IGF1 affects macrophage invasion and activation and TNF-α production in the sciatic nerves of female SOD1G93A mice

Ji, Yingxiao; Duan, Weisong; Liu, Yaling; Liu, Yakun; Liu, Chang; Li, Yuanyuan; Wen, Di; Li, Zhongyao; Li, Chunyan

doi:10.1016/j.neulet.2017.12.062

Cited by 8 publications

(7 citation statements)

References 36 publications

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“…It is well documented that inflammatory cytokines attenuate IGF1 production (Maggio et al 2013 ; Rajpathak et al 2008 ), but IGF1 also plays an important role in regulating innate and acquired immunity—including the production of inflammatory cytokines (Heemskerk et al 1999 ). Clinical data have recently implicated low IGF1 in flare-ups of inflammatory bowel disease (Krakowska-Stasiak et al 2017 ), while basic studies have demonstrated that IGF1 directly inhibits pro-inflammatory cytokines in multiple animal cell types (Ji et al 2017 ; Onnureddy et al 2015 ), inducing LPS-induced cytokine expression (Onnureddy et al 2015 ). This latter finding may have important implications for present findings, as microbial LPS may stimulate inflammatory cytokine production.…”

Section: Discussionmentioning

confidence: 99%

Composition and richness of the serum microbiome differ by age and link to systemic inflammation

et al. 2018

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Advanced age has been associated with alterations to the microbiome within the intestinal tract as well as intestinal permeability (i.e., “leaky gut”). Prior studies suggest that intestinal permeability may contribute to increases in systemic inflammation—an aging hallmark—possibly via microorganisms entering the circulation. Yet, no studies exist describing the state of the circulating microbiome among older persons. To compare microbiota profiles in serum between healthy young (20–35 years, n = 24) and older adults (60–75 years, n = 24) as well as associations between differential microbial populations and prominent indices of age-related inflammation. Unweighted Unifrac analysis, a measure of β-diversity, revealed that microbial communities clustered differently between young and older adults. Several measures of α-diversity, including chao1 (p = 0.001), observed species (p = 0.001), and phylogenetic diversity (p = 0.002) differed between young and older adults. After correction for false discovery rate (FDR), age groups differed (all p values ≤ 0.016) in the relative abundance of the phyla Bacteroidetes, SR1, Spirochaetes, Bacteria_Other, TM7, and Tenericutes. Significant positive correlations (p values ≤ 0.017 after FDR correction) were observed between IGF1 and Bacteroidetes (ρ = 0.380), Spirochaetes (ρ = 0.528), SR1 (ρ = 0.410), and TM7 (ρ = 0.399). Significant inverse correlations were observed for IL6 with Bacteroidetes (ρ = − 0.398) and TM7 (ρ = − 0.423), as well as for TNFα with Bacteroidetes (ρ = − 0.344). Similar findings were observed at the class taxon. These data are the first to demonstrate that the richness and composition of the serum microbiome differ between young and older adults and that these factors are linked to indices of age-related inflammation.

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Section: Discussionmentioning

confidence: 99%

Composition and richness of the serum microbiome differ by age and link to systemic inflammation

et al. 2018

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“…It has previously been shown that treatment of glial cultures with pro-inflammatory stimuli such as lipopolysaccharide (LPS), results in the induction of the HSR, as determined by an increase in Hsp27 expression [38]. In order to examine whether the differential expression of Hsp25 in different brain regions had implications for the stress response of astrocytes in the spinal cord and cortex, we examined Hsp25 expression following treatment of mixed glial cultures with the inflammatory mediators LPS, a bacterial endotoxin that activates the NF-kB-mediated inflammatory pathway [39], or tumor necrosis factor a (TNFα), a pro-inflammatory cytokine previously shown to be upregulated in response to mutant SOD1 [40][41][42][43].…”

Section: Expression Of Hsp25 In Cortical and Spinal Cord Mixed Glial Culturesmentioning

confidence: 99%

Regional Differences in Heat Shock Protein 25 Expression in Brain and Spinal Cord Astrocytes of Wild-Type and SOD1 G93A Mice

Gil

Clarke

Ecroyd

et al. 2021

Cells

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Heterogeneity of glia in different CNS regions may contribute to the selective vulnerability of neuronal populations in neurodegenerative conditions such as amyotrophic lateral sclerosis (ALS). Here, we explored regional variations in the expression of heat shock protein 25 in glia under conditions of acute and chronic stress. Hsp27 (Hsp27; murine orthologue: Hsp25) fulfils a number of cytoprotective functions and may therefore be a possible therapeutic target in ALS. We identified a subpopulation of astrocytes in primary murine mixed glial cultures that expressed Hsp25. Under basal conditions, the proportion of Hsp25-positive astrocytes was twice as high in spinal cord cultures than in cortical cultures. To explore the physiological role of the elevated Hsp25 expression in spinal cord astrocytes, we exposed cortical and spinal cord glia to acute stress, using heat stress and pro-inflammatory stimuli. Surprisingly, we observed no stress-induced increase in Hsp25 expression in either cortical or spinal cord astrocytes. Similarly, exposure to endogenous stress, as modelled in glial cultures from SOD1 G93A-ALS mice, did not increase Hsp25 expression above that observed in astrocytes from wild-type mice. In vivo, Hsp25 expression was greater under conditions of chronic stress present in the spinal cord of SOD1 G93A mice than in wild-type mice, although this increase in expression is likely to be due to the extensive gliosis that occurs in this model. Together, these results show that there are differences in the expression of Hsp25 in astrocytes in different regions of the central nervous system, but Hsp25 expression is not upregulated under acute or chronic stress conditions.

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“…BMP-7 signi cantly reduced proin ammatory M1 macrophages and increased anti-in ammatory M2 macrophages in BMP-7-treated mice [18]. Some studies indicated that PIGF [19], IGF1 [20], SCF [21] and GH [22] reduced in ammation and played a critical role in polarizing the M1/M2 phenotypes via speci c growth factor receptor pathways.…”

Section: Discussionmentioning

confidence: 99%

Placental mesenchymal stem cells ameliorate NLRP3 inflammasome induced ovarian insufficiency by modulating macrophage M2 polarization

Chen

Xing

et al. 2022

Preprint

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Background: Premature ovarian insufficiency (POI) is a common clinical problem but there are currently no effective therapies. Pyroptosis induced by the NLRP3 inflammasome is considered a possible mechanism of POI. Placental mesenchymal stem cells(PMSCs) have excellent immunomodulatory potential and offer a promising method for treating POI. Methods: Female Sprague–Dawley rats were randomly divided into four treatment groups: control (no POI), POI with no PMSCs, POI with PMSCs transplant, and POI with hormones (estrogen+progesterone) as positive control. POI was induced by exposure to 4-vinylcyclohexene diepoxide (VCD) for 15 days. After four weeks, all animals were euthanized and examined for pathology. Hormone levels were measured and ovarian function was evaluated in relation to the estrous cycle. Levels of NLRP3 inflammasome pathway proteins were determined by immunohistochemistry and western blot. Results: VCD significantly damaged rat follicles at different estrous stages. Injection of human PMSCs improved ovarian function and reproductive ability of POI rats compared to the sham and hormone groups. Our data also showed that PMSCs could remarkably suppress cell pyroptosis via downregulation of the NLRP3 inflammasome, caspase-1, IL-1β and IL-18 compared to the other two groups. The human PMSCs increased the expression of IL-4 and IL-10 and decreased pro-inflammatory factors by phenotypic changes in macrophages. Conclusions: Our findings revealed a novel mechanism of follicular dysfunction and ovarian fibrosis via activation of the NLRP3 inflammasome followed by secretion of pro-inflammatory factors. Transplantation of PMSCs into POI rats suppressed pro-inflammatory factor production, NLRP3 inflammasome formation and pyroptosis, and improved ovarian function.

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IGF1 affects macrophage invasion and activation and TNF-α production in the sciatic nerves of female SOD1G93A mice

Cited by 8 publications

References 36 publications

Composition and richness of the serum microbiome differ by age and link to systemic inflammation

Composition and richness of the serum microbiome differ by age and link to systemic inflammation

Regional Differences in Heat Shock Protein 25 Expression in Brain and Spinal Cord Astrocytes of Wild-Type and SOD1 G93A Mice

Placental mesenchymal stem cells ameliorate NLRP3 inflammasome induced ovarian insufficiency by modulating macrophage M2 polarization

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