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  • 1
    Online Resource
    Online Resource
    Role of RGC-32 in multiple sclerosis and neuroinflammation – few answers and many questions
    Frontiers Media SA ; 2022
    In:  Frontiers in Immunology Vol. 13 ( 2022-9-12)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 13 ( 2022-9-12)
    Abstract: Recent advances in understanding the pathogenesis of multiple sclerosis (MS) have brought into the spotlight the major role played by reactive astrocytes in this condition. Response Gene to Complement (RGC)-32 is a gene induced by complement activation, growth factors, and cytokines, notably transforming growth factor β, that is involved in the modulation of processes such as angiogenesis, fibrosis, cell migration, and cell differentiation. Studies have uncovered the crucial role that RGC-32 plays in promoting the differentiation of Th17 cells, a subtype of CD4 + T lymphocytes with an important role in MS and its murine model, experimental autoimmune encephalomyelitis. The latest data have also shown that RGC-32 is involved in regulating major transcriptomic changes in astrocytes and in favoring the synthesis and secretion of extracellular matrix components, growth factors, axonal growth molecules, and pro-astrogliogenic molecules. These results suggest that RGC-32 plays a major role in driving reactive astrocytosis and the generation of astrocytes from radial glia precursors. In this review, we summarize recent advances in understanding how RGC-32 regulates the behavior of Th17 cells and astrocytes in neuroinflammation, providing insight into its role as a potential new biomarker and therapeutic target.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    DOI: 10.3389/fimmu.2022.979414
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2606827-8
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  • 2
    Online Resource
    Online Resource
    DataSheet_1.zip
    Frontiers Media SA ; 2021
    In:  Frontiers in Immunology Vol. 12 ( 2021-7-29)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 12 ( 2021-7-29)
    Abstract: Response Gene to Complement 32 (RGC-32) is an important mediator of the TGF-β signaling pathway, and an increasing amount of evidence implicates this protein in regulating astrocyte biology. We showed recently that spinal cord astrocytes in mice lacking RGC-32 display an immature phenotype reminiscent of progenitors and radial glia, with an overall elongated morphology, increased proliferative capacity, and increased expression of progenitor markers when compared to their wild-type (WT) counterparts that make them incapable of undergoing reactive changes during the acute phase of experimental autoimmune encephalomyelitis (EAE). Here, in order to decipher the molecular networks underlying RGC-32’s ability to regulate astrocytic maturation and reactivity, we performed next-generation sequencing of RNA from WT and RGC-32 knockout (KO) neonatal mouse brain astrocytes, either unstimulated or stimulated with the pleiotropic cytokine TGF-β. Pathway enrichment analysis showed that RGC-32 is critical for the TGF-β-induced up-regulation of transcripts encoding proteins involved in brain development and tissue remodeling, such as axonal guidance molecules, transcription factors, extracellular matrix (ECM)-related proteins, and proteoglycans. Our next-generation sequencing of RNA analysis also demonstrated that a lack of RGC-32 results in a significant induction of WD repeat and FYVE domain-containing protein 1 (Wdfy1) and stanniocalcin-1 (Stc1). Immunohistochemical analysis of spinal cords isolated from normal adult mice and mice with EAE at the peak of disease showed that RGC-32 is necessary for the in vivo expression of ephrin receptor type A7 in reactive astrocytes, and that the lack of RGC-32 results in a higher number of homeodomain-only protein homeobox (HOPX) + and CD133 + radial glia cells. Collectively, these findings suggest that RGC-32 plays a major role in modulating the transcriptomic changes in astrocytes that ultimately lead to molecular programs involved in astrocytic differentiation and reactive changes during neuroinflammation.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    URL: Article
    DOI: 10.3389/fimmu.2021.705308
    DOI: 10.3389/fimmu.2021.705308.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2606827-8
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  • 3
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    Online Resource
    DataSheet_1.pdf
    Frontiers Media SA ; 2021
    In:  Frontiers in Immunology Vol. 11 ( 2021-1-25)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 11 ( 2021-1-25)
    Abstract: Astrocytes are increasingly recognized as critical contributors to multiple sclerosis pathogenesis. We have previously shown that lack of Response Gene to Complement 32 (RGC-32) alters astrocyte morphology in the spinal cord at the peak of experimental autoimmune encephalomyelitis (EAE), suggesting a role for RGC-32 in astrocyte differentiation. In this study, we analyzed the expression and distribution of astrocytes and astrocyte progenitors by immunohistochemistry in spinal cords of wild-type (WT) and RGC-32-knockout (KO) mice with EAE and of normal adult mice. Our analysis showed that during acute EAE, WT astrocytes had a reactive morphology and increased GFAP expression, whereas RGC-32 KO astrocytes had a morphology similar to that of radial glia and an increased expression of progenitor markers such as vimentin and fatty acid binding protein 7 (FABP7). In control mice, GFAP expression and astrocyte density were also significantly higher in the WT group, whereas the number of vimentin and FABP7-positive radial glia was significantly higher in the RGC-32 KO group. In vitro studies on cultured neonatal astrocytes from WT and RGC-32 KO mice showed that RGC-32 regulates a complex array of molecular networks pertaining to signal transduction, growth factor expression and secretion, and extracellular matrix (ECM) remodeling. Among the most differentially expressed factors were insulin-like growth factor 1 (IGF1), insulin-like growth factor binding proteins (IGFBPs), and connective tissue growth factor (CTGF); their expression was downregulated in RGC-32-depleted astrocytes. The nuclear translocation of STAT3, a transcription factor critical for astrogliogenesis and driving glial scar formation, was also impaired after RGC-32 silencing. Taken together, these data suggest that RGC-32 is an important regulator of astrocyte differentiation during EAE and that in the absence of RGC-32, astrocytes are unable to fully mature and become reactive astrocytes.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    URL: Article
    DOI: 10.3389/fimmu.2020.608294
    DOI: 10.3389/fimmu.2020.608294.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2606827-8
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  • 4
    Online Resource
    Online Resource
    Data_Sheet_1.pdf
    Frontiers Media SA ; 2022
    In:  Frontiers in Neurology Vol. 12 ( 2022-2-1)
    Details
    In: Frontiers in Neurology, Frontiers Media SA, Vol. 12 ( 2022-2-1)
    Abstract: Malnutrition is common after stroke and can affect rehabilitation and healthcare costs. A comprehensive overview of stroke patients' nutritional condition from the hyperacute to the chronic phase is lacking. This systematic review aimed to investigate the prevalence of impaired nutritional condition (INC) across the continuum of care in specific phases after stroke. Methods CAB ABSTRACTS, Embase, MEDLINE, were used to collect studies published between 01-01-1999 and 26-08-2020. Primary and secondary outcomes were prevalence of INC and prevalence of malnutrition, respectively. Exploratory outcomes were prevalence of INC at follow-up, nutritional examination methods, prevalence of dysphagia, stroke severity, adverse events, and continent-specific prevalence of INC. A random-effects meta-analysis model was used to estimate the phase-specific pooled prevalence of INC and malnutrition. Results The dataset consisted of 78 study groups selected over a total of 1,244 identified records. The pooled prevalence of INC and malnutrition were 19% (95%CI:7–31) ( N = 4) and 19% (95%CI:9–29) ( N = 3), 34% (95%CI:25–43) ( N = 34) and 26% (95%CI:18–35) ( N = 29), 52% (95%CI:43–61) ( N = 34) and 37% (95%CI:28–45) ( N = 31), 21% (95%CI:12–31) ( N = 3) and 11% (95%CI:0–24) ( N = 3) and 72% (95%CI:41–100) ( N = 3) and 30% (95%CI:0–76) ( N = 2) in the hyperacute, acute, early subacute, late subacute, and chronic phase, respectively. Conclusion INC and malnutrition are highly prevalent in all stages of stroke care. Since malnutrition has been shown to negatively affect clinical outcomes, mortality, and overall healthcare expenditure in stroke survivors, it is essential to examine and monitor the nutritional status of stroke patients throughout their care journey to guide and plan, timely nutritional support and dietary modification.
    Type of Medium: Online Resource
    ISSN: 1664-2295
    URL: Article
    URL: Article
    DOI: 10.3389/fneur.2021.780080
    DOI: 10.3389/fneur.2021.780080.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2564214-5
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