Complement and blood–brain barrier integrity

Jacob, Alexander; Alexander, Jessy J.

doi:10.1016/j.molimm.2014.06.039

Cited by 62 publications

(43 citation statements)

References 65 publications

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“…Because EC loss and subsequent vasoregression contribute to neurodegeneration in cerebral ischemia, DR, peripheral neuropathy, and age-related neurodegenerative diseases [ 75 ], it is likely that PPAR α -mediated vasoprotection contributes to the observed neuroprotective effects in these models.…”

Section: Beneficial Effects Of Ppar α In Microvmentioning

confidence: 99%

Therapeutic Effects of PPARαon Neuronal Death and Microvascular Impairment

Moran

Xing

2015

PPAR Research

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Peroxisome-proliferator activated receptor-alpha (PPARα) is a broadly expressed nuclear hormone receptor and is a transcription factor for diverse target genes possessing a PPAR response element (PPRE) in the promoter region. The PPRE is highly conserved, and PPARs thus regulate transcription of an extensive array of target genes involved in energy metabolism, vascular function, oxidative stress, inflammation, and many other biological processes. PPARα has potent protective effects against neuronal cell death and microvascular impairment, which have been attributed in part to its antioxidant and anti-inflammatory properties. Here we discuss PPARα's effects in neurodegenerative and microvascular diseases and also recent clinical findings that identified therapeutic effects of a PPARα agonist in diabetic microvascular complications.

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Section: Beneficial Effects Of Ppar α In Microvmentioning

confidence: 99%

Therapeutic Effects of PPARαon Neuronal Death and Microvascular Impairment

Moran

Xing

2015

PPAR Research

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“…CD59 is a GPI-anchored membrane-associated molecule and its appearance in the fluid phase requires either shedding on lipid vesicles with an intact GPI anchor or enzymatic anchor cleavage and release as a soluble, unanchored molecule; sCD59 in urine has been shown to be anchor-free, likely derived by enzymatic cleavage from renal tubular cells. [28][29][30] In order to investigate the nature of sCD59 in CSF we performed high-speed centrifugation to remove microparticles and re-measured sCD59 in a subset of CSF samples. Measured levels were little affected by centrifugation, indicating that CSF sCD59 was anchor free; this was further confirmed by showing that passage of the few CSF samples available in sufficient quantities through a 0.2µM filter did not reduce measured sCD59 levels.…”

Section: Discussionmentioning

confidence: 99%

Measurement of soluble CD59 in CSF in demyelinating disease: Evidence for an intrathecal source of soluble CD59

et al. 2018

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“…Activation of the complement system is critical in the innate immune system’s defense against infection and has been clearly demonstrated in the development of inflammation and neuronal dysfunction that precedes SAE (53–56). Once the complement cascade is activated by endotoxin, C5a acts upon cerebral endothelium, microglia, and brain parenchymal neurons.…”

Section: Molecular Mechanisms: Complement Cytokines and Mechanism Omentioning

confidence: 99%

Sepsis-Associated Encephalopathy: The Blood–Brain Barrier and the Sphingolipid Rheostat

Kuperberg

Wadgaonkar

2017

Front. Immunol.

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Sepsis is not only a significant cause of mortality worldwide but has particularly devastating effects on the central nervous system of survivors. It is therefore crucial to understand the molecular structure, physiology, and events involved in the pathogenesis of sepsis-associated encephalopathy, so that potential therapeutic advances can be achieved. A key determinant to the development of this type of encephalopathy is morphological and functional modification of the blood–brain barrier (BBB), whose function is to protect the CNS from pathogens and toxic threats. Key mediators of pathologic sequelae of sepsis in the brain include cytokines, including TNF-α, and sphingolipids, which are biologically active components of cellular membranes that possess diverse functions. Emerging data demonstrated an essential role for sphingolipids in the pulmonary vascular endothelium. This raises the question of whether endothelial stability in other organs systems such as the CNS may also be mediated by sphingolipids and their receptors. In this review, we will model the structure and vulnerability of the BBB and hypothesize mechanisms for therapeutic stabilization and repair following a confrontation with sepsis-induced inflammation.

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Complement and blood–brain barrier integrity

Cited by 62 publications

References 65 publications

Therapeutic Effects of PPARαon Neuronal Death and Microvascular Impairment

Therapeutic Effects of PPARαon Neuronal Death and Microvascular Impairment

Measurement of soluble CD59 in CSF in demyelinating disease: Evidence for an intrathecal source of soluble CD59

Sepsis-Associated Encephalopathy: The Blood–Brain Barrier and the Sphingolipid Rheostat

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