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首页> 外文期刊>International Journal of Molecular Sciences >Exogenous PTHrP Repairs the Damaged Fracture Healing of PTHrP+/? Mice and Accelerates Fracture Healing of Wild Mice
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Exogenous PTHrP Repairs the Damaged Fracture Healing of PTHrP+/? Mice and Accelerates Fracture Healing of Wild Mice

机译:外源性PTHrP修复PTHrP + /?的受损骨折愈合。小鼠并促进野生小鼠的骨折愈合

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Bone fracture healing is a complicated physiological regenerative process initiated in response to injury and is similar to bone development. To demonstrate whether an exogenous supply of parathyroid hormone–related protein (PTHrP) helps in bone fracture healing, closed mid-diaphyseal femur fractures were created and stabilized with intramedullary pins in eight-week-old wild-type (WT) PTHrP+/+ and PTHrP+/? mice. After administering PTHrP for two weeks, callus tissue properties were analyzed at one, two, and four weeks post-fracture (PF) by various methods. Bone formation–related genes and protein expression levels were evaluated by real-time reverse transcriptase–polymerase chain reaction and Western blots. At two weeks PF, mineral density of callus, bony callus areas, mRNA levels of alkaline phosphatase (ALP), type I collagen, Runt-related transcription factor 2 (Runx-2), and protein levels of Runx-2 and insulin-like growth factor-1 decreased in PTHrP+/? mice compared with WT mice. At four weeks PF, total collagen-positive bony callus areas, osteoblast number, ALP-positive areas, and type I collagen-positive areas all decreased in PTHrP+/? mice. At both two and four weeks PF, tartrate-resistant acid phosphatase–positive osteoclast number and surface decreased a little in PTHrP+/? mice. The study indicates that exogenous PTHrP provided by subcutaneous injection could redress impaired bone fracture healing, leading to mutation of activated PTHrP by influencing callus areas, endochondral bone formation, osteoblastic bone formation, and bone turnover.
机译:骨折愈合是响应损伤而启动的复杂的生理再生过程,类似于骨骼发育。为了证明甲状旁腺激素相关蛋白(PTHrP)的外源供应是否有助于骨折愈合,在八周大的野生型(WT)PTHrP + / +中使用闭合的髓内针形成了闭合的干dia端股骨骨折并使其稳定。 PTHrP + /?老鼠。施用PTHrP 2周后,通过各种方法在骨折后(PF)的第1、2和4周分析愈伤组织的特性。通过实时逆转录酶-聚合酶链反应和蛋白质印迹评估骨形成相关基因和蛋白质表达水平。在PF的两周时,愈伤组织的矿物质密度,骨性愈伤组织区域,碱性磷酸酶(ALP)的mRNA水平,I型胶原蛋白,Runt相关转录因子2(Runx-2)以及Runx-2和类似胰岛素的蛋白质水平PTHrP + /?中生长因子-1降低小鼠与野生型小鼠相比。 PF 4周时,PTHrP + /?的总胶原阳性骨call区域,成骨细胞数目,ALP阳性区域和I型胶原阳性区域均下降。老鼠。在PF的两周和四周时,PTHrP + /?的抗酒石酸酸性磷酸酶阳性的破骨细胞数量和表面均略有下降。老鼠。研究表明,皮下注射提供的外源性PTHrP可以纠正受损的骨折愈合,并通过影响愈伤组织区域,软骨内骨形成,成骨细胞形成和骨转换来导致活化的PTHrP突变。

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