Tissue Transglutaminase in Marmoset Experimental Multiple Sclerosis: Discrepancy between White and Grey Matter

Pinzon, Nathaly Espitia; Stroo, Esther; Hart, Bert A. ’t; Bol, John G.J.M.; Drukarch, Benjamin; Bauer, Jan; Dam, Anne‐Marie van

doi:10.1371/journal.pone.0100574

Cited by 12 publications

(9 citation statements)

References 87 publications

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“…Another feature of reactive ASTRs is increased deposition of ECM proteins. Upon toxin-induced demyelination, ASTRs transiently deposit several ECM proteins, including CSPGs and fibronectin, which add to resolve injury and promote recovery [221,[235][236][237][238][239]. The composition of the ECM affects OPC behavior; fibronectin increases OPC proliferation and migration and inhibits OPC differentiation [236,[239][240][241][242][243][244][245][246][247][248], while CSPGs inhibit OPC proliferation, migration and differentiation [239,[249][250][251][252][253].…”

Section: Astrocyte Diversity and Remyelinationmentioning

confidence: 99%

Macroglial diversity: white and grey areas and relevance to remyelination

Werkman

Lentferink

Baron

2020

Cell. Mol. Life Sci.

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Macroglia, comprising astrocytes and oligodendroglial lineage cells, have long been regarded as uniform cell types of the central nervous system (CNS). Although regional morphological differences between these cell types were initially described after their identification a century ago, these differences were largely ignored. Recently, accumulating evidence suggests that macroglial cells form distinct populations throughout the CNS, based on both functional and morphological features. Moreover, with the use of refined techniques including single-cell and single-nucleus RNA sequencing, additional evidence is emerging for regional macroglial heterogeneity at the transcriptional level. In parallel, several studies revealed the existence of regional differences in remyelination capacity between CNS grey and white matter areas, both in experimental models for successful remyelination as well as in the chronic demyelinating disease multiple sclerosis (MS). In this review, we provide an overview of the diversity in oligodendroglial lineage cells and astrocytes from the grey and white matter, as well as their interplay in health and upon demyelination and successful remyelination. In addition, we discuss the implications of regional macroglial diversity for remyelination in light of its failure in MS. Since the etiology of MS remains unknown and only disease-modifying treatments altering the immune response are available for MS, the elucidation of macroglial diversity in grey and white matter and its putative contribution to the observed difference in remyelination efficiency between these regions may open therapeutic avenues aimed at enhancing endogenous remyelination in either area.

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Section: Astrocyte Diversity and Remyelinationmentioning

confidence: 99%

Macroglial diversity: white and grey areas and relevance to remyelination

Werkman

Lentferink

Baron

2020

Cell. Mol. Life Sci.

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“…Our group was the first to observe the appearance of immunoreactive TG2 in infiltrated macrophages in white matter lesions of MS patients (van Strien et al 2015 ). In addition, TG2 appeared in the CNS of marmosets suffering from experimental autoimmune encephalomyelitis (EAE), a non-human primate model for MS (Espitia Pinzon et al 2014 ). In active white matter lesions in these animals, TG2 immunoreactivity was observed in round-shaped cells localized in proximity to the blood vessel.…”

Section: Tg2 In Inflammatory Diseasesmentioning

confidence: 99%

Is monocyte- and macrophage-derived tissue transglutaminase involved in inflammatory processes?

et al. 2016

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Monocytes and macrophages are key players in inflammatory processes following an infection or tissue damage. Monocytes adhere and extravasate into the inflamed tissue, differentiate into macrophages, and produce inflammatory mediators to combat the pathogens. In addition, they take up dead cells and debris and, therefore, take part in the resolution of inflammation. The multifunctional enzyme tissue Transglutaminase (TG2, tTG) is known to participate in most of those monocyte- and macrophage-mediated processes. Moreover, TG2 expression and activity can be regulated by inflammatory mediators. In the present review, we selectively elaborate on the expression, regulation, and contribution of TG2 derived from monocytes and macrophages to inflammatory processes mediated by those cells. In addition, we discuss the role of TG2 in certain pathological conditions, in which inflammation and monocytes and/or macrophages are prominently present, including atherosclerosis, sepsis, and multiple sclerosis. Based on the studies and considerations reported in this review, we conclude that monocyte- and macrophage-derived TG2 is clearly involved in various processes contributing to inflammation. However, TG2’s potential as a therapeutic target to counteract the possible detrimental effects or stimulate the potential beneficial effects on monocyte and macrophage responses during inflammation should be carefully considered. Alternatively, as TG2-related parameters can be used as a marker of disease, e.g., in celiac disease, or of disease-stage, e.g., in cancer, we put forward that this could be subject of research for monocyte- or macrophage-derived TG2 in inflammatory diseases.

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“…TG2 belongs to a class of enzymes known as the transglutaminases. TG2 is unique in this class of proteins, as it is ubiquitously expressed in all cell types within the brain, and can be found in most subcellular compartments (Espitia Pinzon et al, 2014; Grosso and Mouradian, 2012; Hilton et al, 1997; Hwang et al, 2009; Kim et al, 1999; Lesort et al, 1998; Lesort et al, 1999; Lorand and Graham, 2003; Mastroberardino et al, 2006; Piacentini et al, 2002; Piacentini et al, 2014; van Strien et al, 2011a; van Strien et al, 2011b). …”

Section: Introductionmentioning

confidence: 99%

Transglutaminase 2 modulation of NF-κB signaling in astrocytes is independent of its ability to mediate astrocytic viability in ischemic injury

et al. 2017

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Transglutaminase 2 (TG2) is a multifunctional protein that can contribute to cell death and cell survival processes in a variety of disease contexts. Within the brain, TG2 has been shown to promote cell death in ischemic injury when expressed in astrocytes (Colak and Johnson, 2012). However, the specific functions and characteristics of astrocytic TG2 that mediate this effect are largely unknown. Therefore, the goal of this study was to investigate the role of astrocytic TG2 in mediating cellular viability processes in the context of ischemic injury, with a specific focus on its contributions to intracellular signaling cascades. We show that, in response to oxygen/glucose deprivation (OGD), acute lentiviral-mediated knockdown of TG2, as well as inhibition with an irreversible TG2 inhibitor, enhances cell survival. We also show that TG2 depletion increases nuclear factor-κB (NF-κB) signaling, whereas inhibition reduces NF-κB activity. Despite its clear contribution to NF-κB signaling, however, TG2 modulation of NF-κB signaling is not likely to be a major contributor to its ability to mediate astrocytic viability in this context. Overall, the results of this study provide insight into the role of TG2 in astrocytes and suggest possible avenues for future study of the relationship between astrocytic TG2 and ischemic injury.

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Tissue Transglutaminase in Marmoset Experimental Multiple Sclerosis: Discrepancy between White and Grey Matter

Cited by 12 publications

References 87 publications

Macroglial diversity: white and grey areas and relevance to remyelination

Macroglial diversity: white and grey areas and relevance to remyelination

Is monocyte- and macrophage-derived tissue transglutaminase involved in inflammatory processes?

Transglutaminase 2 modulation of NF-κB signaling in astrocytes is independent of its ability to mediate astrocytic viability in ischemic injury

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