title: Effects of CCN3 on rat cartilage endplate chondrocytes cultured under serum deprivation in vitro.
abstract: The presence of apoptotic cells and loss of extracellular matrix (ECM) are common characteristics of degenerated cartilage endplates (CEPs). In addition, therapeutic efficacy is hampered by an incomplete understanding regarding the mechanisms underlying CEP homeostasis and degeneration. The CCN proteins have recently emerged as important regulators of cell‑ECM interactions, and have been identified as key mediators of nucleus pulposus ECM composition and tissue homeostasis. However, whether CCN3 is associated with CEP homeostasis has yet to be elucidated. The present study aimed to investigate the effects of CCN3 on the apoptosis and ECM synthesis of CEP cells cultured under serum deprivation. Rat CEP cells were confirmed to be of the chondrocytic phenotype by toluidine blue staining. The mRNA expression levels of CCN3 were markedly increased, and a dose‑dependent increase of apoptotic rate was detected under serum deprivation conditions following treatment with recombinant CCN3, whereas CCN3 did not exert a proapoptotic effect on cells cultured under normal conditions. Furthermore, CCN3‑treated cells exhibited a decrease in the expression levels of aggrecan and collagen II in both groups. These results suggested that CCN3 may act as a regulator, rather than an initiator, of serum deprivation‑induced cellular apoptosis, and that CCN3 has a catabolic effect on the mediation of ECM synthesis under both normal and serum deprivation conditions. Therefore, CCN3 may represent a novel therapeutic target for the prevention of CEP degeneration.
authors.affiliation: Department of Orthopedic Surgery, Jinshan Hospital, Fudan University, Shanghai 201508, P.R. China.
authors.forename: Lei
authors.initials: L
authors.lastname: Ding
authors.affiliation: Department of Orthopedic Surgery, Jinshan Hospital, Fudan University, Shanghai 201508, P.R. China.
authors.forename: Jingping
authors.initials: J
authors.lastname: Wu
authors.affiliation: Department of Orthopedic Surgery, Jinshan Hospital, Fudan University, Shanghai 201508, P.R. China.
authors.forename: Defang
authors.initials: D
authors.lastname: Li
authors.affiliation: Department of Orthopedic Surgery, Jinshan Hospital, Fudan University, Shanghai 201508, P.R. China.
authors.forename: Houlei
authors.initials: H
authors.lastname: Wang
authors.affiliation: Department of Orthopedic Surgery, Second Affiliated Hospital of Anhui University of Medicine, Hefei, Anhui 230601, P.R. China.
authors.forename: Bin
authors.initials: B
authors.lastname: Zhu
authors.affiliation: Department of Orthopedic Surgery, Jinshan Hospital, Fudan University, Shanghai 201508, P.R. China.
authors.forename: Wei
authors.initials: W
authors.lastname: Lu
authors.affiliation: Center Laboratory, Jinshan Hospital, Fudan University, Shanghai 201508, P.R. China.
authors.forename: Guoxiong
authors.initials: G
authors.lastname: Xu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D002358:Cartilage, Articular / Q000473:pathology*; D002478:Cells, Cultured; D019902:Chondrocytes / Q000187:drug effects / Q000378:metabolism*; D016895:Culture Media, Serum-Free; D016326:Extracellular Matrix Proteins / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D008297:Male; D055514:Nephroblastoma Overexpressed Protein / Q000494:pharmacology*; D010641:Phenotype; D017207:Rats, Sprague-Dawley
chemical_list: D016895:Culture Media, Serum-Free; D016326:Extracellular Matrix Proteins; D055514:Nephroblastoma Overexpressed Protein