Wang Bin, Mai Caiyuan, Pan Lei
Department of Orthopedics, Foshan Sanshui District People's Hospital, Foshan 528100, China.
Department of Obstetrics, Guangdong Women and Children's Hospital, Guangzhou 510010, China.
Emerg Med Int. 2022 Oct 29;2022:1022078. doi: 10.1155/2022/1022078. eCollection 2022.
The classical osteoporotic signaling pathways include the four key genes (LRP5, Runx2, Osterix, and RANKL) influencing the regulation of osteogenesis and osteoclastogenesis. This study investigates the expression of these four genes associated with bone remodeling during fracture healing.
Ovariectomized rats as an osteoporotic group were randomly divided into three groups-group A, group B, and group C. Nonosteoporotic rats as the control group were likewise divided into three groups A0, B0, and C0, using the same method. The rats were killed on the third day of fractures in groups A and A0, on the seventh day of fractures in groups B and B0, and on the fourteenth day of fractures in groups C and C0. The bone specimens were taken from the femoral fracture site, and the expression level of each gene in the bone specimens was detected using RT-qPCR, Western blotting, and immunohistochemistry.
LRP5, Runx2, and Osterix expressions were decreased in osteoporotic rat fractures and then increased over time. The expression of RANKL was elevated in osteoporotic rat bone specimens, which decreased after that.
The expressions of the four genes varied with time after fracture, which could be associated with the various stages of bone repair. The four genes can inform practice in ideal interventions in the prevention and management of osteoporosis.
经典的骨质疏松信号通路包括影响成骨和破骨细胞生成调节的四个关键基因(LRP5、Runx2、Osterix和RANKL)。本研究调查骨折愈合过程中这四个与骨重塑相关基因的表达情况。
将去卵巢大鼠作为骨质疏松组随机分为三组——A组、B组和C组。将非骨质疏松大鼠作为对照组,同样采用相同方法分为A0组、B0组和C0组。A组和A0组大鼠在骨折后第3天处死,B组和B0组在骨折后第7天处死,C组和C0组在骨折后第14天处死。从股骨骨折部位采集骨标本,采用RT-qPCR、蛋白质免疫印迹法和免疫组织化学法检测骨标本中各基因的表达水平。
LRP5、Runx2和Osterix在骨质疏松大鼠骨折中的表达降低,随后随时间增加。RANKL在骨质疏松大鼠骨标本中的表达升高,之后降低。
骨折后四个基因的表达随时间变化,这可能与骨修复的不同阶段有关。这四个基因可为骨质疏松预防和管理的理想干预措施提供实践依据。