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author:("Jiang, xiamen")
1.  Does phosphorylation of cofilin affect the progression of human bladder cancer? 
BMC Cancer  2013;13:45.
We determined the differently expressed protein profiles and their functions in bladder cancer tissues with the aim of identifying possible target proteins and underlying molecular mechanisms for taking part in their progression.
We examined the expression of proteins by proteomic analysis and western blot in normal urothelium, non-muscle-invasive bladder cancers (NMIBCs), and muscle-invasive bladder cancers (MIBCs). The function of cofilin was analyzed using T24 human bladder cancer cells.
The expression levels of 12 proteins were altered between bladder cancers and normal bladder tissues. Of these proteins, 14-3-3σ was upregulated in both NMIBCs and MIBCs compared with controls. On the other hand, myosin regulatory light chain 2, galectin-1, lipid-binding AI, annexin V, transthyretin, CARD-inhibitor of NF-κB-activating ligand, and actin prepeptide were downregulated in cancer samples. Cofilin, an actin-depolymerizing factor, was prominent in both NMIBCs and MIBCs compared with normal bladder tissues. Furthermore, we confirmed that cofilin phosphorylation was more prominent in MIBCs than in NMIBCs using immunoblotting and immunohistochemcal analyses. Epidermal growth factor (EGF) increased the phosphorylation of cofilin and elevated the migration in T24 cells. Knockdown of cofilin expression with small interfering RNA attenuated the T24 cell migration in response to EGF.
These results demonstrate that the increased expression and phosphorylation of cofilin might play a role in the occurrence and invasiveness of bladder cancer. We suspected that changes in cofilin expression may participate in the progression of the bladder cancer.
PMCID: PMC3568060  PMID: 23374291
Cofilin; Phosphorylation; Invasion; Urothelial cell carcinoma
2.  Denervation impairs bone regeneration during distraction osteogenesis in rabbit tibia lengthening 
Acta Orthopaedica  2012;83(4):406-410.
Background and purposes
The nervous system plays an important role in bone metabolism. However, the effect of denervation on bone formation during distraction osteogenesis (DO) remains unclear. We studied neural influence on bone regeneration during DO in a rabbit model.
24 New Zealand male white rabbits underwent left tibial osteodistraction. Before distraction, the animals were randomly divided into group R (resected left sciatic nerve) and group I (intact left sciatic nerve). 8 weeks after completion of distraction, the animals were killed and the lengthened tibias were harvested for radiography, micro-CT, histological evaluation, and mechanical testing.
New regenerated bone was present in the distraction gaps of all animals at the end of the study, as revealed by radiography, micro-CT, and histology. However, less new bone formation and a lower degree of mineralization were observed in group R. The mechanical strength of the distraction gap in group I was 1.3-fold greater than that in group R when measured using the 3-point bending test.
The results suggest that the nervous system plays an essential role during DO: the denervation appears to have an inhibitory effect on bone formation.
PMCID: PMC3427633  PMID: 22880710
3.  Tetrahydrobiopterin Inhibits PDGF-stimulated Migration and Proliferation in Rat Aortic Smooth Muscle Cells via the Nitric Oxide Synthase-independent Pathway 
Tetrahydrobiopterin (BH4), an essential cofactor for nitric oxide synthase (NOS) activity, is known to play important roles in modulating both NO and superoxide production during vascular diseases such as atherosclerosis. However, the role of BH4 in functions of vascular smooth muscle cells is not fully known. In this study, we tested the effects of BH4 and dihydrobiopterin (BH2), a BH4 precursor, on migration and proliferation in response to platelet-derived growth factor-BB (PDGF-BB) in rat aortic smooth muscle cells (RASMCs). Cell migration and proliferation were measured using a Boyden chamber and a 5-bromo-2'-deoxyuridine incorporation assay, respectively, and these results were confirmed with an ex vivo aortic sprout assay. Cell viability was examined by 2,3-bis [2-methoxy-4-nitro-5-sulfophenyl]-2H-tetrazolium-5-carboxanilide assays. BH4 and BH2 decreased PDGF-BB-induced cell migration and proliferation in a dose-dependent manner. The inhibition of cell migration and proliferation by BH4 and BH2 was not affected by pretreatment with NG-nitro-L-arginine methyl ester, a NOS inhibitor. Moreover, the sprout outgrowth formation of aortic rings induced by PDGF-BB was inhibited by BH4 and BH2. Cell viability was not inhibited by BH4 and BH2 treatment. The present results suggest that BH4 and BH2 may inhibit PDGF-stimulated RASMC migration and proliferation via the NOS-independent pathway. Therefore, BH4 and its derivative could be useful for the development of a candidate molecule with an NO-independent anti-atherosclerotic function.
PMCID: PMC2902810  PMID: 20631891
Tetrahydrobiopterin; Migration; Nitric oxide; Proliferation; Rat aortic smooth muscle cells

Results 1-3 (3)