FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2896811704> ?p ?o ?g. }

• W2896811704 endingPage "5303" @default.
• W2896811704 startingPage "5287" @default.
• W2896811704 abstract "Abstract microRNA (miR) has been shown to be involved in the treatment of diseases such as osteoarthritis (OA). This study aims to investigate the role of miR‐206 in regulating insulin‐like growth factor‐1 (IGF‐1) in chondrocyte autophagy and apoptosis in an OA rat model via the phosphoinositide 3‐kinase (P13K)/protein kinase B (AKT)‐mechanistic target of rapamycin (mTOR) signaling pathway. Wistar rats were used to establish the OA rat model, followed by the observation of histopathological changes, Mankin score, and the detection of IGF‐1‐positive expression and tissue apoptosis. The underlying regulatory mechanisms of miR‐206 were analyzed in concert with treatment by an miR‐206 mimic, an miR‐206 inhibitor, or small interfering RNA against IGF‐1 in chondrocytes isolated from OA rats. Then, the expression of miR‐206, IGF‐1, and related factors in the signaling pathway, cell cycle, and apoptosis, as well as inflammatory factors, were determined. Subsequently, chondrocyte proliferation, cell cycle distribution, apoptosis, autophagy, and autolysosome were measured. OA articular cartilage tissue exhibited a higher Mankin score, promoted cell apoptotic rate, increased expression of IGF‐1, Beclin1, light chain 3 (LC3), Unc‐51‐like autophagy activating kinase 1 (ULK1), autophagy‐related 5 (Atg5), caspase‐3, and Bax, yet exhibited decreased expression of miR‐206, P13K, AKT, mTOR, and Bcl‐2. Besides, miR‐206 downregulated the expression of IGF‐1 and activated the P13K/AKT signaling pathway. Moreover, miR‐206 overexpression and IGF‐1 silencing inhibited the interleukins levels (IL‐6, IL‐17, and IL‐18), cell apoptotic rate, the formation of autolysosome, and cell autophagy while promoting the expression of IL‐1β and cell proliferation. The findings from our study provide a basis for the efficient treatment of OA by investigating the inhibitory effects of miR‐206 on autophagy and apoptosis of articular cartilage in OA via activating the IGF‐1‐mediated PI3K/AKT‐mTOR signaling pathway." @default.
• W2896811704 created "2018-10-26" @default.
• W2896811704 creator A5034982613 @default.
• W2896811704 creator A5041858328 @default.
• W2896811704 creator A5056122667 @default.
• W2896811704 creator A5060010401 @default.
• W2896811704 creator A5090957978 @default.
• W2896811704 date "2018-10-18" @default.
• W2896811704 modified "2023-10-06" @default.
• W2896811704 title "microRNA‐206 is required for osteoarthritis development through its effect on apoptosis and autophagy of articular chondrocytes via modulating the phosphoinositide 3‐kinase/protein kinase B‐mTOR pathway by targeting insulin‐like growth factor‐1" @default.
• W2896811704 cites W1964420304 @default.
• W2896811704 cites W1965671005 @default.
• W2896811704 cites W1969708590 @default.
• W2896811704 cites W1976178491 @default.
• W2896811704 cites W1979161900 @default.
• W2896811704 cites W1985262555 @default.
• W2896811704 cites W1985406857 @default.
• W2896811704 cites W1990435491 @default.
• W2896811704 cites W1992735807 @default.
• W2896811704 cites W2003375725 @default.
• W2896811704 cites W2020405841 @default.
• W2896811704 cites W2021387873 @default.
• W2896811704 cites W202319641 @default.
• W2896811704 cites W2042787577 @default.
• W2896811704 cites W2042814728 @default.
• W2896811704 cites W2061599785 @default.
• W2896811704 cites W2065824624 @default.
• W2896811704 cites W2065977480 @default.
• W2896811704 cites W2067692987 @default.
• W2896811704 cites W2068859480 @default.
• W2896811704 cites W2070759795 @default.
• W2896811704 cites W2076542702 @default.
• W2896811704 cites W2096894782 @default.
• W2896811704 cites W2108888253 @default.
• W2896811704 cites W2113017107 @default.
• W2896811704 cites W2118476803 @default.
• W2896811704 cites W2122799748 @default.
• W2896811704 cites W2123728720 @default.
• W2896811704 cites W2130979840 @default.
• W2896811704 cites W2133915381 @default.
• W2896811704 cites W2140513563 @default.
• W2896811704 cites W2157741650 @default.
• W2896811704 cites W2159926715 @default.
• W2896811704 cites W2277285115 @default.
• W2896811704 cites W2416573624 @default.
• W2896811704 cites W2546109636 @default.
• W2896811704 cites W2625804785 @default.
• W2896811704 cites W2740975586 @default.
• W2896811704 cites W2755427773 @default.
• W2896811704 cites W2766191041 @default.
• W2896811704 cites W2766416282 @default.
• W2896811704 cites W2786784128 @default.
• W2896811704 cites W2793175077 @default.
• W2896811704 cites W4211256917 @default.
• W2896811704 cites W4379017299 @default.
• W2896811704 doi "https://doi.org/10.1002/jcb.27803" @default.
• W2896811704 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30335903" @default.
• W2896811704 hasPublicationYear "2018" @default.
• W2896811704 type Work @default.
• W2896811704 sameAs 2896811704 @default.
• W2896811704 citedByCount "18" @default.
• W2896811704 countsByYear W28968117042019 @default.
• W2896811704 countsByYear W28968117042020 @default.
• W2896811704 countsByYear W28968117042021 @default.
• W2896811704 countsByYear W28968117042022 @default.
• W2896811704 countsByYear W28968117042023 @default.
• W2896811704 crossrefType "journal-article" @default.
• W2896811704 hasAuthorship W2896811704A5034982613 @default.
• W2896811704 hasAuthorship W2896811704A5041858328 @default.
• W2896811704 hasAuthorship W2896811704A5056122667 @default.
• W2896811704 hasAuthorship W2896811704A5060010401 @default.
• W2896811704 hasAuthorship W2896811704A5090957978 @default.
• W2896811704 hasConcept C104317684 @default.
• W2896811704 hasConcept C105702510 @default.
• W2896811704 hasConcept C119056186 @default.
• W2896811704 hasConcept C145059251 @default.
• W2896811704 hasConcept C170493617 @default.
• W2896811704 hasConcept C184235292 @default.
• W2896811704 hasConcept C185592680 @default.
• W2896811704 hasConcept C190283241 @default.
• W2896811704 hasConcept C203522944 @default.
• W2896811704 hasConcept C22615655 @default.
• W2896811704 hasConcept C2775960820 @default.
• W2896811704 hasConcept C2780550940 @default.
• W2896811704 hasConcept C2780689927 @default.
• W2896811704 hasConcept C2781322055 @default.
• W2896811704 hasConcept C2781403057 @default.
• W2896811704 hasConcept C29537977 @default.
• W2896811704 hasConcept C502942594 @default.
• W2896811704 hasConcept C54009773 @default.
• W2896811704 hasConcept C55493867 @default.
• W2896811704 hasConcept C62478195 @default.
• W2896811704 hasConcept C75217442 @default.
• W2896811704 hasConcept C86554907 @default.
• W2896811704 hasConcept C86803240 @default.
• W2896811704 hasConcept C95444343 @default.
• W2896811704 hasConceptScore W2896811704C104317684 @default.
• W2896811704 hasConceptScore W2896811704C105702510 @default.

• next