ABSTRACT
Objective: To explore the application value of MR ultrashort echo time (UTE) sequence and conventional sequence imaging for displaying lumbar intervertebral disc (IVD) cartilage endplate (CEP) injury. Methods: Totally 87 volunteers underwent conventional and UTE lumbar spine MRI. The correlation between UTE sequence of lumbar IVD CEP injury and vertebral Modic changes classification, Pfirrmann disc degeneration grade were analyzed. Results: UTE showed linear hyperintense uncalcified CEP and hypointense calcified CEP between nucleus pulposus and vertebral body. There was a positive correlation between cartilage endplate injury in L1-S1 and vertebral Modic changes classification, Pfirrmann disc degeneration grade (all P<0.001). Conclusion: MR UTE can clearly show the lamination and damage of CEP, and there is certain relationship between cartilage endplate injury and lumbar degeneration.
ABSTRACT
Current studies find that degenerated cartilage endplates (CEP) of vertebrae, with fewer diffusion areas, decrease nutrient supply and accelerate intervertebral disc degeneration. Many more apoptotic cells have been identified in degenerated than in normal endplates, and may be responsible for the degenerated grade. Previous findings suggest that inhibition of apoptosis is one possible approach to improve disc regeneration. It is postulated that inhibition of CEP cell apoptosis may be responsible for the regeneration of endplates. Caspase-3, involved in the execution phase of apoptosis, is a candidate for regulating the apoptotic process. In the present study, CEP cells were incubated in 1% fetal bovine serum. Activated caspases were detected to identify the apoptotic pathway, and apoptosis was quantified by flow cytometry. Lentiviral caspase-3 short hairpin RNA (shRNA) was employed to study its protective effects against serum deprivation. Silencing of caspase-3 expression was quantified by reverse transcription-polymerase chain reaction and Western blots, and inhibition of apoptosis was quantified by flow cytometry. Serum deprivation increased apoptosis of rat CEP cells through activation of a caspase cascade. Lentiviral caspase-3 shRNA was successfully transduced into CEP cells, and specifically silenced endogenous caspase-3 expression. Surviving cells were protected by the downregulation of caspase-3 expression and activation. Thus, lentiviral caspase-3 shRNA-mediated RNAi successfully silenced endogenous caspase-3 expression, preventing inappropriate or premature apoptosis.