Phospholipid transfer protein (PLTP) deficiency impaired blood–brain barrier integrity by increasing cerebrovascular oxidative stress

Zhou, Ting; He, Qihua; Tong, Yawei; Zhan, Rui; Xu, Feng; Fan, Dongsheng; Guo, Xiangyang; Han, Hongbin; Qin, Shucun; Chui, Dehua

doi:10.1016/j.bbrc.2014.01.194

Cited by 34 publications

(22 citation statements)

References 23 publications

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“…PLTP deletion was demonstrated to increase amyloid--induced memory deficits in mice (24). Compared with the whole brain, the PLTP mRNA expression level is 6.8-fold higher in cerebral vessels (25) and PLTP may play a role in maintaining blood-brain barrier integrity, possibly through its ability to transfer vitamin E and modulate cerebrovascular oxidative stress (26). These findings collectively suggest a significant role of PLTP in both physiological and pathophysiological processes in the brain.…”

Section: Phospholipid Transfer Proteinmentioning

confidence: 85%

Phospholipid transfer protein: its impact on lipoprotein homeostasis and atherosclerosis

Jiang

2018

Journal of Lipid Research

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Phospholipid transfer protein (PLTP) is one of the major modulators of lipoprotein metabolism and atherosclerosis development in humans; however, we still do not quite understand the mechanisms. In mouse models, PLTP overexpression induces atherosclerosis, while its deficiency reduces it. Thus, mouse models were used to explore the mechanisms. In this review, I summarize the major progress made in the PLTP research field and emphasize its impact on lipoprotein metabolism and atherosclerosis, as well as its regulation.

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Section: Phospholipid Transfer Proteinmentioning

confidence: 85%

Phospholipid transfer protein: its impact on lipoprotein homeostasis and atherosclerosis

Jiang

2018

Journal of Lipid Research

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“…Moreover, an in vitro study provides supporting data that Vitamin C reversed hyperglycemia-mediated BBB disruption [57]. Similar to Vitamin C, Vitamin E is also reported to prevent BBB breakdown induced by oxidative stress by attenuation of endothelial oxidative stress and via increasing the expression of tight junction proteins in vivo [58]. In rats with convulsion under hyperthermic conditions, Vitamin E showed beneficial effects on modulation of BBB permeability [59].…”

Section: Antioxidants Cognitive Decline and Blood-brain Barriermentioning

confidence: 98%

Antioxidants and Dementia Risk: Consideration through a Cerebrovascular Perspective

2016

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A number of natural and chemical compounds that exert anti-oxidative properties are demonstrated to be beneficial for brain and cognitive function, and some are reported to reduce the risk of dementia. However, the detailed mechanisms by which those anti-oxidative compounds show positive effects on cognition and dementia are still unclear. An emerging body of evidence suggests that the integrity of the cerebrovascular blood-brain barrier (BBB) is centrally involved in the onset and progression of cognitive impairment and dementia. While recent studies revealed that some anti-oxidative agents appear to be protective against the disruption of BBB integrity and structure, few studies considered the neuroprotective effects of antioxidants in the context of cerebrovascular integrity. Therefore, in this review, we examine the mechanistic insights of antioxidants as a pleiotropic agent for cognitive impairment and dementia through a cerebrovascular axis by primarily focusing on the current available data from physiological studies. Conclusively, there is a compelling body of evidence that suggest antioxidants may prevent cognitive decline and dementia by protecting the integrity and function of BBB and, indeed, further studies are needed to directly examine these effects in addition to underlying molecular mechanisms.

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“…PLTP's primary activity involves the transfer of phospholipids between HDL particles, thus modulating HDL size and composition, and transferring lipids between apoB-containing lipoproprotein particles and HDL [53]. Within the CNS, PLTP is highly expressed by neurons, astrocytes, microglia, oligodendrocytes, BBB endothelial cells, choroid plexus ependymal cells and can be found both in brain tissue and CSF in human and animals [57][58][59][60][61]. Within CSF, PLTP is associated with apoE-containing lipoproteins where it actively participates in phospholipid transport [13,62,63] with activity corresponding to 15% of plasma levels in humans [62] and 23% of plasma levels in rabbits [59].…”

Section: Enzymes Involved In Lipoprotein Metabolismmentioning

confidence: 99%

“…Intriguingly, whereas PLTP synthesis by neurons and glia is increased in the early stages of AD [62], its levels, and more importantly, its activity are reduced in brain tissue and CSF of AD patients in later stages [57,63]. In mice, deletion of Pltp increases cerebral oxidative stress, elevates Aβ42, reduces synaptophysin expression, increases BBB permeability and decreases expression of tight junction proteins under basal conditions [61,248]. Further, intracerebroventricular injection of an oligomeric Aβ peptide leads to exacerbated cognitive impairment in Pltp-/mice compared to wild-type controls [248].…”

Section: Lcat Pltp and Cetp In Admentioning

confidence: 99%

Lipids and Lipoproteins in Alzheimer’s Disease

Stukas¹,

Kulic²,

Zareyan³

et al. 2015

Alzheimer's Disease - Challenges for the Future

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Cholesterol is a key structural component of the brain, and cholesterol transport and distribution within the central nervous system CNS is mediated by a lipid metabolic cycle that includes generation of apolipoproteins as lipid carriers, lipidation by cholesterol and phospholipid transporters, enzyme remodeling of these particles and their receptor-mediated uptake and turnover in cells. It is becoming increasingly appreciated that "lzheimer's Disease "D patients often have comorbid conditions such as cardiovascular disease, type II diabetes mellitus, or hypertension, each of which can greatly affect lipoprotein metabolism, especially at the vessel wall and thereby possibly contribute to "D pathogenesis. Here we review the known biology of lipids and lipoproteins in the CNS and discuss how alterations in lipid metabolism may impact "D pathogenesis. "polipoprotein E APOE is the best established genetic risk factor for "D and the major apolipoprotein expressed in the brain. In addition, genome-wide association studies GW"S have identified several other genes associated with "D risk that function in lipid or lipoprotein metabolism, including clusterin CLU , "TP binding cassette ""C transporter " ABCA7 , and apoE receptors. Understanding how lipid/lipoprotein metabolism in the brain and body affect cognitive function may therefore offer new insights in developing more effective therapeutic approaches for dementia.

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Phospholipid transfer protein (PLTP) deficiency impaired blood–brain barrier integrity by increasing cerebrovascular oxidative stress

Cited by 34 publications

References 23 publications

Phospholipid transfer protein: its impact on lipoprotein homeostasis and atherosclerosis

Phospholipid transfer protein: its impact on lipoprotein homeostasis and atherosclerosis

Antioxidants and Dementia Risk: Consideration through a Cerebrovascular Perspective

Lipids and Lipoproteins in Alzheimer’s Disease

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