Up-regulation of multiple proteins and biological processes during maxillary expansion in rats.
BACKGROUND
Maxillary expansion (ME) is a common practice in orthodontics that aims to increase the constricted maxillary arch width. Relapse often occurs, however, and better treatment strategies are needed. In order to develop a more effective method, this study was designed to further examine the process of tissue remodeling during ME, to identify the changes in expression of several proteins of interest, and to clarify the molecular mechanism responsible for tissue remodeling.


METHODS
Male Wistar rats were randomly divided into control and ME groups. The rats were euthanized at various intervals over 11 days, and the dissected palates were prepared for histological examination. The structure of the midpalatal sutures changed little during the first three days. Proteins from samples in the ground midpalatal tissues obtained on the third day were subjected to two-dimensional polyacrylamide gel electrophoresis (2-DE) and matrix assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF MS) analysis. Validation of protein expression was performed by Western blot analyses.


RESULTS
From day 5, chondrocytes in the inner layer of suture cartilage and osteoblasts at the end of the suture cartilage began to proliferate, and the skeletal matrix increased later adjacent to the cartilage in the ME group. Comparative proteomic analysis showed increases in 22 protein spots present in the ME group. The changes in three proteins closely related to osteogenesis (parathyroid hormone, osteoprotegerin and vimentin) were confirmed by Western blotting.


CONCLUSIONS
Many proteins are over-expressed during ME, and they may play an important role in the remodeling process.
Ma
Junqing
J
Institute of Stomatology, School of Stomatology, Nanjing Medical University, PR China. majunq@163.com
Wu
Yunxia
Y
Zhang
Weibing
W
Smales
Roger J
RJ
Huang
You
Y
Pan
Yongchu
Y
Wang
Lin
L
D000818:Animals; D001835:Body Weight / Q000502:physiology; D002356:Cartilage / Q000378:metabolism / Q000473:pathology; D049109:Cell Proliferation; D024042:Collagen Type I / Q000378:metabolism; D008297:Male; D018919:Neovascularization, Physiologic / Q000502:physiology; D010006:Osteoblasts / Q000378:metabolism / Q000473:pathology; D010012:Osteogenesis / Q000502:physiology*; D053244:Osteoprotegerin / Q000235:genetics / Q000378:metabolism*; D010155:Palatal Expansion Technique; D010159:Palate / Q000098:blood supply; D010281:Parathyroid Hormone / Q000235:genetics / Q000378:metabolism*; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D015854:Up-Regulation / Q000235:genetics / Q000502:physiology*; D014746:Vimentin / Q000235:genetics / Q000378:metabolism*
D024042:Collagen Type I; D053244:Osteoprotegerin; D010281:Parathyroid Hormone; D018809:Proliferating Cell Nuclear Antigen; D014746:Vimentin