ABSTRACT
Objective To investigate the effect of preptin on proliferation and differentiation of human osteoblasts. Methods After human osteoblasts were incubated with 10-10, 10-9, 10-8 , 10-7 mol/L preptin for 24 h,the proliferation of osteoblasts was determined by[3H]thymidine incorporation and alkaline phosphatase (ALP)activity was assayed by spectrophotometric measurement. The phosphorylation levels of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase ( MAPK), extracellular signal-regulated kinase (ERK) 1/2 were assayed by Western blot. ERK inhibitor PD98059, p38MAPK inhibitor SB203580, and JNK inhibitor SP600125were used for investigating the signal pathway of preptin-stimulated osteoblast proliferation and differentiation.Results Preptin dose-dependently increased human proliferation of osteoblasts and ALP activity with the maximum effect at the concentration of l0-9 mol/L (both P<0.01 ). Preptin stimulated ERK phosphorylation in human osteoblasts, but not p38 MAPK and JNK phosphorylation. PD98059 blocked preptin-sitmulated human osteoblasts proliferation and ALP activity (both P<0.05 ), while SB203580 and SP600125 had no effect. Conclusions Preptin promotes the proliferation and differentiation of human osteoblasts through ERK pathway.
ABSTRACT
Objective To investigate the effect and mechnism of preptin on connect tissue growth factor (CTGF) in human osteoblasts. Methods Recombinant human preptin was used to treat primary human osteoblasts, and Western blot was used to detect CTGF protein level. Mitogen-activated protein kinase p38(p38MAPK), extracellular signal-regulated kinase (ERK1/2), c-jun N-terminal Kinase (JNK), and their phosphorylation levels were also detected by Western blot. MAPK inhibitors (PD98059, SP600125, or SB203580)were used to elucidate the mechnism of preptin induced expression of CTGF in human osteoblasts. Results Treatment of human osteoblasts with preptin caused a time and dose-dependent increase in CTGF secretion. Preptin induced activation of ERK, but not p38MAPK or JNK in human osteoblasts. Furhermore, pretreatment of human osteoblasts with the ERK inhibitor PD98059 abolished the preptin-induced CTGF secretion. Conclusion Preptin induces CTGF expression in human osteoblasts by means of ERK/MAPK pathway.
ABSTRACT
Fasting plasma preptin level was assayed by RIA in the patients with different glucose tolerances. Regarding fasting plasma preptin levels, it was higher in females than in males. Fasting plasma preptin level was increased in patients with type 2 diabetes as compared with subjects of impaired glucose tolerance and normal controls, and there were positive correlations with diastolic blood pressure, blood triglyceride, total cholesterol, high-density lipoprotein-cholesterol, free fatty acids, 2 h plasma glucose after glucose load, HbA1C and HOMA-IR, suggesting a potential link between preptin and glucose-lipid metabolism and insulin resistance.