Dissertation
Dissertation > Medicine, health > Surgery > Orthopaedic Surgery ( movement system diseases,orthopedic surgery )

Zinc Deficiency Induced Mouse Bone Rarefaction and ZnTs

Author YeFang
Tutor YangMaoWei
School China Medical University
Course Surgery
Keywords ZnT (zinc transportor) chondrocyte epiphyseal growth plate
CLC R68
Type Master's thesis
Year 2008
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Zinc is an important element of the growth and development of children, and in recent years has gradually been recognized. Normal zinc nutrition can promote the healthy development of children, compared to the height of children of the same age zinc deficiency were significantly different: decreased bone density, the length of the femur was significantly lower than the control group, the morphological development of the flat bone deformity. Yuehong growing rats found that changes in the under zinc deficiency environmental, epiphyseal plate morphology, narrow, irregular, distorted. Epiphyseal plate chondrocytes deformity, the epiphyseal plate proliferative belt and the mast with reduction in the number of chondrocytes, not was typical columnar arrangement. Throughout the epiphyseal plate was to the degradation like change, does not have a normal morphology and function, thus affecting the growth and development of bones. Shows that zinc deficiency inhibit epiphyseal cartilage cell proliferation and differentiation, is likely to be caused by endochondral bone disorders and retardation of the main reasons to cause bone. Litchfield add the right amount of zinc in serum-free medium epiphyseal plate chondrocytes can promote the cartilage cell protein content and secretion of type II collagen, the appropriate concentration of zinc promote chondrocyte proliferation split, such as from the medium using zinc ion chelation Mixture the TPEN rid zinc, protein content within the cartilage cells and decrease in type II collagen. This result confirmed that zinc is an important factor to promote chondrocyte proliferation and differentiation. Wang Xinbin chicks give zinc deficiency food after three days of the epiphyseal plate chondrocytes by TUNEL and BrdU detection epiphyseal plate chondrocyte apoptosis has increased chondrocyte proliferation and differentiation of obstacles while using immune histochemical methods detected the epiphyseal plate growth factor levels yet reduce zinc deficiency environment chondrocyte differentiation disorders may be very close relationship with the growth factor, with zinc deficiency itself caused changes. According to the above results, we analyzed the zinc deficiency cause bone damage to the environment may be due to the epiphyseal plate chondrocytes zinc homeostasis damage, affecting the normal metabolism of zinc the normal chondrocytes proliferation and differentiation, and ultimately lead to developmental disorders of bone . Zinc ion is consumed in the process of cell metabolism must be replenished constantly. In the same time, the zinc ions can not pass freely through the cells within the film structure, only by a specific transporter protein and membrane channels in the cells normal metabolism. Recent studies indicate that, in mammalian cells, there are a class similar to ATP enzyme protein --- zinc transporters protein family the (Zinc transporters, ZnTs), zinc ion can be transporter, and adjust the zinc ion concentration of the plasma membrane. Zinc transporter proteins for a group of similar structure and function of the protein, and they all have six transmembrane region and has a region rich in histidine, this region may contain zinc ion binding site, and must be combined with zinc ions can play role. ZnTs expression by extracellular loop of the regulation of the level of domestic and zinc ions, the decreased expression of the the zinc deficiency environment ZnTs of so far in the zinc transporter protein family has seven members ZnT1 ~ 7 cloned. Zinc transporter ZnT1 ZnTs family is the first to be discovered, located in the cell membrane, zinc ions out of cells, play an important role in the regulation of the cell cycle, and expression in chondrocytes. ZnT5, and ZnT7 and osteoblast differentiation relationship, may be distributed in the intracellular vesicles surface, and is closely related with the release of the distribution and accumulation of the zinc ion. Chondrocyte differentiation process in cell cycle we speculate that the change ZnTs, caused by a metabolic disorder of the cartilage cells within the zinc ion, the normal zinc ions chondrocytes release chondrocyte proliferation and differentiation of obstacles, leading to bone damage. Zinc deficiency after epiphyseal plate chondrocytes pathological changes from the start to explore the changes of the biological characteristics of the chondrocytes after zinc deficiency, especially ZnT5, and ZnT7 and dynamic changes of intracellular zinc ions, trying to reveal the zinc deficiency epiphyseal plate cartilage cell differentiation the mechanism of the obstacles: Zinc deficiency, due to the decline in expression of ZnT5 and ZnT7 caused aggregation of zinc ions obstacles, resulting in the epiphyseal plate chondrocyte differentiation obstacles, and ultimately lead to bone development disorder.

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