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JNK phosphorylation promotes natural degeneration of cervical endplate chondrocytes by down-regulating expression of ANK.
Eur Rev Med Pharmacol Sci 2013; 17(17):2335-44ER

Abstract

BACKGROUND

Endplate degeneration leads to accelerated degeneration of the intervertebral disc. The importance of endplate chondrocytes in this process is unclear. Many cellular processes in chondrocytes are controlled by activated c-Jun N-terminal kinases (JNK) and protein kinase B (AKT). However, the involvement of their pathways in the degeneration process needs to be elucidated.

AIM

To study activation of JNK and AKT signaling pathways and their significance for degeneration of endplate chondrocytes, as well as involvement of progressive ankylosis protein (ANK) in this process.

MATERIALS AND METHODS

Rat primary chondrocytes were grown to confluence and subcultured until passage 4. Morphological appearances (microscope, hematoxylin & eosin staining, toluidine blue staining) and proliferation rates of cells (MTT test) were observed. Further, levels of type II collagen, aggrecan, phosphorylated JNK and AKT, total JNK, AKT and ANK were evaluated by qPCR, flow cytometry and Western blot assays. Furthermore, inhibition experiments with SP600125, the JNK inhibitor, were carried out in the passage 4 cells to assess the effects of the JNK pathway on natural degeneration of endplate chondrocytes.

RESULTS

The proliferative speed of endplate chondrocytes progressively decreased during passaging. Expressions of type II collagen and aggrecan were significantly decreased with cells at higher passages. Furthermore, phosphorylation of JNK, but not AKT, was significantly up-regulated and accompanied by reduced ANK expression. Inhibition of the JNK pathway increased expression of type II collagen, aggrecan and ANK and facilitated proliferation rates.

CONCLUSIONS

Phosphorylation of JNK promotes natural degeneration of cervical endplate chondrocytes, likely by down-regulating ANK expression.

Authors+Show Affiliations

Department of Orthopedic Surgery, Yijishan Hospital, Wannan Medical College, Wuhu, People's Republic of China. pumchxuhg@126.com.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24065227

Citation

Xu, H-G, et al. "JNK Phosphorylation Promotes Natural Degeneration of Cervical Endplate Chondrocytes By Down-regulating Expression of ANK." European Review for Medical and Pharmacological Sciences, vol. 17, no. 17, 2013, pp. 2335-44.
Xu HG, Cheng JF, Peng HX, et al. JNK phosphorylation promotes natural degeneration of cervical endplate chondrocytes by down-regulating expression of ANK. Eur Rev Med Pharmacol Sci. 2013;17(17):2335-44.
Xu, H. G., Cheng, J. F., Peng, H. X., Lv, K., Wang, H., Liu, P., ... Zhang, M. Y. (2013). JNK phosphorylation promotes natural degeneration of cervical endplate chondrocytes by down-regulating expression of ANK. European Review for Medical and Pharmacological Sciences, 17(17), pp. 2335-44.
Xu HG, et al. JNK Phosphorylation Promotes Natural Degeneration of Cervical Endplate Chondrocytes By Down-regulating Expression of ANK. Eur Rev Med Pharmacol Sci. 2013;17(17):2335-44. PubMed PMID: 24065227.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - JNK phosphorylation promotes natural degeneration of cervical endplate chondrocytes by down-regulating expression of ANK. AU - Xu,H-G, AU - Cheng,J-F, AU - Peng,H-X, AU - Lv,K, AU - Wang,H, AU - Liu,P, AU - Zhong,M, AU - Zhang,M-Y, PY - 2013/9/26/entrez PY - 2013/9/26/pubmed PY - 2013/12/16/medline SP - 2335 EP - 44 JF - European review for medical and pharmacological sciences JO - Eur Rev Med Pharmacol Sci VL - 17 IS - 17 N2 - BACKGROUND: Endplate degeneration leads to accelerated degeneration of the intervertebral disc. The importance of endplate chondrocytes in this process is unclear. Many cellular processes in chondrocytes are controlled by activated c-Jun N-terminal kinases (JNK) and protein kinase B (AKT). However, the involvement of their pathways in the degeneration process needs to be elucidated. AIM: To study activation of JNK and AKT signaling pathways and their significance for degeneration of endplate chondrocytes, as well as involvement of progressive ankylosis protein (ANK) in this process. MATERIALS AND METHODS: Rat primary chondrocytes were grown to confluence and subcultured until passage 4. Morphological appearances (microscope, hematoxylin & eosin staining, toluidine blue staining) and proliferation rates of cells (MTT test) were observed. Further, levels of type II collagen, aggrecan, phosphorylated JNK and AKT, total JNK, AKT and ANK were evaluated by qPCR, flow cytometry and Western blot assays. Furthermore, inhibition experiments with SP600125, the JNK inhibitor, were carried out in the passage 4 cells to assess the effects of the JNK pathway on natural degeneration of endplate chondrocytes. RESULTS: The proliferative speed of endplate chondrocytes progressively decreased during passaging. Expressions of type II collagen and aggrecan were significantly decreased with cells at higher passages. Furthermore, phosphorylation of JNK, but not AKT, was significantly up-regulated and accompanied by reduced ANK expression. Inhibition of the JNK pathway increased expression of type II collagen, aggrecan and ANK and facilitated proliferation rates. CONCLUSIONS: Phosphorylation of JNK promotes natural degeneration of cervical endplate chondrocytes, likely by down-regulating ANK expression. SN - 1128-3602 UR - https://www.unboundmedicine.com/medline/citation/24065227/JNK_phosphorylation_promotes_natural_degeneration_of_cervical_endplate_chondrocytes_by_down_regulating_expression_of_ANK_ L2 - http://www.europeanreview.org/article/5110 DB - PRIME DP - Unbound Medicine ER -