Abstract
Diabetes mellitus is a multiorgan disorder affecting many types of connective tissues, including bone and cartilage. High glucose could accelerate the autophagy in nucleus pulposus (NP) cells. In our present study, we investigated whether peroxisome proliferator-activated receptor γ (PPAR-γ) pathway is involved into autophagy regulation in NP cells under high glucose condition. After NP cells were treated with different high glucose concentrations for 72 hours, the rate of autophagy increased. Moreover, the levels of PPARγ, Beclin-1, and LC3II were significantly increased and p62 was significantly decreased compared to control group. Then, NP cells were treated with high glucose plus PPARγ agonist or PPARγ antagonist, respectively. The rate of autophagy and the levels of Beclin-1 and LC3II increased, but p62 decreased when PPARγ agonist was used. On the contrary, the rate of autophagy and the levels of Beclin-1 and LC3II decreased, while p62 increased when PPARγ antagonist was added. These results suggested that autophagy induced by high glucose in NP cells was through PPARγ-dependent pathway.
Highlights
Low back pain is highly prevalent and accounts for low life quality, and it is widely accepted that back pain has relationship with lumbar disc degeneration (LDD)
To be consistent with those previous results, our findings emphasize that high glucose could significantly enhance autophagy in nucleus pulposus (NP) cells
We have found both mRNA and protein levels of Beclin-1 and LC3B increased after high glucose treatment
Summary
Low back pain is highly prevalent and accounts for low life quality, and it is widely accepted that back pain has relationship with lumbar disc degeneration (LDD). The decrease in the number of viable nucleus pulposus (NP) cells in diabetes was thought to be one of the initial triggers of disc degeneration. High glucose has been proved to accelerate autophagy [5], apoptosis [6], and senescence [7] in adult rat NP cells in a dose- and timedependent manner. Both apoptosis and senescence of IVD cells can lead to the decrease of viable cells. Autophagy can promote cell survival and avert apoptosis during stress responses by turning over the intracellular organelles and molecules through the lysosomal pathway. The mechanism of autophagy in NP cell under high glucose is still unclear
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