MicroRNA-125b-1-3p mediates intervertebral disc degeneration in rats by targeting teashirt zinc finger homeobox 3

Meng, Xiaotong; Zhu, Yue; Lin, Tao; Zhao, Sichao; Qiu, Shui

doi:10.3892/etm.2018.5715

Cited by 9 publications

(7 citation statements)

References 43 publications

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“…Previous studies reported that miRNAs are involved in cell growth, proliferation and cell death in different diseases (10–12). It has been shown that some miRNAs exert an important role in the development of IDD, such as miR-194, miR-3150a and miR-125b-1 (13–15).…”

Section: Introductionmentioning

confidence: 99%

miR‑222 induces apoptosis in human intervertebral disc nucleus pulposus cells by targeting Bcl‑2

Wang

Zhang

et al. 2019

Mol Med Report

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intervertebral disc degeneration (idd) is characterized by abnormal induction of apoptosis in intervertebral disc nucleus pulposus (nP) cells. Previous studies indicated that mir-222 was upregulated in patients with rheumatoid arthritis. However, the effects of mir-222 in idd remain unclear. The present study aimed to demonstrate the role of mir-222 in nP cells. The levels of mir-222 in patients with idd were measured by reverse transcription-quantitative Pcr. cell counting Kit-8 and western blotting assays were used to detect cell proliferation and apoptosis-associated protein levels, respectively. in addition, luciferase reporter assays were performed to validate the predicted target genes of miR-222. miR-222 was significantly upregulated in patients with idd. overexpression of mir-222 inhibited cell proliferation and induced cell apoptosis. Moreover, overexpression of mir-222 resulted in an upregulation in the levels of Bax and cleaved caspase 3, and a downregulation in the levels of Bcl-2 in nP cells. The luciferase reporter assays demonstrated that Bcl-2 is a target of mir-222. Furthermore, overexpression of mir-222 increased the levels of cytochrome c, apoptotic protease activating factor-1 and cleaved caspase 9 in nP cells. conversely, downregulation of mir-222 could promote the proliferation of nP cells. The present data demonstrated that mir-222 induced apoptosis in nP cells by directly targeting Bcl-2. Therefore, mir-222 may act as a potential therapeutic target for the treatment of idd.

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Section: Introductionmentioning

confidence: 99%

miR‑222 induces apoptosis in human intervertebral disc nucleus pulposus cells by targeting Bcl‑2

Wang

Zhang

et al. 2019

Mol Med Report

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“…Melatonin has been shown to trigger apoptosis in human alveolar rhabdomyosarcoma cells and could be considered a promising drug for future multitargeted therapies (28), but the role of melatonin in osteoblast apoptosis remains unclear. our previous study demonstrated that a high concentration of melatonin could increase the concentration of calcium ions, causing an imbalance in the homeostasis of intracellular calcium, thus leading to calcium overload (15)(16)(17)(18)(19)(20). calcium overload induces erS, which is associated with autophagy and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…our previous studies demonstrated that melatonin exerts a dual effect on osteoblast proliferation that is dependent on concentration; 1 nM-100 µM melatonin can stimulate cell proliferation, whereas 1 mM melatonin can significantly delay osteoblast proliferation (13)(14). it was also found that melatonin could upregulate the concentration of calcium ions, activate the calcium pathway, disrupt homeostasis of intracellular calcium, and lead to calcium overload (15)(16)(17)(18)(19)(20). calcium overload induces endoplasmic reticulum stress (erS), which is associated with autophagy and apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Relationship between autophagy, apoptosis and endoplasmic reticulum stress induced by melatonin in osteoblasts by septin7 expression

et al. 2020

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Melatonin secreted by the pineal body is associated with the occurrence and development of idiopathic scoliosis. Melatonin has a concentration-dependent dual effect on osteoblast proliferation, in which higher concentrations can inhibit osteoblast proliferation and induce apoptosis; however, the underlying mechanism remains unclear. in the present study, flow cytometry was used to demonstrate that osteoblast cells treated with melatonin exhibited significantly increased early and late stage apoptotic rates as the concentration increased. chromatin condensation in the nucleus and apoptotic body formation could be observed using fluorescent microscopy in osteoblast cells treated with 2 mM melatonin. Western blotting results showed that there was an upregulation in the expression of apoptosis marker proteins [poly (adP-ribose) polymerase 1 (ParP-1)], endoplasmic reticulum stress [erS; c/eBP homologous protein (cHoP) and glucose-regulated protein, 78 kda (GrP78)] and autophagy [microtubule-associated protein 1 light chain 3β (lc3)-i/lc3ii]. ParP-1 expression was not altered when treated with erS inhibitor 4PBa and autophagy inhibitor 3Ma, whereas 4PBa or 3Ma in combination with 2 mM melatonin (or the three together) significantly increased ParP-1 expression. Furthermore, the use of septin7 small interfering RNA confirmed that increased expression of GrP78 and cHoP was related to septin7, and melatoninmediated erS was necessary for septin7 activation. These findings suggest that ERS and autophagy might occur in the early stage of treatment with a high concentration of melatonin, and each might play a protective role in promoting survival; in a later stage, erS and autophagy might interact and contribute to the induction of apoptosis. overall, the results indicated that septin7 may be a target protein of melatonin-induced erS.

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“…The increased expression of miR-665 not only promotes NPC proliferation, but also reduces aggrecan and type II collagen expression and increases MMP-3 and MMP-13 expression by inhibiting the expression of growth differentiation factor 5 in NPCs (42). miR-125b-1-3p regulates the cell cycle proteins cyclin D1 and B1 by targeting teashirt zinc finger homeobox 3, which may be involved in the regulation of NPC proliferation (43). In addition, miR-184 was elevated in degenerative NP tissues and promoted abnormal proliferation of NPCs via the growth arrest-specific 1/Akt pathway (44).…”

Section: Mirnas and Npc Proliferationmentioning

confidence: 99%

Role of microRNAs in intervertebral disc degeneration (Review)

et al. 2021

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The incidence of lower back pain caused by intervertebral disc degeneration (IDD) is gradually increasing. IDD not only affects the quality of life of the patients, but also poses a major socioeconomic burden. There is currently no optimal method for delaying or reversing IDD, mainly due to its unknown pathogenesis. MicroRNAs (miRNAs/miRs) participate in the development of a number of diseases, including IDD. Abnormal expression of miRNAs in the intervertebral disc is implicated in various pathological processes underlying the development of IDD, including nucleus pulposus (NP) cell (NPC) proliferation, NPC apoptosis, extracellular matrix remodeling, inflammation and cartilaginous endplate changes, among others. The focus of the present review was the advances in research on the involvement of miRNAs in the mechanism underlying IDD. Further research is expected to identify markers for early diagnosis of IDD and new targets for delaying or reversing IDD.

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MicroRNA-125b-1-3p mediates intervertebral disc degeneration in rats by targeting teashirt zinc finger homeobox 3

Cited by 9 publications

References 43 publications

miR‑222 induces apoptosis in human intervertebral disc nucleus pulposus cells by targeting Bcl‑2

miR‑222 induces apoptosis in human intervertebral disc nucleus pulposus cells by targeting Bcl‑2

Relationship between autophagy, apoptosis and endoplasmic reticulum stress induced by melatonin in osteoblasts by septin7 expression

Role of microRNAs in intervertebral disc degeneration (Review)

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