PMID- 23292283
OWN - NLM
STAT- MEDLINE
DCOM- 20130710
LR  - 20220331
IS  - 1791-244X (Electronic)
IS  - 1107-3756 (Linking)
VI  - 31
IP  - 3
DP  - 2013 Mar
TI  - Osteogenic potential of bone marrow stromal cells derived from 
      streptozotocin-induced diabetic rats.
PG  - 614-20
LID - 10.3892/ijmm.2013.1227 [doi]
AB  - Type 1 diabetes mellitus (T1DM) is associated with a series of bone 
      complications, which are still a great challenge in the clinic. Bone marrow 
      stromal cells (BMSCs) are crucial to bone remodeling and are attractive 
      candidates for tissue engineering. Hence, we aimed to investigate whether 
      impaired functions of BMSCs play a role in the pathogenesis of bone complications 
      associated with T1DM. BMSCs were isolated from normal and streptozotocin-induced 
      diabetic rats, and their proliferation and osteogenic differentiation ability 
      were analyzed. Diabetic BMSCs demonstrated reduced proliferation ability, 
      osteoblast gene expression, alkaline phosphatase activity and mineralization. 
      Nude mice transplanted with diabetic BMSCs in a calcium phosphate cement scaffold 
      exhibited reduced new bone formation, as detected by hematoxylin and eosin 
      staining and immunohistochemistry. These changes may be partially related to 
      impaired insulin and insulin-like growth factor 1 (IGF-1) signaling. Weak gene 
      expression of insulin receptor (IR), IGF-1, insulin-like growth factor 1 receptor 
      (IGF-1R), and insulin receptor substrate-1 (IRS-1) was observed in the diabetic 
      BMSCs compared with normal BMSCs, together with decreased protein level of IGF-1, 
      IGF-1R, IRS-1 and phosphorylated extracellular signal-regulated kinase. 
      Therefore, impaired proliferation and osteogenic potential of BMSCs may be 
      responsible for bone complications related to T1DM, mediated partially by 
      impaired insulin and IGF-1 signaling. These findings may provide a new target 
      with which to devise strategies for therapy.
FAU - Zhao, Yan-Fang
AU  - Zhao YF
AD  - Department of Prosthodontics, Ninth People's Hospital affiliated to Shanghai Jiao 
      Tong University School of Medicine, Shanghai, PR China.
FAU - Zeng, De-Liang
AU  - Zeng DL
FAU - Xia, Lun-Guo
AU  - Xia LG
FAU - Zhang, Song-Mei
AU  - Zhang SM
FAU - Xu, Lian-Yi
AU  - Xu LY
FAU - Jiang, Xin-Quan
AU  - Jiang XQ
FAU - Zhang, Fu-Qiang
AU  - Zhang FQ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130103
PL  - Greece
TA  - Int J Mol Med
JT  - International journal of molecular medicine
JID - 9810955
RN  - 0 (Insulin)
RN  - 5W494URQ81 (Streptozocin)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - EC 2.7.10.1 (Receptor, IGF Type 1)
RN  - EC 2.7.10.1 (Receptor, Insulin)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
RN  - EC 3.1.3.1 (Alkaline Phosphatase)
SB  - IM
MH  - Alkaline Phosphatase/metabolism
MH  - Animals
MH  - Bone Marrow Cells/metabolism
MH  - Calcification, Physiologic
MH  - Cell Differentiation/genetics
MH  - Cell Proliferation
MH  - Cells, Cultured
MH  - Diabetes Mellitus, Experimental/*metabolism
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - Gene Expression
MH  - Insulin/*metabolism
MH  - Insulin-Like Growth Factor I/biosynthesis/genetics/*metabolism
MH  - Male
MH  - Mesenchymal Stem Cells/*metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Osteoblasts/cytology/metabolism
MH  - Osteogenesis/genetics
MH  - Phosphorylation
MH  - Rats
MH  - Rats, Wistar
MH  - Receptor, IGF Type 1/biosynthesis/genetics
MH  - Receptor, Insulin/biosynthesis/genetics
MH  - Signal Transduction
MH  - Streptozocin
EDAT- 2013/01/08 06:00
MHDA- 2013/07/11 06:00
CRDT- 2013/01/08 06:00
PHST- 2012/09/29 00:00 [received]
PHST- 2012/11/09 00:00 [accepted]
PHST- 2013/01/08 06:00 [entrez]
PHST- 2013/01/08 06:00 [pubmed]
PHST- 2013/07/11 06:00 [medline]
AID - 10.3892/ijmm.2013.1227 [doi]
PST - ppublish
SO  - Int J Mol Med. 2013 Mar;31(3):614-20. doi: 10.3892/ijmm.2013.1227. Epub 2013 Jan 
      3.