Insulin-like growth factor 1 antagonizes lumbar disc degeneration through enhanced autophagy.
Autophagy has been shown to antagonize the development of Lumbar disc degeneration (LDD), whereas the molecular regulation of autophagy is unknown. We recently reported a potential role of Insulin-like growth factor 1 receptor (IGF1R)/phosphatidylinositol-3 kinase (PI3k)/Akt signaling in the initiation and progression of LDD. Here, we studied the effects of IGF1R signaling on disc cell autophagy. We showed a correction of activation of IGF1R and disc cell autophagy in the resected discs in LDD patients. In vitro, activation of IGF1R signaling antagonized the decreases in cell viability of human disc cells, HNPSV, through suppression of apoptosis and enhancement of autophagy. Suppression of IGF1R signaling or inhibition of autophagy abolished the effects of activation of IGF1R signaling on disc cell survival upon compression. Together, our data suggest that activation of IGF1R may antagonize LDD, at least partially through enhanced autophagy.
Department of Orthopedics, Qingpu Branch of Zhongshan Hospital Affiliated to Fudan University 1158 Gongyuan East Road, Shanghai 201700, China.
Zuo-Qing
ZQ
Liu
Department of Orthopedics, Qingpu Branch of Zhongshan Hospital Affiliated to Fudan University 1158 Gongyuan East Road, Shanghai 201700, China.
Shan
S
Zhao
Department of Orthopedics, Qingpu Branch of Zhongshan Hospital Affiliated to Fudan University 1158 Gongyuan East Road, Shanghai 201700, China.
Wen-Qin
WQ
Fu
Lumbar disc degeneration (LDD); apoptosis; autophagy; insulin-like growth factor 1 receptor (IGF1R)