Potential role for S100A4 in the disruption of the blood–brain barrier in collagen-induced arthritic mice, an animal model of rheumatoid arthritis

Nishioku, Tsuyoshi; Furusho, Koki; Tomita, Akira; Ohishi, Hanako; Dohgu, Shinya; Shuto, Hideki; Yamauchi, Atsushi; Kataoka, Yasufumi

doi:10.1016/j.neuroscience.2011.05.044

Cited by 40 publications

(37 citation statements)

References 37 publications

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“…Several S100 proteins, such as S100B (46), S100A1, S100A2 (47), S100A4 (48), S100A6, S100A11 (24,32) and S100A14 (49) have been shown to interact with MDM2. Direct protein-protein interactions between S100 proteins and MDM2 promote the degradation of p53, as has been demonstrated for S100B and S100A4 (12,48,50). This results in the loss of p53-dependent tumor suppressor activities.…”

Section: +mentioning

confidence: 79%

S100 family signaling network and related proteins in pancreatic cancer (Review)

Huang

Jiang

et al. 2014

International Journal of Molecular Medicine

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Abstract. The occurrence and development of pancreatic cancer is a complex process convoluted by multi-pathogenies, multi-stages and multi-factors. S100 proteins are members of the S100 family that regulate multiple cellular pathways related to pancreatic cancer progression and metastasis. S100 proteins have a broad range of intracellular and extracellular functions, including the regulation of protein phosphorylation and enzyme activity, calcium homeostasis and the regulation of cytoskeletal components and transcriptional factors. S100 proteins interact with receptor for advanced glycation end-products (RAGE), p53 and p21, which play a role in the degradation of the extracellular matrix (ECM) and metastasis, and also interact with cytoskeletal proteins and the plasma membrane in pancreatic cancer progression and metastasis. S100A11 and S100P are significant tumor markers for pancreatic cancer and unfavorable predictors for the prognosis of patients who have undergone surgical resection. Recently, S100A2 has been suggested to be a negative prognostic biomarker in pancreatic cancer, and the expression of S100A6 may be an independent prognostic impact factor. The expression of S100A4 and S100P is associated with drug resistance, differentiation, metastasis and clinical outcome. This review summarizes the role and significance of the S100 family signaling network and related proteins in pancreatic cancer.

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Section: +mentioning

confidence: 79%

S100 family signaling network and related proteins in pancreatic cancer (Review)

Huang

Jiang

et al. 2014

International Journal of Molecular Medicine

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“…It was thought that these features were simply secondary to the peripheral manifestations of the disease. However, the above findings suggest the BBB may be more porous in RA (Nishioku et al, 2011)and that intracerebral TNFα activity has been demonstrated and (Thomson et al, 2014), thus, opens the possibility of a primary, cerebral etiology for neuropsychiatric symptoms as proposed by Rech et al (2013). …”

Section: Risk Of Infectionmentioning

confidence: 97%

Section: Risk Of Infectionmentioning

confidence: 99%

“…Increased cerebrovascular permeability has been demonstrated in mice challenged with the collagen-induced arthritis (CIA) model (Nishioku et al, 2011). The same group have also proposed that the S100A4 protein mediates disruption of the BBB by increasing vascular permeability (Nishioku et al, 2011). Further evidence that the BBB is not as immunologically a privileged site as previously thought is supported by the recent observations in mice with systemic inflammation triggered by a peripheral LPS challenge show activation of interferon-stimulated genes (ISGs) and TNFα in the brain (Thomson et al, 2014), as illustrated in Figure 1.…”

Section: Risk Of Infectionmentioning

confidence: 99%

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New insights into the impact of neuro-inflammation in rheumatoid arthritis

et al. 2014

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Rheumatoid arthritis (RA) is considered to be, in many respects, an archetypal autoimmune disease that causes activation of pro-inflammatory pathways resulting in joint and systemic inflammation. RA remains a major clinical problem with the development of several new therapies targeted at cytokine inhibition in recent years. In RA, biologic therapies targeted at inhibition of tumor necrosis factor alpha (TNFα) have been shown to reduce joint inflammation, limit erosive change, reduce disability and improve quality of life. The cytokine TNFα has a central role in systemic RA inflammation and has also been shown to have pro-inflammatory effects in the brain. Emerging data suggests there is an important bidirectional communication between the brain and immune system in inflammatory conditions like RA. Recent work has shown how TNF inhibitor therapy in people with RA is protective for Alzheimer's disease. Functional MRI studies to measure brain activation in people with RA to stimulus by finger joint compression, have also shown that those who responded to TNF inhibition showed a significantly greater activation volume in thalamic, limbic, and associative areas of the brain than non-responders. Infections are the main risk of therapies with biologic drugs and infections have been shown to be related to disease flares in RA. Recent basic science data has also emerged suggesting that bacterial components including lipopolysaccharide induce pain by directly activating sensory neurons that modulate inflammation, a previously unsuspected role for the nervous system in host-pathogen interactions. In this review, we discuss the current evidence for neuro-inflammation as an important factor that impacts on disease persistence and pain in RA.

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“…S100A4 is reported to stimulate expression and proteolytic activation of matrix metalloproteinases (MMPs) in endothelial cells. MMPs are known to disrupt the BBB (Nishioku et al, 2011). Microvascular tight junctions (TJs) maintain the integrity of the BBB.…”

Section: Discussionmentioning

confidence: 99%

Activation of p38-mitogen-activated protein kinase contributes to ischemia reperfusion in rat brain

Song¹,

Zou²,

Zhao³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Inflammation plays an important role in cerebral ischemia reperfusion, which can cause severe damage to the brain and may lead to cerebral hemorrhage transformation. p38-mitogen-activated protein kinase (p38mapk) has been implicated in the etiology of a number of diseases because it is a cause of inflammation, but comparatively little research has been carried out into its role in the etiology of ischemia reperfusion. We investigated the expression of p38mapk in cerebral ischemia reperfusion to gain a better understanding of its potential role in hemorrhagic transformation (HT). One hundred rats were randomly divided into three groups: an ischemia reperfusion group, an ischemia group, and a sham-operated group. We carried out neurological deficit assessments, infarct volume measurements, histopathological examinations, and immunohistochemistry analyses. p38mapk was 2 Y.Q. Song et al. Genetics and Molecular Research 15 (3): gmr.15038492 overexpressed in the ischemia reperfusion group, which exhibited severe tissue damage and greater edema than the other two groups. These results suggest that p38mapk plays an important role in cerebral ischemia reperfusion, and may be one of the causes of HT.

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Potential role for S100A4 in the disruption of the blood–brain barrier in collagen-induced arthritic mice, an animal model of rheumatoid arthritis

Cited by 40 publications

References 37 publications

S100 family signaling network and related proteins in pancreatic cancer (Review)

S100 family signaling network and related proteins in pancreatic cancer (Review)

New insights into the impact of neuro-inflammation in rheumatoid arthritis

Activation of p38-mitogen-activated protein kinase contributes to ischemia reperfusion in rat brain

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