THE ROLE OF INSULIN-LIKE GROWTH-FACTOR-II IN MAGNETIC-FIELD REGULATION OF BONE-FORMATION

被引:13
作者
RYABY, JT
FITZSIMMONS, RJ
KHIN, NA
CULLEY, PL
MAGEE, FP
WEINSTEIN, AM
BAYLINK, DJ
机构
[1] LOMA LINDA UNIV,JERRY L PETTIS MEM VET HOSP,DEPT MINERAL METAB,LOMA LINDA,CA 92357
[2] LOMA LINDA UNIV,SCH MED,DEPT MED,LOMA LINDA,CA 92357
[3] ARIZONA STATE UNIV,DEPT BIOENGN,TEMPE,AZ 85287
来源
BIOELECTROCHEMISTRY AND BIOENERGETICS | 1994年 / 35卷 / 1-2期
关键词
INSULIN-LIKE GROWTH FACTOR; BONE FORMATION; COMBINED MAGNETIC FIELD;
D O I
10.1016/0302-4598(94)87016-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Musculoskeletal tissue is uniquely sensitive to biophysical input, as demonstrated by both mechanical and electrical stimulation experiments. However, the mechanism by which biophysical input couples to cellular processes is not well understood. The results presented in these studies suggest that these stimuli are bioactive due to stimulation of growth factor biosynthesis by musculoskeletal target cells. We chose insulin-like growth factors (IGFs) as the model growth factor, as the IGFs are capable of stimulating chemotaxis, proliferation, and differentiation of osteoprogenitor cells. These specific studies addressed whether short-term exposure to combined a.c. and d.c. magnetic fields (CMF) would increase production of IGF-II by both osteoblast-like cell cultures as well as rat fracture callus cultures. In vitro studies on human osteoblast-like cell cultures demonstrated statistically significant increases in IGF-II levels and DNA synthesis after only 30 min CMF exposure. In rat fracture callus explant cultures, IGF-II levels were increased at least two-fold dependent on the callus differentiation stage, and these results were comparable with the effect of the osteotropic agent, parathyroid hormone. In summary, these results suggest that the mechanism by which CMF, and other biophysical stimuli, regulate musculoskeletal repair is by modulation of endogenous growth factor (IGF-II) synthesis and secretion.
引用
收藏
页码:87 / 91
页数:5
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