Pleiotropic Hes-1 Concomitant with its Differential Activation Mediates Neural Stem Cell Maintenance and Radial Glial Propensity in Developing Neocortex

Dhanesh, Sivadasan Bindu; Subashini, Chandramohan; Riya, Paul Ann; Rasheed, Vazhanthodi Abdul; James, Jackson

doi:10.1093/cercor/bhw207

Cited by 5 publications

(3 citation statements)

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“…Previous studies have shown neurogenesis to be enhanced by TGFβ (Mathieu et al, 2010) and by TGFβ+ activated microglia in the context of neurodegeneration (De Lucia et al, 2016). In addition, TGFβ has been identified as a factor inducing Notch-independent HES-1 signalling (Chacón and Rodríguez-Tébar, 2012), which would specifically contribute to the maintenance of a primitive neural stem cell pool (Dhanesh et al, 2017). This would support the idea that, as for acute ECS, chronic treatment would tend to increase the activity of the innate immune system and simultaneously contribute to proliferative neurogenic processes 4 h later.…”

Section: Resultsmentioning

confidence: 99%

The innate immune system and neurogenesis as modulating mechanisms of electroconvulsive therapy in pre-clinical studies

2020

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Background: Electroconvulsive therapy (ECT) is a powerful and fast-acting anti-depressant strategy, often used in treatment-resistant patients. In turn, patients with treatment-resistant depression often present an increased inflammatory response. The impact of ECT on several pathophysiological mechanisms of depression has been investigated, with a focus which has largely been on cellular and synaptic plasticity. Although changes in the immune system are known to influence neurogenesis, these processes have principally been explored independently from each other in the context of ECT. Objective: The aim of this review was to compare the time-dependent consequences of acute and chronic ECT on concomitant innate immune system and neurogenesis-related outcomes measured in the central nervous system in pre-clinical studies. Results: During the few hours following acute electroconvulsive shock (ECS), the expression of the astrocytic reactivity marker glial fibrillary acidic protein (GFAP) and inflammatory genes, such as cyclooxygenase-2 (COX2), were significantly increased together with the neurogenic brain-derived neurotrophic factor (BDNF) and cell proliferation. Similarly, chronic ECS caused an initial upregulation of the same astrocytic marker, immune genes, and neurogenic factors. Interestingly, over time, inflammation appeared to be dampened, while glial activation and neurogenesis were maintained, after either acute or chronic ECS. Conclusion: Regardless of treatment duration ECS would seemingly trigger a rapid increase in inflammatory molecules, dampened over time, as well as a long-lasting activation of astrocytes and production of growth and neurotrophic factors, leading to cell proliferation. This suggests that both innate immune system response and neurogenesis might contribute to the efficacy of ECT.

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Section: Resultsmentioning

confidence: 99%

The innate immune system and neurogenesis as modulating mechanisms of electroconvulsive therapy in pre-clinical studies

2020

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“…A reduction in Hes-1 impairs differentiation and cell proliferation in the epidermis and hair follicles and reduces the pluripotency of stem cells in the skin [ 87 ]. In hair follicles, the expression of the target gene Hes-1 may be related to changes in Jagged-1 ligand gene expression [ 88 ]. Studies have found that reduced Hes-1 expression limits the ligand–receptor interaction and reduces Hes-1 signaling [ 89 ].…”

Section: Reviewmentioning

confidence: 99%

Regulation of signaling pathways in hair follicle stem cells

Wang

Liu

et al. 2022

Burns &Amp; Trauma

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Hair follicle stem cells (HFSCs) reside in the bulge region of the outer root sheath of the hair follicle. They are considered slow-cycling cells that are endowed with multilineage differentiation potential and superior proliferative capacity. The normal morphology and periodic growth of HFSCs play a significant role in normal skin functions, wound repair and skin regeneration. The HFSCs involved in these pathophysiological processes are regulated by a series of cell signal transduction pathways, such as lymphoid enhancer factor/T-cell factor, Wnt/β-catenin, transforming growth factor-β/bone morphogenetic protein, Notch and Hedgehog. The mechanisms of the interactions among these signaling pathways and their regulatory effects on HFSCs have been previously studied, but many mechanisms are still unclear. This article reviews the regulation of hair follicles, HFSCs and related signaling pathways, with the aims of summarizing previous research results, revealing the regulatory mechanisms of HFSC proliferation and differentiation and providing important references and new ideas for treating clinical diseases.

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“…NICD also controls NF-kß expression through Hairy and enhancer of split1 (Hes1)(Espinosa et al, 2010). This protein controls neurogenesis and it has been shown to be expressed following a cyclic pattern during certain stages of development(Dhanesh et al, 2016) as well as it occurs with miR-29a. Moreover, miR-29a controls Nuclear factor I A (Nfia) expression, a transcription factor repressor of Hes1 expression(Liu et al, 2015).…”

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confidence: 99%

Interaction of opioid and Notch signaling cascades. Implications in dopaminergic development after morphine administration

Concejo¹

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Opioids, primarily used for pain relief, are still nowadays the preferred analgesics for the treatment of chronic pain. Among them, morphine is the most used molecule, although it is well known for inducing the appearance of tolerance and addiction after prolonged administration. This opiate binds to the mu opioid receptor (Oprm1) with the highest affinity and, therefore, the effects of this drug, especially in the central nervous system (CNS), are mediated by the activation of this receptor (Pert et al., 1987). Opioid receptors are G-protein coupled receptors and the signaling cascade triggered by them induces the activity of several transcription factors, including cAMP Response Element Binding (CREB) protein (Impey et al., 2004; Ma et al., 2001), a transcription factor involved in many molecular pathways by controlling the transcription of different genes. Morphine also alters calcium and potassium signaling and controls PKA activity by the inhibition of adenylate cyclase (AC); in this way it also induces changes in gene expression in the target cell (Kumar et al., 2010). It is also known that morphine regulates nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kß) activation through IP3/Akt pathway, although the molecular mechanism implicated in this situation still remains uncharacterized (Chen et al., 2006). equal (Mohammed et al., 2014), indicating that the process of splicing is not only a maturation process but also a regulatory mechanism that controls the expression of each of the mature miRNAs. After the pri-miRNA has been transcribed, it is cleaved by several processing enzymes such as Dicer, leading to a shorter hairpin-like structured named precursor miRNA (pre-miRNA). After this processing, pre-miRNAs are transported into the cytoplasm by exportin-5 and they suffer another splicing by the processing enzyme Drosha. After this process, two mature miRNAs are generated. In general terms, only one of these two miRNAs exert its function, although several cases have been described in which both molecules may have their own regulatory roles. These molecules control gene expression by binding to complementary sequences in the 3′ untranslated region (3′ UTR) of their target mRNA transcripts to facilitate their degradation and/or inhibit their translation (Bartel, 2009), although binding to other regions have been described (Doench and Sharp, 2004; Greco and Rameshwar, 2007). miRNAs are involved in many developmental processes, such as differentiation and proliferation and their dysregulation has been linked to a wide variety of diseases (Sidhu regulation of myoblasts proliferation and differentiation in part by regulating the YY1-miR-29 negative regulatory circuit. Developmental changes and cell type-specific distribution of miR-29 expression, such as that reported in the murine lung (Cushing et al., 2011), further support the presence of dynamic regulation of the expression of miR-29. miR-29a has also been shown to regulate the expression of ADAM12 expression by binding to the 3'UTR region ...

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Pleiotropic Hes-1 Concomitant with its Differential Activation Mediates Neural Stem Cell Maintenance and Radial Glial Propensity in Developing Neocortex

Cited by 5 publications

References 62 publications

The innate immune system and neurogenesis as modulating mechanisms of electroconvulsive therapy in pre-clinical studies

The innate immune system and neurogenesis as modulating mechanisms of electroconvulsive therapy in pre-clinical studies

Regulation of signaling pathways in hair follicle stem cells

Interaction of opioid and Notch signaling cascades. Implications in dopaminergic development after morphine administration

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