17ß-estradiol protects nucleus pulposus cells from serum deprivation-induced apoptosis and regulates expression of MMP-3 and MMP-13 through promotion of autophagy.

Serum deprivation is a likely contributor to intervertebral disc (IVD) degeneration (IVDD).17ß-estradiol (E2) have been noted to protect nucleus pulposus cells (NPCs) against apoptosis. Autophagy and apoptosis play a paramount role in maintaining the homeostasis of IVD. So far, little research has been published on whether autophagy plays a role for the E2 mediated protection of NPCs. The aim of this study is to understand whether autophagy is involved in the protective effect of E2 against serum deprivation-induced cell apoptosis and expression of matrix metalloproteinase (MMP)-3 and MMP-13. mCherry-GFP-LC3-adenovirus transfection is used to monitor autophagy detection. The expression levels of autophagy-related proteins were measured by Western blotting, Apoptosis and MMPs were detected by flow cytometry and Western blotting. Accordingly, Autophagy and apoptosis was detected in NP cells under serum deprivation conditions, the autophagy incidence began to reached a peak value at 48 h, the apoptosis and MMPs incidence began reached a minimum value treat with E2 (10-7 M). Whereas the combined use of E2 and 3-MA led to a dramatic decrease in autophagy, while aberrantly elevated expression levels of apoptotic and MMPs. These data suggest that serum deprivation-induced apoptosis and MMP-3, MMP-13, which was efficiently suppressed by the E2 through promoting autophagy in rat NPCs.

A Modified Laminoplasty Technique to Treat Cervical Myelopathy Secondary to Ossification of the Posterior Longitudinal Ligament (OPLL).

BACKGROUND This study aimed to evaluate the validity of modified laminoplasty in treating close-base OPLL with an occupying ratio of more than 60%. MATERIAL AND METHODS Forty-seven close-base OPLL patients with an occupying ratio of more than 60% were treated through modified laminoplasty (N=22) and combined anterior-posterior approach (N=25) in the study, including 17 females and 30 males, with a mean age of 60.59±6.76 years (ranging from 46 to 75 years). The patients' characteristics, the recovery rate of neurological function, length of the operation, intraoperative blood loss, hospital costs, and complications were recorded and compared between the 2 groups. RESULTS The recovery rate of neurological function did not demonstrate a significant difference between the 2 groups (P=0.886). However, length of the operation and intraoperative blood loss in the modified laminoplasty group were shorter than those in the combined anterior-posterior approach group (P=0.001 and P=0.023). Moreover, the mean hospital costs in the modified laminoplasty group (5166.61±123.27 USD) decreased by 33.6% compared with the combined anterior-posterior approach group (7780.12±256.73 USD). Additionally, the complications of the modified laminoplasty group were lower than in the combined anterior-posterior approach group. CONCLUSIONS Modified laminoplasty may be considered a safe and effective strategy for patients that have demonstrated close-base OPLL with an occupying ratio of more than 60% and who cannot endure the trauma caused by the combined anterior-posterior approach due to medical disease.

Autophagy Protects Advanced Glycation End Product-Induced Apoptosis and Expression of MMP-3 and MMP-13 in Rat Chondrocytes.

Aging is one of the most prominent risk factors for the pathological progression of osteoarthritis (OA). One feature of age-related changes in OA is advanced glycation end products (AGEs) accumulation in articular cartilage. Autophagy plays a cellular housekeeping role by removing dysfunctional cellular organelles and proteins. However, the relationship between autophagy and AGE-associated OA is unknown. The aim of this study is to determine whether autophagy participates in the pathology of AGE-treated chondrocytes and to investigate the exact role of autophagy in AGE-induced cell apoptosis and expression of matrix metalloproteinase- (MMP-) 3 and MMP-13. AGEs induced notable apoptosis that was detected by Annexin V/PI double-staining, and the upregulation of MMP-3 and MMP-13 was confirmed by Western blotting. Autophagy-related proteins were also determined by Western blotting, and chondrocytes were transfected with mCherry-GFP-LC3B-adenovirus to monitor autophagic flux. As a result, autophagy significantly increased in chondrocytes and peaked at 6 h. Furthermore, rapamycin (RA) attenuated AGE-induced apoptosis and expression of MMP-3 and MMP-13 by autophagy activation. In contrast, pretreatment with autophagy inhibitor 3-methyladenine (3-MA) enhanced the abovementioned effects of AGEs. We therefore demonstrated that autophagy is linked with AGE-related pathology in rat chondrocytes and plays a protective role in AGE-induced apoptosis and expression of MMP-3 and MMP-13.