Yong Zhang1, Yuan Zhang2, Kun Yang3, Weizhong Guo3, Xiaojun Ma3, Xingming Ma3, Zengliang Wang4. 1. Department of Trauma and Joint, The Second Hospital of Qinhuangdao, Qinhuangdao, Hebei, 066600, China. zhangyong_tijh@126.com. 2. Department of Gastroenterology and Nephrology, The Second Hospital of Qinhuangdao, Qinhuangdao, Hebei, 066600, China. 3. Department of Trauma and Joint, The Second Hospital of Qinhuangdao, Qinhuangdao, Hebei, 066600, China. 4. Department of Osteology, Tianjin Hospital, No. 406, Jiefang South Road, Tianjin, 300211, China. wangzengliang_tijh@163.com.
Abstract
BACKGROUND: Most fractures could heal after treatment, around 5-10 % of patients still develop delayed union and nonunion. Evidence has increasingly shown that abnormal expression of long noncoding RNAs is closely related to the occurrence and development of various diseases including fracture healing. However, evidence regarding the effect of MALAT1 on fracture healing remains limited. OBJECTIVES: In this study, we attempt to explore the role of MALAT1 during the process of femoral neck fracture healing and elucidate the underlying mechanism of this disease. METHODS: We first detect the expression of lncRNAs in serums from 3 pairs of patients with delayed femoral neck fracture healing and healthy volunteers using lncRNA microarray. And the expression of long noncoding RNA MALAT1 in serums and LPS-treated MG-63 cells was measured using qRT-PCR. CCK-8 assay, cell migration and qRT-PCR were applied to the role of MALAT1 knockdown in LPS-treated MG-63 cells. ELISA was used for the measurement of inflammatory cytokines in serums of patients and healthy volunteers. The bioinformatics analysis and the rescue experiment were devoted to the underlying mechanism. RESULTS: MALAT1 expression was up-regulated in serum of patients with delayed union of femoral neck fracture. MALAT1 knockdown promoted cell viability and migration, reduced inflammation in LPS-treated MG-63 cells. The bioinformatics analysis showed MALAT1 acts as a molecular sponge for miR-212. And SOX6 was a target of miR-212. Besides, MALAT1 knockdown suppressed SOX6 expression via targeting miR-212 in LPS-treated MG-63 cells. CONCLUSIONS: These data suggest MALAT1 knockdown promoted the biological behavior of LPS-treated MG-63 cells via sponging miR-212, which may provide a new therapeutic avenue for delayed union of femoral neck fracture.
BACKGROUND: Most fractures could heal after treatment, around 5-10 % of patients still develop delayed union and nonunion. Evidence has increasingly shown that abnormal expression of long noncoding RNAs is closely related to the occurrence and development of various diseases including fracture healing. However, evidence regarding the effect of MALAT1 on fracture healing remains limited. OBJECTIVES: In this study, we attempt to explore the role of MALAT1 during the process of femoral neck fracture healing and elucidate the underlying mechanism of this disease. METHODS: We first detect the expression of lncRNAs in serums from 3 pairs of patients with delayed femoral neck fracture healing and healthy volunteers using lncRNA microarray. And the expression of long noncoding RNA MALAT1 in serums and LPS-treated MG-63 cells was measured using qRT-PCR. CCK-8 assay, cell migration and qRT-PCR were applied to the role of MALAT1 knockdown in LPS-treated MG-63 cells. ELISA was used for the measurement of inflammatory cytokines in serums of patients and healthy volunteers. The bioinformatics analysis and the rescue experiment were devoted to the underlying mechanism. RESULTS: MALAT1 expression was up-regulated in serum of patients with delayed union of femoral neck fracture. MALAT1 knockdown promoted cell viability and migration, reduced inflammation in LPS-treated MG-63 cells. The bioinformatics analysis showed MALAT1 acts as a molecular sponge for miR-212. And SOX6 was a target of miR-212. Besides, MALAT1 knockdown suppressed SOX6 expression via targeting miR-212 in LPS-treated MG-63 cells. CONCLUSIONS: These data suggest MALAT1 knockdown promoted the biological behavior of LPS-treated MG-63 cells via sponging miR-212, which may provide a new therapeutic avenue for delayed union of femoral neck fracture.