β-Dystroglycan cleavage by matrix metalloproteinase-2/-9 disturbs aquaporin-4 polarization and influences brain edema in acute cerebral ischemia

Yan, Weigang; Zhao, Xinyu; Chen, H.; Zhong, Di; Jin, Jiashun; Qin, Qi‐Long; Zhang, H.; Ma, Shuainan; Li, Guozhong

doi:10.1016/j.neuroscience.2016.03.055

Cited by 24 publications

(16 citation statements)

References 51 publications

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“…A similar increase in glutamate surge occurs during reperfusion to the micro-ischemic area resulting in further enhancement of blood barrier leakages and causing microbleed. MMP-2/-9 mediated β-dystroglycan cleavage in ischemic conditions induces redistribution of aquaporin-4 in astrocytes and causes both cytotoxic and vasogenic edema [242][243][244]. These aquaporinsare sensitive to heavy metals such as Zn 2+ , Mn, Pb [245,246].…”

Section: Mmps Expressionmentioning

confidence: 99%

Heavy Metal-Induced Cerebral Small Vessel Disease: Insights into Molecular Mechanisms and Possible Reversal Strategies

Patwa

Flora

2020

IJMS

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Heavy metals are considered a continuous threat to humanity, as they cannot be eradicated. Prolonged exposure to heavy metals/metalloids in humans has been associated with several health risks, including neurodegeneration, vascular dysfunction, metabolic disorders, cancer, etc. Small blood vessels are highly vulnerable to heavy metals as they are directly exposed to the blood circulatory system, which has comparatively higher concentration of heavy metals than other organs. Cerebral small vessel disease (CSVD) is an umbrella term used to describe various pathological processes that affect the cerebral small blood vessels and is accepted as a primary contributor in associated disorders, such as dementia, cognitive disabilities, mood disorder, and ischemic, as well as a hemorrhagic stroke. In this review, we discuss the possible implication of heavy metals/metalloid exposure in CSVD and its associated disorders based on in-vitro, preclinical, and clinical evidences. We briefly discuss the CSVD, prevalence, epidemiology, and risk factors for development such as genetic, traditional, and environmental factors. Toxic effects of specific heavy metal/metalloid intoxication (As, Cd, Pb, Hg, and Cu) in the small vessel associated endothelium and vascular dysfunction too have been reviewed. An attempt has been made to highlight the possible molecular mechanism involved in the pathophysiology, such as oxidative stress, inflammatory pathway, matrix metalloproteinases (MMPs) expression, and amyloid angiopathy in the CSVD and related disorders. Finally, we discussed the role of cellular antioxidant defense enzymes to neutralize the toxic effect, and also highlighted the potential reversal strategies to combat heavy metal-induced vascular changes. In conclusion, heavy metals in small vessels are strongly associated with the development as well as the progression of CSVD. Chelation therapy may be an effective strategy to reduce the toxic metal load and the associated complications.

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Section: Mmps Expressionmentioning

confidence: 99%

Heavy Metal-Induced Cerebral Small Vessel Disease: Insights into Molecular Mechanisms and Possible Reversal Strategies

Patwa

Flora

2020

IJMS

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“…In addition, brain edema is the primary cause of IS mortality. The mechanism underlying this phenomenon may be the rapid disturbance of water contributing to abnormal elevation in intracranial pressure and/or intracranial fluid [116,117].…”

Section: Potential Dm-induced Mechanisms Leading To Diabetic Strokementioning

confidence: 99%

Potential Biochemical Mechanisms of Brain Injury in Diabetes Mellitus

Xing¹,

Tang²,

Lei³

et al. 2020

Aging and disease

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The goal of this review was to summarize current biochemical mechanisms of and risk factors for diabetic brain injury. We mainly summarized mechanisms published in the past three years and focused on diabetes induced cognitive impairment, diabetes-linked Alzheimer's disease, and diabetic stroke. We think there is a need to conduct further studies with increased sample sizes and prolonged period of follow-ups to clarify the effect of DM on brain dysfunction. Additionally, we also think that enhancing experimental reproducibility using animal models in conjunction with application of advanced devices should be considered when new experiments are designed. It is expected that further investigation of the underlying mechanisms of diabetic cognitive impairment will provide novel insights into therapeutic approaches for ameliorating diabetes-associated injury in the brain.

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“…During reperfusion following initial ischemia in the stroke, with the activation of Na + /K + -ATPase, more Na + release than K + uptake occurs in a 3:2 ratio, which drives NKCC1 to move more ions into the cell, leading to the development of cytotoxic cell swelling (Wang and Parpura, 2016 ). All these pathological processes are associated with malfunctioned uptake machinery for K + and glutamate (Steiner et al, 2012 ; Yan et al, 2016 ) and fluid volume transfer through AQP4 (Anderova et al, 2014 ) by astrocytes during ischemic stroke. Additionally, there is an increased level of extracellular VP during ischemic stroke (Jia et al, 2016 ).…”

Section: Astrocytes and Intracellular Cerebral Edemamentioning

confidence: 99%

Astroglial Modulation of Hydromineral Balance and Cerebral Edema

Wang

Parpura

2018

Front. Mol. Neurosci.

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Maintenance of hydromineral balance (HB) is an essential condition for life activity at cellular, tissue, organ and system levels. This activity has been considered as a function of the osmotic regulatory system that focuses on hypothalamic vasopressin (VP) neurons, which can reflexively release VP into the brain and blood to meet the demand of HB. Recently, astrocytes have emerged as an essential component of the osmotic regulatory system in addition to functioning as a regulator of the HB at cellular and tissue levels. Astrocytes express all the components of osmoreceptors, including aquaporins, molecules of the extracellular matrix, integrins and transient receptor potential channels, with an operational dynamic range allowing them to detect and respond to osmotic changes, perhaps more efficiently than neurons. The resultant responses, i.e., astroglial morphological and functional plasticity in the supraoptic and paraventricular nuclei, can be conveyed, physically and chemically, to adjacent VP neurons, thereby influencing HB at the system level. In addition, astrocytes, particularly those in the circumventricular organs, are involved not only in VP-mediated osmotic regulation, but also in regulation of other osmolality-modulating hormones, including natriuretic peptides and angiotensin. Thus, astrocytes play a role in local/brain and systemic HB. The adaptive astrocytic reactions to osmotic challenges are associated with signaling events related to the expression of glial fibrillary acidic protein and aquaporin 4 to promote cell survival and repair. However, prolonged osmotic stress can initiate inflammatory and apoptotic signaling processes, leading to glial dysfunction and a variety of brain diseases. Among many diseases of brain injury and hydromineral disorders, cytotoxic and osmotic cerebral edemas are the most common pathological manifestation. Hyponatremia is the most common cause of osmotic cerebral edema. Overly fast correction of hyponatremia could lead to central pontine myelinolysis. Ischemic stroke exemplifies cytotoxic cerebral edema. In this review, we summarize and analyze the osmosensory functions of astrocytes and their implications in cerebral edema.

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β-Dystroglycan cleavage by matrix metalloproteinase-2/-9 disturbs aquaporin-4 polarization and influences brain edema in acute cerebral ischemia

Cited by 24 publications

References 51 publications

Heavy Metal-Induced Cerebral Small Vessel Disease: Insights into Molecular Mechanisms and Possible Reversal Strategies

Heavy Metal-Induced Cerebral Small Vessel Disease: Insights into Molecular Mechanisms and Possible Reversal Strategies

Potential Biochemical Mechanisms of Brain Injury in Diabetes Mellitus

Astroglial Modulation of Hydromineral Balance and Cerebral Edema

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