathic scoliosis as control and IDD as degenerate groups. We found that CK8 expression decreased in IDD with an increased phosphorylation in degenerate NP cells. Moreover, NP cells were cultured under different compressive load schemes for diverse time duration. We found that compressive loads resulted in phosphorylation and disassembly of CK8 in a time-dependent and degree-dependent manner in vitro. The activation of protein kinase C was a significant molecular factor contributing to this phenomenon. Taken together, this study is the first to address the molecular mechanisms of CK8 downregulation in NP cells. Importantly, our findings provide clues regarding a molecular link between compressive loads and CK8 alterations, which shed a novel light on the etiology of IDD.
Persistent Identifierhttp://hdl.handle.net/10722/203245
ISSN
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSun, Zen_US
dc.contributor.authorGuo, YSen_US
dc.contributor.authorYan, SJen_US
dc.contributor.authorWan, ZYen_US
dc.contributor.authorGao, Ben_US
dc.contributor.authorWang, Len_US
dc.contributor.authorLiu, ZHen_US
dc.contributor.authorGao, Yen_US
dc.contributor.authorSamartzis, Den_US
dc.contributor.authorLan, LFen_US
dc.contributor.authorWang, HQen_US
dc.contributor.authorLuo, ZJen_US
dc.date.accessioned2014-09-19T13:11:30Z-
dc.date.available2014-09-19T13:11:30Z-
dc.date.issued2013en_US
dc.identifier.citationLab Invest, 2013, v. 93 n. 12, p. 1323-30en_US
dc.identifier.issn1530-0307 (Electronic) 0023-6837 (Linkinen_US
dc.identifier.urihttp://hdl.handle.net/10722/203245-
dc.description.abstractCytokeratin 8 (CK8) is a member of the cytokeratins family with multiple functions on the basis of its unique structural hallmark. The aberrant expression of CK8 and its phosphorylation are pertinent with various diseases. We have previously shown that CK8 exists in normal human nucleus pulposus (NP) cells and decreases as the intervertebral disc degenerates. However, the underlying molecular regulatory machinery of CK8 in intervertebral disc degeneration (IDD) has not been clarified. Here, we collected NP samples from patients with idiopathic scoliosis as control and IDD as degenerate groups. We found that CK8 expression decreased in IDD with an increased phosphorylation in degenerate NP cells. Moreover, NP cells were cultured under different compressive load schemes for diverse time duration. We found that compressive loads resulted in phosphorylation and disassembly of CK8 in a time-dependent and degree-dependent manner in vitro. The activation of protein kinase C was a significant molecular factor contributing to this phenomenon. Taken together, this study is the first to address the molecular mechanisms of CK8 downregulation in NP cells. Importantly, our findings provide clues regarding a molecular link between compressive loads and CK8 alterations, which shed a novel light on the etiology of IDD.en_US
dc.languageengen_US
dc.relation.ispartofLab Investen_US
dc.titleCK8 phosphorylation induced by compressive loads underlies the downregulation of CK8 in human disc degeneration by activating protein kinase Cen_US
dc.typeArticleen_US
dc.identifier.emailSamartzis, D: dspine@hku.hken_US
dc.identifier.authoritySamartzis, D=rp01430en_US
dc.identifier.doi10.1038/labinvest.2013.122en_US
dc.identifier.pmid24166186-
dc.identifier.hkuros238000en_US
dc.identifier.volume93en_US
dc.identifier.issue12en_US
dc.identifier.spage1323en_US
dc.identifier.epage30en_US
dc.identifier.isiWOS:000327795600007-

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