title: Acidic pH environment induces autophagy in osteoblasts.
abstract: Osteoblasts (OBs) play an important role in bone fracture healing, yet the extreme adverse microenvironment in fracture sites has a negative impact on the survival of OBs. Therefore, it is important to study how OBs behave in the complex fracture microenvironment. Studies have shown that autophagy plays a pivotal role in maintaining cellular homeostasis and defending the cell against adverse microenvironments. In this study we found the induction of autophagy in OBs at femoral bone fracture sites, which may be a result of ischemia, oxidative stress and hypoxia within the local area. At fracture sites a low pH environment also developed. Until now it has been unclear whether the induction of autophagy in osteoblasts is triggered by the acidic pH environment. Therefore, we cultured OBs in vitro in media of different pH values, and found both autophagy and apoptosis increased in OBs in acidic conditions. However, when autophagy inhibitor chloroquine (CQ) was used, apoptosis increased significantly compared with that without CQ. Thus indicating that inhibition of autophagy may promote apoptosis in OBs in an acidic environment, which may provide a new therapeutic strategy to decrease cell apoptosis in OBs through the use of drugs that modulate the autophagic state.
authors.affiliation: Department of Oral and Maxillofacial Surgery, the Second Hospital of Shandong University, Jinan, China.|School of Stomatology, Shandong University, Jinan, China.
authors.forename: Zhichao
authors.initials: Z
authors.lastname: Zhang
authors.affiliation: Department of Oral and Maxillofacial Surgery, the Second Hospital of Shandong University, Jinan, China.
authors.forename: Qingguo
authors.initials: Q
authors.lastname: Lai
authors.affiliation: School of Medicine, Shandong University, Jinan, China.
authors.forename: Yanan
authors.initials: Y
authors.lastname: Li
authors.affiliation: School of Stomatology, Shandong University, Jinan, China.
authors.forename: Chao
authors.initials: C
authors.lastname: Xu
authors.affiliation: Department of Oral and Maxillofacial Surgery, the Second Hospital of Shandong University, Jinan, China.
authors.forename: Xiaopeng
authors.initials: X
authors.lastname: Tang
authors.affiliation: Department of Oral and Maxillofacial Surgery, the Second Hospital of Shandong University, Jinan, China.
authors.forename: Jiangbo
authors.initials: J
authors.lastname: Ci
authors.affiliation: School of Stomatology, Shandong University, Jinan, China.
authors.forename: Shaolong
authors.initials: S
authors.lastname: Sun
authors.affiliation: School of Stomatology, Shandong University, Jinan, China.
authors.forename: Bingbing
authors.initials: B
authors.lastname: Xu
authors.affiliation: School of Medicine, Shandong University, Jinan, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Li
mesh_terms: D000143:Acids / Q000494:pharmacology*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D000071182:Autophagosomes / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D001343:Autophagy / Q000187:drug effects*; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D050723:Fractures, Bone / Q000473:pathology; D006863:Hydrogen-Ion Concentration; D008297:Male; D051379:Mice; D010006:Osteoblasts / Q000166:cytology* / Q000187:drug effects / Q000648:ultrastructure; D051381:Rats
chemical_list: D000143:Acids