Pattern of axonal injury in murine myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis: Implications for multiple sclerosis

Herrero-Herranz, Eva; Pardo, Luis A.; Gold, Ralf; Linker, Ralf A.

doi:10.1016/j.nbd.2008.01.001

Cited by 119 publications

(92 citation statements)

References 52 publications

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“…To investigate the role of the Ang-(1-7)/Mas axis on macrophages in vivo, we used two different animal models: EAE, a mouse model for multiple sclerosis (20), and hypercholesterinemic apolipoproteinE knockout (ApoEKO), a mouse model for human atherosclerosis (21).…”

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confidence: 99%

Role of the receptor Mas in macrophage-mediated inflammation in vivo

Hammer

Yang

Friedrich

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Recently, an alternative renin–angiotensin system pathway has been described, which involves binding of angiotensin-(1–7) to its receptor Mas. The Mas axis may counterbalance angiotensin-II–mediated proinflammatory effects, likely by affecting macrophage function. Here we investigate the role of Mas in murine models of autoimmune neuroinflammation and atherosclerosis, which both involve macrophage-driven pathomechanisms. Mas signaling affected macrophage polarization, migration, and macrophage-mediated T-cell activation. Mas deficiency exacerbated the course of experimental autoimmune encephalomyelitis and increased macrophage infiltration as well as proinflammatory gene expression in the spleen and spinal cord. Furthermore, Mas deficiency promoted atherosclerosis by affecting macrophage infiltration and migration and led to increased oxidative stress as well as impaired endothelial function in ApoE-deficient mice. In summary, we identified the Mas axis as an important factor in macrophage function during inflammation of the central nervous and vascular system in vivo. Modulating the Mas axis may constitute an interesting therapeutic target in multiple sclerosis and/or atherosclerosis.

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confidence: 99%

Role of the receptor Mas in macrophage-mediated inflammation in vivo

Hammer

Yang

Friedrich

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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“…One such approach is the pharmacological blockade of the AT1R by losartan, which in contrast to other AT1R blockers, like telmisartan, does not display additional peroxisome proliferator-activating receptor (PPAR)␥ agonistic effects (9). Here we investigate the role of the RAS during autoimmune inflammation of the CNS in the model of myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis (MOG-EAE), which mimics many aspects of multiple sclerosis (10). In particular, MOG-EAE is characterized by Th1 and Th17 responses, infiltration of macrophages, and a critical role of different antigen presenting cell (APC) populations, like CNS-derived dendritic cells (DCs) (11), but no relation of the inflammatory response to the blood pressure.…”

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confidence: 99%

Role of the renin-angiotensin system in autoimmune inflammation of the central nervous system

Stegbauer

Lee

Seubert

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Angiotensin II is the principle effector molecule of the renin angiotensin system (RAS). It exerts its various actions on the cardiovascular and renal system, mainly via interaction with the angiotensin II type-1 receptor (AT1R), which contributes to blood pressure regulation and development of hypertension but may also mediate effects on the immune system. Here we study the role of the RAS in myelinoligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis ( antigen presenting cell ͉ blood pressure ͉ chemokine ͉ multiple sclerosis

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“…Axonal damage appears microscopically as distinct, elongated APP+ blots following the course of the axon, or a succession of discontinuous APP+ punctate dots that look as if they are lodged within the axon (Figure 1). Immunocytochemistry for APP is a useful method of detecting axonal injury in human and animal nerve tissue preparations (Sherriff et al, 1994b;Herrero-Herranz et al, 2008). Staining of other fast axonal transport substances is often used to determine or verify axonal injury, including synaptic vesicle terminal or synaptophisin protein (SPY) (Frischer et al 2009).…”

Section: Amyloid Precursor Protein (App)mentioning

confidence: 99%

“…Distinct patterns of axonal pathology are present in different histopathogenetic stages of MS lesions (Table 2, Han et al, 2008;Frischer et al, 2009). Active and chronic MS white matter lesions exhibit axonal injury profiles corresponding with the degree of inflammation (Bitsch et al, 2000;Herrero-Herranz, 2008;Frischer et al, 2009). …”

Section: Patterns Of Axonal Pathology In Msmentioning

confidence: 99%

“…Identification of degenerating nerve fibers outside inflammatory foci in the normal appearing white matter (NAWM) of post-mortem MS brains shows that the neurodegenerative process can occur independently -at least topgraphically-of inflammation and demyelination (Bjartmar et al, 2001). However, there is a strong correlation between the degree of axonal injury and inflammation in all MS lesion stages and normal appearing white matter (Bitsch et al, 2000;Herrero-Herranz, 2008;Frischer et al, 2009). Moreover, progressive patients exhibit extensive neurodegeneration against a background of massive inflammation and glial activation (Kutzeinigg et al, 2005).…”

Section: Axonal Loss As a Distant Pathological Processmentioning

confidence: 99%

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