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mTOR pathway 期刊论文

编号：

66d52ce8-00e6-466c-8323-439ac4977312
作者：

Sun, Jie(孙杰)#^[1]Song, Xin(宋鑫)^[1]Su, Ling^[2];Cao, Shifeng(曹师锋)*^[1]
语种：

英文
期刊：

INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY ISSN：1936-2625 2018 年 11 卷 6 期 (3000 - 3009)
收录：
关键词：

Osteoarthritis LncHIFCAR HIF-1 alpha VEGF BNIP3 PI3K/AKT/mTOR pathway
摘要：

Osteoarthritis (OA) is a progressive disease that characterized by synovial inflammation and loss of cartilage in the joint. This study aimed to elucidate the potential role of long non-coding RNA LncHIFCAR in the development of osteoarthritis (OA). Expression of LncHIFCAR and HIF-1 alpha in OA and normal cartilage tissues were determined. ATDC5 chondrocyte cells were cultured under hypoxia condition to establish a cell model of OA. Additionally, LncHIFCAR was suppressed in ATDC5 cells and the effects of LncHIFCAR suppression on hypoxia-induced cell injury were investigated by assessing cell proliferation, apoptosis, inflammatory response, and matrix synthesis. Furthermore, interactions between LncHIFCAR and HIF-1 alpha as well as HIF-1 alpha target genes (VEGF and BNIP3) were explored. Additionally, whether LncHIFCAR affected the expression of PI3K/AKT/mTOR pathway-related proteins was detected. LncHIFCAR and HIF-1 alpha were up-regulated in OA tissues. Hypoxia induced ATDC5 cell injury and increased LncHIFCAR expression. Suppression of LncHIFCAR significantly improved hypoxia-induced cell injury by promoting cell proliferation, inhibiting apoptosis, decreasing the secretion of TNF-alpha and IL-6, and suppressing the synthesis of MMPs. In addition, LncHIFCAR positively regulated HIF-1 alpha and HIF-1 alpha target genes (VEGF and BNIP3). LncHIFCAR promoted hypoxia-induced inflammatory response and matrix synthesis by upregulation of VEGF, and induced hypoxia-induced apoptosis via upregulation of BNIP3. Furthermore, LncHIFCAR significantly inhibited hypoxia-induced activation of PI3K/AKT/mTOR pathway. Our results indicate that LncHIFCAR is up-regulated in OA tissues and suppression of LncHIFCAR may improve hypoxia-induced cell injury via positively regulating HIF-1 alpha and HIF-1 alpha target genes (VEGF and BNIP3). The PI3K/AKT/mTOR pathway may thus be a possible mechanism to mediate LncHIFCAR function in OA development.
推荐引用方式
GB/T 7714：

Sun Jie,Song Xin,Su Ling, et al. Long non-coding RNA LncHIFCAR promotes osteoarthritis development via positively regulating HIF-1 alpha and activating the PI3K/AKT/mTOR pathway [J].INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY,2018,11(6):3000-3009.
APA：

Sun Jie,Song Xin,Su Ling,Cao Shifeng.(2018).Long non-coding RNA LncHIFCAR promotes osteoarthritis development via positively regulating HIF-1 alpha and activating the PI3K/AKT/mTOR pathway .INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY,11(6):3000-3009.
MLA：

Sun Jie, et al. "Long non-coding RNA LncHIFCAR promotes osteoarthritis development via positively regulating HIF-1 alpha and activating the PI3K/AKT/mTOR pathway" .INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY 11,6(2018):3000-3009.
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