MicroRNA-378 regulates neural stem cell proliferation and differentiation in vitro by modulating Tailless expression

Huang, Yanxia; Liu, Xiaoguai; Wang, Yaping

doi:10.1016/j.bbrc.2015.09.011

Cited by 25 publications

(20 citation statements)

References 44 publications

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“…This event affects the status of progenitor proliferation and differentiation [51]. Tlx is also regulated by another miR, let-7b and miR378, both of them increasing NSC differentiation [52, 113]. Emerging evidence suggests that microRNAs promote factors that induce differentiation by modulating Tlx expression in neuroprogenitor cells, and by interplay with TLX, these miRs appear to be involved in neurological disorders and neural tumours, as described below.…”

Section: Introductionmentioning

confidence: 99%

TLX—Its Emerging Role for Neurogenesis in Health and Disease

Sobhan

Funa

2016

Mol Neurobiol

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The orphan nuclear receptor TLX, also called NR2E1, is a factor important in the regulation of neural stem cell (NSC) self-renewal, neurogenesis, and maintenance. As a transcription factor, TLX is vital for the expression of genes implicated in neurogenesis, such as DNA replication, cell cycle, adhesion and migration. It acts by way of repressing or activating target genes, as well as controlling protein-protein interactions. Growing evidence suggests that dysregulated TLX acts in the initiation and progression of human disorders of the nervous system. This review describes recent knowledge about TLX expression, structure, targets, and biological functions, relevant to maintaining adult neural stem cells related to both neuropsychiatric conditions and certain nervous system tumours.

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Section: Introductionmentioning

confidence: 99%

TLX—Its Emerging Role for Neurogenesis in Health and Disease

Sobhan

Funa

2016

Mol Neurobiol

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“…Neonatal astrocytes were extracted from 1‐ to 2‐day‐old postnatal SD rats and adult astrocytes were extracted from 8‐week‐old SD rats. Preparation of the astrocytes has been described previously . When the neonatal and adult astrocytes reached approximately 80% confluence at the third passage, the cells were treated with fresh DMEM/F12 plus 5 μg/ml lipopolysaccharide (LPS) (Sigma Aldrich, St. Louis, MO, http://www.sigmaaldrich.com).…”

Section: Methodsmentioning

confidence: 99%

“…Compared with neonates, NSC self‐renewal, and the corresponding capacity for endogenous repair, in the adult brain is poor . Though it has previously been demonstrated that a series of substances can promote the proliferation of endogenous NSCs, it should be noted that the capacity for neural repair by endogenous NSCs postinjury remains severely limited. This results in irreversible damage and lasting neurological deficits after neuronal injury such as TBI.…”

Section: Introductionmentioning

confidence: 99%

Effects and Mechanism of Action of Neonatal Versus Adult Astrocytes on Neural Stem Cell Proliferation After Traumatic Brain Injury

et al. 2019

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Due to the limited capacity of brain tissue to self-regenerate after traumatic brain injury (TBI), the mobilization of endogenous neural stem cells (NSCs) is a popular research topic. In the clinic, the neurogenic abilities of adults versus neonates vary greatly, which is likely related to functional differences in NSCs. Recent studies have demonstrated that the molecules secreted from astrocytes play important roles in NSC fate determination. In this study, conditioned media (CM) derived from neonatal or adult rat astrocytes, which were unstimulated or stimulated by lipopolysaccharide (LPS), were prepared to treat NSCs. Our results revealed that neonatal rat astrocytes can significantly promote the proliferation of NSCs, compared with adult rat astrocytes, regardless of whether or not they were stimulated by LPS. Furthermore, we used mass spectrometry to detect the constituents of the CM from each group. We analyzed and screened for a protein, Tenascin-C (TNC), which was highly expressed in the neonatal group but poorly expressed in the adult group. We found that TNC can bind to the NSC surface epidermal growth factor receptor and promote proliferation through the PI3K-AKT pathway in vitro. Additionally, we confirmed in vivo that TNC can promote damage repair in a rat model of TBI, through enhancing the proliferation of endogenous NSCs. We believe that these findings provide a mechanistic understanding of why neonates show better neuroregenerative abilities than adults. This also provides a potential future therapeutic target, TNC, for injury repair after TBI. STEM CELLS

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“…Various studies have demonstrated that miR-378 could regulate Wnt/β-catenin signaling, i.e. miR-378 could increase neural stem cell differentiation through Wnt/β-catenin signaling; 21 A colon cancer study also revealed that miR-378 attenuates malignant phenotypes of colon cancer cells via suppressing Wnt/β-catenin pathway. 22 More importantly, miR-378a-3p could suppress Wnt/β-catenin signaling in hepatic stellate cells via targeting Wnt10a.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-378 suppressed osteogenesis of mesenchymal stem cells and impaired bone formation via inactivating Wnt/β-catenin signaling

Zhang

Shi

et al. 2019

Preprint

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37MicroRNAs (miRNAs) have been reported to serve as silencers to repress gene 38 expression at post-transcriptional level. Multiple miRNAs have been demonstrated to 39 play important roles in osteogenesis. MiR-378, a conserved miRNA, was reported to 40 mediate bone metabolism and influence bone development, but the detailed function 41 and underlying mechanism remain obscure. In this study, the miR-378 transgenic (TG) 42 mouse was developed to study the role of miR-378 in osteogenic differentiation as 43 well as bone formation. The abnormal bone tissues and impaired bone quality were 44 displayed in the miR-378 TG mice, and a delayed healing effect was observed during 45 bone fracture of the miR-378 TG mice. The osteogenic differentiation of MSCs 46 derived from this TG mouse was also inhibited. We also found that miR-378 mimics 47 suppressed while anti-miR-378 promoted osteogenesis of human MSCs. Two Wnt 48 family members Wnt6 and Wnt10a were identified as bona fide targets of miR-378, 49 and their expression were decreased by this miRNA, which eventually induced the 50 inactivation of Wnt/β-catenin signaling. Finally, the sh-miR-378 modified MSCs were 51 locally injected into the fracture sites in an established mouse fracture model. The 52 results indicated that miR-378 inhibitor therapy could promote bone formation and 53 stimulate healing process in vivo. In conclude, miR-378 suppressed osteogenesis and 54 bone formation via inactivating Wnt/β-catenin signaling, suggesting miR-378 may be 55 a potential therapeutic target for bone diseases.56 Key words: miR-378; mesenchymal stem cells; osteogenesis; Wnt/β-catenin 57 signaling; bone formation 58 59 Bone regeneration is very important for the recovery of some diseases including 60 osteoporosis and bone fracture trauma. It is a multiple step and multiple gene involved 61 complex process, including osteoblast-mediated bone formation and 62 osteoclast-mediated bone resorption. During this process, mesenchymal stem cells 63 (MSCs) gradually differentiate into osteoblasts, which produce a variety of 64 extracellular matrix and thus induce the initiation of bone formation. Hence, 65 improving the osteoblast differentiation of MSCs is crucial for the development of 66 therapeutic strategy for bone diseases. 67 Over the past few years, microRNAs (miRNAs) have emerged as gene silencers to 68 suppress gene expression at post-transcriptional level. Multiple miRNAs have been 69 demonstrated to play important roles in biological activities including osteogenic 70 differentiation and skeletal development. For example, miR-26a, miR-29b, miR-125b, 71 miR-133, miR-135 and miR-196a, have been reported to be involved in 72 osteogenesis. 1-5 Our previous reports also demonstrated that miR-20a and 20b 73 promoted whereas miR-637 suppressed osteoblast differentiation. 6-7 Therefore, 74 miRNAs have been considered as potential candidates to mediate osteogenic 75 differentiation and may be acted as therapeutic targets for bone regeneration.76 MiR-378, which is derived from a ...

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MicroRNA-378 regulates neural stem cell proliferation and differentiation in vitro by modulating Tailless expression

Cited by 25 publications

References 44 publications

TLX—Its Emerging Role for Neurogenesis in Health and Disease

TLX—Its Emerging Role for Neurogenesis in Health and Disease

Effects and Mechanism of Action of Neonatal Versus Adult Astrocytes on Neural Stem Cell Proliferation After Traumatic Brain Injury

MicroRNA-378 suppressed osteogenesis of mesenchymal stem cells and impaired bone formation via inactivating Wnt/β-catenin signaling

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