The fast track to canonical Wnt signaling in MC3T3-E1 cells protected by substance P against serum deprivation-induced apoptosis.
The canonical Wnt pathway is vital to bone physiology by increasing bone mass through elevated osteoblast survival. Although investigated extensively in stem cells, its role in osteoblastic MC3T3-E1 cells has not been completely determined. To explore how this pathway is regulated by different conditions, we assessed the anti-apoptotic effects of substance P on the canonical Wnt pathway in MC3T3-E1 cells by treating cells with serum deprivation or serum starving with "substance P," a neuropeptide demonstrated to promote bone growth and stimulate Wnt signaling. The results showed that serum deprivation both induced apoptosis and activated Wnt signal transduction while substance P further stimulated the Wnt pathway via the NK-1 receptor but protected the cells from apoptotic death. Fast-tracking of Wnt signaling by substance P was also noted. These results indicate that nutritional deprivation and substance P synergistically activated the canonical Wnt pathway, a finding that helps to reveal the role of Wnt signaling in bone physiology affected by nutritional deprivation and neuropeptide substance P.
Department of Orthopedics and Traumatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong Province, 510515, China.|Department of Orthopaedics, Huhhot First Hospital, Hohhot, Inner Mongolia, 010020, China.
Jianguo
J
Yang
Department of Hand Surgery, The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia, 010030, China.
Jiping
J
Nie
School of Engineering and Materials Science, Queen Mary University of London, Mile End Road, London, E1 4NS, UK.
Su
S
Fu
Department of Orthopedics and Traumatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong Province, 510515, China.
Song
S
Liu
Department of Orthopedics and Traumatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong Province, 510515, China.
Jianqun
J
Wu
Department of Orthopaedics, Huhhot First Hospital, Hohhot, Inner Mongolia, 010020, China.
Liang
L
Cui
Department of Orthopaedics, Affiliated Hospital of Hebei University of Engineering, Handan, Hebei, 056002, China.
Yongtao
Y
Zhang
Department of Orthopedics and Traumatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong Province, 510515, China.
Bin
B
Yu
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002460:Cell Line; D002467:Cell Nucleus / Q000378:metabolism; D016895:Culture Media, Serum-Free; D019610:Cytoprotection / Q000187:drug effects*; D051379:Mice; D018040:Receptors, Neurokinin-1 / Q000378:metabolism; D013373:Substance P / Q000494:pharmacology*; D060449:Wnt Signaling Pathway / Q000187:drug effects*; D051176:beta Catenin / Q000378:metabolism
D016895:Culture Media, Serum-Free; D018040:Receptors, Neurokinin-1; D051176:beta Catenin; D013373:Substance P
MC3T3-E1 cells; Wnt signaling; apoptosis; substance P