miR-140-5p/miR-149 Affects Chondrocyte Proliferation, Apoptosis, and Autophagy by Targeting FUT1 in Osteoarthritis

Wang, Zi; Hu, Jialei; Pan, Yue; Shan, Yujia; Jiang, Liqun; Qi, Xia; Li, Jia

doi:10.1007/s10753-018-0750-6

Cited by 76 publications

(42 citation statements)

References 39 publications

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“…Chondrocytes were extracted from OA cartilage tissues, as previously described 22 . In brief, cartilage specimen was dissected into small sections and subjected to sequential digestion with 0.1% trypsin (Invitrogen, Carlsbad, CA, USA) for 30 min and then with 0.2% collagenase Type II (Millipore Corp., Billerica, MA, USA) in Dulbecco’s modified Eagle’s medium (DMEM) (Gibco) for 10 h at 37 °C.…”

Section: Methodsmentioning

confidence: 99%

Long non-coding RNA HOTAIR promotes osteoarthritis progression via miR-17-5p/FUT2/β-catenin axis

et al. 2018

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Osteoarthritis (OA) is a chronic joint disease and hard to cure at present. Accumulating evidence suggests long noncoding RNA-HOTAIR (lncRNA-HOTAIR) plays important role in OA progression. However, the underlying molecular mechanism of HOTAIR in OA progression has not been well elucidated. In the present study, we identified that HOTAIR level was upregulated in OA cartilage tissues. High expression of HOTAIR was correlated with modified Mankin scale, extracellular matrix (ECM) degradation and chondrocytes apoptosis. The expression of miR-17-5p was down-regulated, while alpha-1, 2 fucosyltransferase 2 (FUT2) was increased in OA progression. Luciferase reporter and RNA immunoprecipitation (RIP) assays indicated that HOTAIR could directly bind to miR-17-5p and indirectly upregulate FUT2 level. Functional investigation revealed HOTAIR and FUT2 aggravated ECM degradation and chondrocytes apoptosis, and this effect could be reversed by miR-17-5p. Altered FUT2 modulated the activity of wnt/β-catenin pathway and HOTAIR/miR-17-5p also mediated wnt/β-catenin pathway through FUT2. Collectively, our findings indicated that HOTAIR/miR-17-5p/FUT2 axis contributed to OA progression via wnt/β-catenin pathway, which might provide novel insights into the function of lncRNA-driven in OA.

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Section: Methodsmentioning

confidence: 99%

Long non-coding RNA HOTAIR promotes osteoarthritis progression via miR-17-5p/FUT2/β-catenin axis

et al. 2018

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“…[ 12 ] Additionally, miR‐149 can suppress the inflammatory response of chondrocytes in osteoarthritis by inhibiting the transduction of TAK1/NF‐kB signaling, [ 26 ] hinder apoptosis and accelerate the proliferation and autophagy of chondrocytes by targeting FUT1. [ 27 ] In summary, we inferred that PVT1 might facilitate the progression of asthma by regulating the expression of miR‐149 in HSAECs. In the present study, we found that the expression of miR‐149 was downregulated in the serum of asthma patients.…”

Section: Discussionmentioning

confidence: 91%

LncRNA PVT1 exacerbates the inflammation and cell‐barrier injury during asthma by regulating miR‐149

Lian-mei

Zhang

Hao

et al. 2020

J Biochem & Molecular Tox

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Background Asthma is a prevailing respiratory disease among children, characterized by allergic airway inflammation, airway remodeling, and airway hyperresponsiveness. Although it is well‐known that long non‐coding RNAs (lncRNAs) are linked to a variety of human diseases and well‐documented, very few studies explore its role in asthma. In this study, we investigate the effects of lncRNA PVT1 on the promotion of airway inflammation and its associated mechanisms. Methods and Materials Human small airway epithelial cells (HSAECs) with PVT1 overexpressed or knocked down were constructed, and platelet activating factor (PAF) was used to treat HSAECs to mimic the pathological process of asthma in vitro. The expressions of prostaglandin E2 (PGE2), interleukin‐1β (IL‐1β), IL‐6, and tumor necrosis factor‐α (TNF‐α) were measured by enzyme‐linked immunosorbent assay (ELISA). The expressions of PKC, MyD88, and NF‐ĸB were measured by Western blot. Monolayer permeability of HSAECs was also compared within different groups. Luciferase reporter gene assay was employed to detect the targeting relationship between PVT1 and miR‐149. Results The knockdown of PVT1 attenuated the levels of inflammatory factors induced by PAF and destruction of cell‐barrier function. The overexpression of PVT1 facilitated the pathological development. Additionally, miR‐149 was identified as a target microRNA of PVT1, and the overexpression of miR‐149 could reverse the effects of PVT1 on PAF‐induced HSAECs. Conclusion These findings suggest that PVT1 may represent a novel potential target for treatment of asthma.

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“…Knee tibial plateau cartilage is primarily composed of chondrocytes and extracellular matrix secreted by the chondrocytes; therefore, chondrocytes determine the physiological state of cartilage tissue 10,11,40,41 . Research on chondrocytes is a hot spot in the eld of knee OA 8,[12][13][14]18,30,31,34 . To date, there are many experimental methods to simulate human knee OA, such as surgical application of traumatic OA, drug injection (such as papain) into the joint to produce knee OA, and external xators to break the knee joint, causing OA 42-45 . However, these are all exogenous interventions.…”

Section: Discussionmentioning

confidence: 99%

“…The key proteins related to chondrocyte autophagy are light chain-3 (LC-3), autophagy-related protein-5 (ATG-5), ATG-7 and Beclin-1 (27)(28)(29). Studies have shown that when OA occurs, the level of autophagy in articular chondrocytes signi cantly decreases (30)(31)(32). Moreover, when the level of autophagy was reduced, the occurrence and development of knee OA were also more rapid (33)(34)(35).…”

Section: Introductionmentioning

confidence: 99%

Loss of autophagy in tibial plateau chondrocytes causes increased apoptosis of chondrocytes in spontaneous osteoarthritis of guinea pigs

Wang¹,

Wei²,

Xing³

et al. 2020

Preprint

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Objective To observe the effect of autophagy in tibial plateau chondrocytes on apoptosis in spontaneous knee osteoarthritis (OA) in guinea pigs. Methods Fifty 2-month-old female Hartley guinea pigs were divided into a normal group, which was euthanized after 7 months, and an OA group, ten of which were euthanized after 10 months. Immunohistochemistry, PCR and western blotting were used to evaluate the level of autophagy, intracellular glycogen accumulation and apoptosis in tibial plateau chondrocytes in vivo and in vitro. The remaining 30 guinea pigs in the OA group were divided into 3 groups: a rapamycin group, a normal saline group and a 3-MA group. Intracellular glycogen accumulation and chondrocyte apoptosis were observed by changing the level of autophagy in tibial plateau chondrocytes in vivo. Results When spontaneous OA occurred in the guinea pigs, the level of autophagy in tibial plateau chondrocytes decreased,and intracellular glycogen accumulation and the rate of chondrocyte apoptosis increased. After enhancing the autophagy level of tibial plateau chondrocytes in OA guinea pigs, the intracellular glycogen accumulation and the rate of chondrocyte apoptosis decreased. When the autophagy level of the chondrocytes was weakened, intracellular glycogen accumulation was further increased, and the apoptosis rate was higher. Conclusions The autophagy function of chondrocytes may be at least partly involved in the catabolism of glycogen in chondrocytes. In OA guinea pigs, the autophagy level in tibial plateau chondrocytes decreased, and the chondrocytes were unable to degrade intracellular glycogen into glucose, leading to less energy for the chondrocytes and increased apoptosis.

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miR-140-5p/miR-149 Affects Chondrocyte Proliferation, Apoptosis, and Autophagy by Targeting FUT1 in Osteoarthritis

Cited by 76 publications

References 39 publications

Long non-coding RNA HOTAIR promotes osteoarthritis progression via miR-17-5p/FUT2/β-catenin axis

Long non-coding RNA HOTAIR promotes osteoarthritis progression via miR-17-5p/FUT2/β-catenin axis

LncRNA PVT1 exacerbates the inflammation and cell‐barrier injury during asthma by regulating miR‐149

Loss of autophagy in tibial plateau chondrocytes causes increased apoptosis of chondrocytes in spontaneous osteoarthritis of guinea pigs

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