Hotair and Malat1 Long Noncoding RNAs Regulate Bdnf Expression and Oligodendrocyte Precursor Cell Differentiation

Khani-Habibabadi, Fatemeh; Zare, Leila; Sahraian, Mohammad Ali; Javan, Mohammad; Behmanesh, Mehrdad

doi:10.1007/s12035-022-02844-0

Cited by 11 publications

(7 citation statements)

References 59 publications

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“…A study has showed that oligodendrocytes in the spinal cord and optic nerve express BDNF mRNA and the expression is increased in Long-Evans shaker rats that lack CNS myelin due to the MBP gene mutation [47]. Another study found that fingolimod treatment resulted in increased BDNF mRNA concomitant with increased OPC differentiation in rat OPC culture [48]. Our results confirm the expression of BDNF in oligodendrocytes in certain brain regions.…”

Section: Discussionsupporting

confidence: 82%

Genetic dissection of BDNF and TrkB expression in glial cells

Niu

Yue

et al. 2023

Preprint

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The brain-derived neurotrophic factor (BDNF) and its high-affinity receptor tropomyosin-related kinase receptor B (TrkB) are widely expressed in the central nervous system. It is well documented that neurons express BDNF and full-length TrkB (TrkB.FL), and a lower level of truncated TrkB (TrkB.T). With conflicting results, glial cells also have been reported to express BDNF and TrkB. In the current study, we employed a more sensitive and reliable genetic method to characterize the expression of BDNF and TrkB in glial cells in the mouse brain. We utilized three Cre mouse strains in which Cre recombinase is expressed in the same cells as BDNF, TrkB.FL, or all TrkB isoforms, and crossed them to Cre-dependent EGFP reporter mice to label BDNF- or TrkB- expressing cells. We performed immunohistochemistry with glial cell markers to examine the expression of BDNF and TrkB in microglia, astrocytes, and oligodendrocytes. Surprisingly, we found no BDNF- or TrkB- expressing microglia in the brain and spinal cord. Consistent with previous studies, most astrocytes only express TrkB.T in the adult brain. Moreover, there are a small number of astrocytes and oligodendrocytes that express BDNF, the function of which is to be determined. We also found that oligodendrocyte precursor cells, but not mature oligodendrocytes, express both TrkB.FL and TrkB.T in the adult brain. These results not only clarify the expression of BDNF and TrkB in glial cells, but also open opportunities to investigate previously unidentified roles of BDNF and TrkB in glial cells.

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Section: Discussionsupporting

confidence: 82%

Genetic dissection of BDNF and TrkB expression in glial cells

Niu

Yue

et al. 2023

Preprint

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“…The data on neurotrophins receptors expression are in line with emerging roles of these molecules in in OPC differentiation and maturation, which are still poorly described, as recently proved for BDNF ( Khani-Habibabadi et al, 2022 ). In the first part of this study, in fact, we demonstrated that mixed OPC/astrocyte cultures produce NGF and respond to NGF during OPC differentiation and OL maturation; that NGF receptors are dynamically expressed throughout the NSC lineage and OPC differentiation process, and that neutralization of endogenous NGF determines an impairment in OPC differentiation.…”

Section: Discussionmentioning

confidence: 57%

Nerve growth factor promotes differentiation and protects the oligodendrocyte precursor cells from in vitro hypoxia/ischemia

Baldassarro

Cescatti²,

Rocco³

et al. 2023

Front. Neurosci.

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IntroductionNerve growth factor (NGF) is a pleiotropic molecule acting on different cell types in physiological and pathological conditions. However, the effect of NGF on the survival, differentiation and maturation of oligodendrocyte precursor cells (OPCs) and oligodendrocytes (OLs), the cells responsible for myelin formation, turnover, and repair in the central nervous system (CNS), is still poorly understood and heavily debated.MethodsHere we used mixed neural stem cell (NSC)-derived OPC/astrocyte cultures to clarify the role of NGF throughout the entire process of OL differentiation and investigate its putative role in OPC protection under pathological conditions.ResultsWe first showed that the gene expression of all the neurotrophin receptors (TrkA, TrkB, TrkC, and p75NTR) dynamically changes during the differentiation. However, only TrkA and p75NTR expression depends on T3-differentiation induction, as Ngf gene expression induction and protein secretion in the culture medium. Moreover, in the mixed culture, astrocytes are the main producer of NGF protein, and OPCs express both TrkA and p75NTR. NGF treatment increases the percentage of mature OLs, while NGF blocking by neutralizing antibody and TRKA antagonist impairs OPC differentiation. Moreover, both NGF exposure and astrocyte-conditioned medium protect OPCs exposed to oxygenglucose deprivation (OGD) from cell death and NGF induces an increase of AKT/pAKT levels in OPCs nuclei by TRKA activation.DiscussionThis study demonstrated that NGF is implicated in OPC differentiation, maturation, and protection in the presence of metabolic challenges, also suggesting implications for the treatment of demyelinating lesions and diseases.

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“…This is supported by evidences that HOTAIR -EZH2-miRNA-141 signaling drives expressional changes in BDNF, and regulates the differentiation of dopaminergic neuron-like cells from human amniotic epithelial stem cells (HuAESCs) (Liu et al 2018b ). Along similar lines, Khani‑Habibabadi et al have recently implicated HOTAIR in the regulation of oligodendrocyte precursor cell differentiation (Khani-Habibabadi et al 2022 ).…”

Section: Hotair In Non-oncological Brain Pathophysiological ...mentioning

confidence: 84%

Roles of HOTAIR Long Non-coding RNA in Gliomas and Other CNS Disorders

Ahmad,

Sudesh,

Ahmed

et al. 2024

Cell Mol Neurobiol

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HOX transcript antisense intergenic RNA (HOTAIR) is a long non-coding RNA (lncRNA) which is increasingly being perceived as a tremendous molecular mediator of brain pathophysiology at multiple levels. Epigenetic regulation of target gene expression carried out by HOTAIR is thorough modulation of chromatin modifiers; histone methyltransferase polycomb repressive complex 2 (PRC2) and histone demethylase lysine-specific demethylase 1 (LSD1). Incidentally, HOTAIR was the first lncRNA shown to elicit sponging of specific microRNA (miRNA or miR) species in a trans-acting manner. It has been extensively studied in various cancers, including gliomas and is regarded as a prominent pro-tumorigenic and pro-oncogenic lncRNA. Indeed, the expression of HOTAIR may serve as glioma grade predictor and prognostic biomarker. The objective of this timely review is not only to outline the multifaceted pathogenic roles of HOTAIR in the development and pathophysiology of gliomas and brain cancers, but also to delineate the research findings implicating it as a critical regulator of overall brain pathophysiology. While the major focus is on neuro-oncology, wherein HOTAIR represents a particularly potent underlying pathogenic player and a suitable therapeutic target, mechanisms underlying the regulatory actions of HOTAIR in neurodegeneration, traumatic, hypoxic and ischemic brain injuries, and neuropsychiatric disorders are also presented. Graphical Abstract HOTAIR-mediated epigenetic DNA regulation and molecular sponging of target miRNAs. While the 5′ end of HOTAIR regulates the H3K27 trimethylation activity of the catalytic subunit enhancer of Zeste homolog 2 (EZH2) of the polycomb repressive complex 2 (PRC2), its 3′ end modulates the H3K4 demethylation activity of lysine-specific demethylase 1 (LSD1). HOTAIR also binds to and competitively inhibits the functions of target miRNAs, altering the expression of downstream genes.

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Hotair and Malat1 Long Noncoding RNAs Regulate Bdnf Expression and Oligodendrocyte Precursor Cell Differentiation

Cited by 11 publications

References 59 publications

Genetic dissection of BDNF and TrkB expression in glial cells

Genetic dissection of BDNF and TrkB expression in glial cells

Nerve growth factor promotes differentiation and protects the oligodendrocyte precursor cells from in vitro hypoxia/ischemia

Roles of HOTAIR Long Non-coding RNA in Gliomas and Other CNS Disorders

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