Involvement of Wnt7a in the role of M2c microglia in neural stem cell oligodendrogenesis

Mecha, Míriam; Yanguas‐Casás, Natalia; Feliú, Ana; Mestre, Leyre; Carrillo‐Salinas, Francisco; Riecken, Kristoffer; Gómez-Nicola, Diego; Guaza, Carmen

doi:10.1186/s12974-020-01734-3

Cited by 26 publications

(17 citation statements)

References 67 publications

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“…It is well known that activated microglia and infiltrating peripheral monocytes in CNS are crucial neuroinflammatory determinants in the pathophysiology of both MS and EAE. Together with primed T cells, they are the main inflammatory players involved in neuronal and oligodendrocyte alterations associated with synaptic dysfunction, subpial and axonal demyelination in MS/EAE (Mandolesi et al, 2015;Dong and Yong, 2019;Mecha et al, 2020). Increased microglial activity in brain regions involved in mood and cognitive control (including PFC and hippocampus) has been detected, by means of both PET and post-mortem clinical studies, in depressed MS patients in comparison to non-depressed MS patients and healthy controls (Politis, 2012).…”

Section: The Role Of Microglia In Ms Depressionmentioning

confidence: 99%

Inflammation-Associated Synaptic Alterations as Shared Threads in Depression and Multiple Sclerosis

Bruno

Dolcetti

Rizzo

et al. 2020

Front. Cell. Neurosci.

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In the past years, several theories have been advanced to explain the pathogenesis of Major Depressive Disorder (MDD), a neuropsychiatric disease that causes disability in general population. Several theories have been proposed to define the MDD pathophysiology such as the classic “monoamine-theory” or the “glutamate hypothesis.” All these theories have been recently integrated by evidence highlighting inflammation as a pivotal player in developing depressive symptoms. Proinflammatory cytokines have been indeed claimed to contribute to stress-induced mood disturbances and to major depression, indicating a widespread role of classical mediators of inflammation in emotional control. Moreover, during systemic inflammatory diseases, peripherally released cytokines circulate in the blood, reach the brain and cause anxiety, anhedonia, social withdrawal, fatigue, and sleep disturbances. Accordingly, chronic inflammatory disorders, such as the inflammatory autoimmune disease multiple sclerosis (MS), have been associated to higher risk of MDD, in comparison with overall population. Importantly, in both MS patients and in its experimental mouse model, Experimental Autoimmune Encephalomyelitis (EAE), the notion that depressive symptoms are reactive epiphenomenon to the MS pathology has been recently challenged by the evidence of their early manifestation, even before the onset of the disease. Furthermore, in association to such mood disturbance, inflammatory-dependent synaptic dysfunctions in several areas of MS/EAE brain have been observed independently of brain lesions and demyelination. This evidence suggests that a fine interplay between the immune and nervous systems can have a huge impact on several neurological functions, including depressive symptoms, in different pathological conditions. The aim of the present review is to shed light on common traits between MDD and MS, by looking at inflammatory-dependent synaptic alterations associated with depression in both diseases.

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Section: The Role Of Microglia In Ms Depressionmentioning

confidence: 99%

Inflammation-Associated Synaptic Alterations as Shared Threads in Depression and Multiple Sclerosis

Bruno

Dolcetti

Rizzo

et al. 2020

Front. Cell. Neurosci.

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“…Inflammatory microglial necroptosis occurs, shutting down proinflammatory signals, and is followed by the repopulation of the lesion with regulatory microglia, a process required for efficient remyelination . Regulatory microglia can also promote SVZ-derived oligodendrogenesis and remyelination via Wnt7a production (Mecha et al, 2020).…”

Section: Roles Of Microglia In Remyelinationmentioning

confidence: 99%

Myelin Repair: From Animal Models to Humans

Cayre

Falque

Mercier

et al. 2021

Front. Cell. Neurosci.

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It is widely thought that brain repair does not occur, but myelin regeneration provides clear evidence to the contrary. Spontaneous remyelination may occur after injury or in multiple sclerosis (MS). However, the efficiency of remyelination varies considerably between MS patients and between the lesions of each patient. Myelin repair is essential for optimal functional recovery, so a profound understanding of the cells and mechanisms involved in this process is required for the development of new therapeutic strategies. In this review, we describe how animal models and modern cell tracing and imaging methods have helped to identify the cell types involved in myelin regeneration. In addition to the oligodendrocyte progenitor cells identified in the 1990s as the principal source of remyelinating cells in the central nervous system (CNS), other cell populations, including subventricular zone-derived neural progenitors, Schwann cells, and even spared mature oligodendrocytes, have more recently emerged as potential contributors to CNS remyelination. We will also highlight the conditions known to limit endogenous repair, such as aging, chronic inflammation, and the production of extracellular matrix proteins, and the role of astrocytes and microglia in these processes. Finally, we will present the discrepancies between observations in humans and in rodents, discussing the relationship of findings in experimental models to myelin repair in humans. These considerations are particularly important from a therapeutic standpoint.

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“…Represented with similar function, NPCs secrete factors like TGF-β2 to transform MG into protective type [102], who in turn to support the maintenance and growth. The reparation on demyelination can also be initiated by M2 microglia, while through NSCs to bring about oligodendrogenesis and myelination [108]. Accumulating evidence has demonstrated that NSCs niches is the utmost region as the origin of the neural regenerative microenvironment, though its program of neurogenesis is a bit distinguished from the pattern after TBI.…”

Section: Nsc Might Integrate the Inflammatory Signal In Neural Regenementioning

confidence: 99%

“…Represented with similar function, NPCs secrete factors like TGF-β2 to transform MG into protective type 102 , who in turn to support the maintenance and growth. The reparation on demyelination can also be initiated by M2 microglia, while through NSCs to bring about oligodendrogenesis and myelination 108 .…”

Section: Communication Crosstalk and Integration In Neuroinflammatiomentioning

confidence: 99%

Niche Cells Crosstalk In Neuroinflammation After Traumatic Brain Injury

Jia¹,

Wang²,

Ye³

et al. 2021

Int. J. Biol. Sci.

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Traumatic brain injury (TBI) is recognized as the disease with high morbidity and disability around world in spite of the work ongoing in neural protection. Due to heterogeneity among the patients, it's still hard to acquire satisfying achievements in clinic. Neuroinflammation, which exists since primary injury occurs, with elusive duality, appear to be of significance from recovery of injury to neurogenesis. In recent years, studied have revealed that communication in neurogenic niche is more than “cell to cell” communication, and study on NSCs represent it as central role in the progress of neural regeneration. Hence, the neuroinflammation-affecting crosstalk after TBI, and clarifying definitive role of NSCs in the course of regeneration is a promising subject for researchers, for its great potential in overcoming the frustrating status quo in clinic, promoting welfare of TBI patient.

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Involvement of Wnt7a in the role of M2c microglia in neural stem cell oligodendrogenesis

Cited by 26 publications

References 67 publications

Inflammation-Associated Synaptic Alterations as Shared Threads in Depression and Multiple Sclerosis

Inflammation-Associated Synaptic Alterations as Shared Threads in Depression and Multiple Sclerosis

Myelin Repair: From Animal Models to Humans

Niche Cells Crosstalk In Neuroinflammation After Traumatic Brain Injury

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