Plasma Immunoproteasome Predicts Early Hemorrhagic Transformation in Acute Ischemic Stroke Patients

Chen, Xingyong; Wang, Yinzhou; Fu, Ming; Lei, Hanhan; Cheng, Qian; Xu, Zhonghua

doi:10.1016/j.jstrokecerebrovasdis.2016.08.027

Cited by 21 publications

(23 citation statements)

References 28 publications

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“…The IP is significantly up-regulated in glia and neurons, in both patients and experimental models of HD (121, 139), AD (112–117), PD (119, 120), MS (41, 98–103, 108–110), ALS (134, 140), neurotrauma (129), ischemic stroke (104, 124, 125), and epilepsy (38, 100, 126, 127). In the context of PD, the induction of IP within glia and DA neurons was recently related to alpha-synuclein degradation and subsequent generation of self-Ag peptides for T-cell presentation by MHC-I (79, 119, 132).…”

Section: The Role Of Proteasomes In Neurons and Gliamentioning

confidence: 99%

A Sentinel in the Crosstalk Between the Nervous and Immune System: The (Immuno)-Proteasome

et al. 2019

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The wealth of recent evidence about a bi-directional communication between nerve- and immune- cells revolutionized the traditional concept about the brain as an “immune-privileged” organ while opening novel avenues in the pathophysiology of CNS disorders. In fact, altered communication between the immune and nervous system is emerging as a common hallmark in neuro-developmental, neurodegenerative, and neuro-immunological diseases. At molecular level, the ubiquitin proteasome machinery operates as a sentinel at the crossroad between the immune system and brain. In fact, the standard proteasome and its alternative/inducible counterpart, the immunoproteasome, operate dynamically and coordinately in both nerve- and immune- cells to modulate neurotransmission, oxidative/inflammatory stress response, and immunity. When dysregulations of the proteasome system occur, altered amounts of standard- vs. immune-proteasome subtypes translate into altered communication between neurons, glia, and immune cells. This contributes to neuro-inflammatory pathology in a variety of neurological disorders encompassing Parkinson's, Alzheimer's, and Huntingtin's diseases, brain trauma, epilepsy, and Multiple Sclerosis. In the present review, we analyze those proteasome-dependent molecular interactions which sustain communication between neurons, glia, and brain circulating T-lymphocytes both in baseline and pathological conditions. The evidence here discussed converges in that upregulation of immunoproteasome to the detriment of the standard proteasome, is commonly implicated in the inflammatory- and immune- biology of neurodegeneration. These concepts may foster additional studies investigating the role of immunoproteasome as a potential target in neurodegenerative and neuro-immunological disorders.

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Section: The Role Of Proteasomes In Neurons and Gliamentioning

confidence: 99%

A Sentinel in the Crosstalk Between the Nervous and Immune System: The (Immuno)-Proteasome

et al. 2019

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“…IL-1 and TNF-a) and reactive oxygen species, and can lead to the breaking of the blood-brain barrier [21,22,42]. Compared to the constitutive proteasome, immunoproteasomes produce more peptides with a hydrophobic C-terminus, which are well suited for presentation on MHC class I molecules [43].…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, mutations in LMP7 and LMP2 in humans cause complex autoimmune and inflammatory phenotypes [39,40]. The literature concerning the role of the immunoproteasome in nuclear factor kappa C (NF-jB) activation is somewhat controversial [42,[44][45][46][47].…”

Section: Discussionmentioning

confidence: 99%

Immunoproteasome in the blood plasma of children with acute appendicitis, and its correlation with proteasome and UCHL1 measured by SPR imaging biosensors

Matuszczak

Sankiewicz

Dębek

et al. 2017

Clinical and Experimental Immunology

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SummaryThe aim of this study was to determinate the immunoproteasome concentration in the blood plasma of children with appendicitis, and its correlation with circulating proteasome and ubiquitin carboxyl-terminal hydrolase L1 (UCHL1). Twenty-seven children with acute appendicitis, managed at the Paediatric Surgery Department, were included randomly into the study (age 2 years 9 months up to 14 years, mean age 9Á5 6 1 years). There were 10 girls and 17 boys; 18 healthy, age-matched subjects, admitted for planned surgeries served as controls. Mean concentrations of immunoproteasome, 20S proteasome and UCHL1 in the blood plasma of children with appendicitis before surgery 24 h and 72 h after the appendectomy were higher than in the control group. The immunoproteasome, 20S proteasome and UCHL1 concentrations in the blood plasma of patients with acute appendicitis were highest before surgery. The immunoproteasome, 20S proteasome and UCHL1 concentration measured 24 and 72 h after the operation decreased slowly over time and still did not reach the normal range (P < 0Á05). There was no statistical difference between immunoproteasome, 20S proteasome and UCHL1 concentrations in children operated on laparoscopically and children after classic appendectomy. The immunoproteasome concentration may reflect the metabolic response to acute state inflammation, and the process of gradual ebbing of the inflammation may thus be helpful in the assessment of the efficacy of treatment. The method of operation -classic open appendectomy or laparoscopic appendectomy -does not influence the general trend in immunoproteasome concentration in children with appendicitis.

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“…The immunoproteasome induction after cerebral ischemia is supposed to play a critical role in coping with the damaged proteins and thus may be of great importance in neuronal survival and death [8]. The plasma level of the immunoproteasome is supposed to be a useful indicator in the early prediction of hemorrhagic transformation after acute ischemic stroke [9].…”

Section: Change Of Immunoproteasome In Cerebral Ischemiamentioning

confidence: 99%

The Role of Ubiquitin-Proteasome Pathway and Autophagy-Lysosome Pathway in Cerebral Ischemia

Chen

Qin

Tan

et al. 2020

Oxidative Medicine and Cellular Longevity

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The ubiquitin-proteasome pathway and autophagy-lysosome pathway are two major routes for clearance of aberrant cellular components to maintain protein homeostasis and normal cellular functions. Accumulating evidence shows that these two pathways are impaired during cerebral ischemia, which contributes to ischemic-induced neuronal necrosis and apoptosis. This review aims to critically discuss current knowledge and controversies on these two pathways in response to cerebral ischemic stress. We also discuss molecular mechanisms underlying the impairments of these protein degradation pathways and how such impairments lead to neuronal damage after cerebral ischemia. Further, we review the recent advance on the understanding of the involvement of these two pathways in the pathological process during many therapeutic approaches against cerebral ischemia. Despite recent advances, the exact role and molecular mechanisms of these two pathways following cerebral ischemia are complex and not completely understood, of which better understanding will provide avenues to develop novel therapeutic strategies for ischemic stroke.

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Plasma Immunoproteasome Predicts Early Hemorrhagic Transformation in Acute Ischemic Stroke Patients

Cited by 21 publications

References 28 publications

A Sentinel in the Crosstalk Between the Nervous and Immune System: The (Immuno)-Proteasome

A Sentinel in the Crosstalk Between the Nervous and Immune System: The (Immuno)-Proteasome

Immunoproteasome in the blood plasma of children with acute appendicitis, and its correlation with proteasome and UCHL1 measured by SPR imaging biosensors

The Role of Ubiquitin-Proteasome Pathway and Autophagy-Lysosome Pathway in Cerebral Ischemia

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