Role of Membrane Lipids and Membrane Fluidity in Thermosensitivity and Thermotolerance of Mammalian Cells

Background: Neuroinflammation plays a critical role in the development and progression of various neurological disorders. Therefore, various studies have focused on the development of neuroinflammation inhibitors as potential therapeutic tools. Recently, the involvement of autophagy in the regulation of neuroinflammation has drawn substantial scientific interest, and a growing number of studies support the role of impaired autophagy in the pathogenesis of common neurodegenerative disorders. Objective: The purpose of this article is to review recent research on the role of autophagy in controlling neuroinflammation. We focus on studies employing both mammalian cells and animal models to evaluate the ability of different autophagic modulators to regulate neuroinflammation. Methods: We have mostly reviewed recent studies reporting anti-neuroinflammatory properties of autophagy. We also briefly discussed a few studies showing that autophagy modulators activate neuroinflammation in certain conditions. Results: Recent studies report neuroprotective as well as anti-neuroinflammatory effects of autophagic modulators. We discuss the possible underlying mechanisms of action of these drugs and their potential limitations as therapeutic agents against neurological disorders. Conclusion: Autophagy activators are promising compounds for the treatment of neurological disorders involving neuroinflammation.

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The Role of Lipids and Membranes in the Pathogenesis of Alzheimer's Disease: A Comprehensive View

Current Alzheimer Research ◽

10.2174/1567205015666180911151716 ◽

2018 ◽

Vol 15 (13) ◽

pp. 1191-1212 ◽

Cited By ~ 23

Author(s):

Botond Penke ◽

Gábor Paragi ◽

János Gera ◽

Róbert Berkecz ◽

Zsolt Kovács ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Signaling Pathways ◽

Membrane Lipids ◽

Specific Protein ◽

Dietary Factors ◽

Lipid Signaling ◽

Special Role ◽

Aβ Peptides

Lipids participate in Amyloid Precursor Protein (APP) trafficking and processing - important factors in the initiation of Alzheimer’s disease (AD) pathogenesis and influence the formation of neurotoxic β-amyloid (Aβ) peptides. An important risk factor, the presence of ApoE4 protein in AD brain cells binds the lipids to AD. In addition, lipid signaling pathways have a crucial role in the cellular homeostasis and depend on specific protein-lipid interactions. The current review focuses on pathological alterations of membrane lipids (cholesterol, glycerophospholipids, sphingolipids) and lipid metabolism in AD and provides insight in the current understanding of biological membranes, their lipid structures and functions, as well as their role as potential therapeutic targets. Novel methods for studying the membrane structure and lipid composition will be reviewed in a broad sense whereas the use of lipid biomarkers for early diagnosis of AD will be shortly summarized. Interactions of Aβ peptides with the cell membrane and different subcellular organelles are reviewed. Next, the details of the most important lipid signaling pathways, including the role of the plasma membrane as stress sensor and its therapeutic applications are given. 4-hydroxy-2-nonenal may play a special role in the initiation of the pathogenesis of AD and thus the “calpain-cathepsin hypothesis” of AD is highlighted. Finally, the most important lipid dietary factors and their possible use and efficacy in the prevention of AD are discussed.

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Role of endosomal membrane lipids and NPC2 in cholesterol transfer and membrane fusion

The Journal of Lipid Research ◽

10.1194/jlr.m003822 ◽

2010 ◽

Vol 51 (7) ◽

pp. 1747-1760 ◽

Cited By ~ 54

Author(s):

Misbaudeen Abdul-Hammed ◽

Bernadette Breiden ◽

Matthew A. Adebayo ◽

Jonathan O. Babalola ◽

Günter Schwarzmann ◽

...

Keyword(s):

Membrane Fusion ◽

Membrane Lipids ◽

Endosomal Membrane

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A new functional role of mitochondria‐anchored protein ligase in peroxisome morphology in mammalian cells

Journal of Cellular Biochemistry ◽

10.1002/jcb.30114 ◽

2021 ◽

Author(s):

Abhishek Mohanty ◽

Rodolfo Zunino ◽

Vincent Soubannier ◽

Shilpa Dilipkumar

Keyword(s):

Mammalian Cells ◽

Functional Role

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Reactive oxygen species in cell responses to toxic agents

Human & Experimental Toxicology ◽

10.1191/0960327102ht216oa ◽

2002 ◽

Vol 21 (2) ◽

pp. 85-90 ◽

Cited By ~ 87

Author(s):

L E Feinendegen

Keyword(s):

Radiation Exposure ◽

Mammalian Cells ◽

Low Dose ◽

X Rays ◽

Low Dose Radiation ◽

Cell Responses ◽

Toxic Agents ◽

Particle Tracks ◽

Dose Radiation

This review first summarizes experimental data on biological effects of different concentrations of ROS in mammalian cells and on their potential role in modifying cell responses to toxic agents. It then attempts to link the role of steadily produced metabolic ROS at various concentrations in mammalian cells to that of environmentally derived ROS bursts from exposure to ionizing radiation. The ROS from both sources are known to both cause biological damage and change cellular signaling, depending on their concentration at a given time. At low concentrations signaling effects of ROS appear to protect cellular survival and dominate over damage, and the reverse occurs at high ROS concentrations. Background radiation generates suprabasal ROS bursts along charged particle tracks several times a year in each nanogram of tissue, i.e., average mass of a mammalian cell. For instance, a burst of about 200 ROS occurs within less than a microsecond from low-LET irradiation such as X-rays along the track of a Compton electron (about 6 keV, ranging about 1 μm). One such track per nanogram tissue gives about 1 mGy to this mass. The number of instantaneous ROS per burst along the track of a 4-meV ¬-particle in 1 ng tissue reaches some 70000. The sizes, types and sites of these bursts, and the time intervals between them directly in and around cells appear essential for understanding low-dose and low dose-rate effects on top of effects from endogenous ROS. At background and low-dose radiation exposure, a major role of ROS bursts along particle tracks focuses on ROS-induced apoptosis of damage-carrying cells, and also on prevention and removal of DNA damage from endogenous sources by way of temporarily protective, i.e., adaptive, cellular responses. A conclusion is to consider low-dose radiation exposure as a provider of physiological mechanisms for tissue homoeostasis.

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A Narrative Review on the Role of AMPK on De Novo Lipogenesis in Non-Alcoholic Fatty Liver Disease: Evidence from Human Studies

Cells ◽

10.3390/cells10071822 ◽

2021 ◽

Vol 10 (7) ◽

pp. 1822

Author(s):

Christian von Loeffelholz ◽

Sina M. Coldewey ◽

Andreas L. Birkenfeld

Keyword(s):

Liver Disease ◽

Fatty Liver ◽

Fatty Liver Disease ◽

Mammalian Cells ◽

De Novo ◽

Adenosine Monophosphate ◽

De Novo Lipogenesis ◽

Alcoholic Fatty Liver ◽

Alcoholic Fatty Liver Disease

5′AMP-activated protein kinase (AMPK) is known as metabolic sensor in mammalian cells that becomes activated by an increasing adenosine monophosphate (AMP)/adenosine triphosphate (ATP) ratio. The heterotrimeric AMPK protein comprises three subunits, each of which has multiple phosphorylation sites, playing an important role in the regulation of essential molecular pathways. By phosphorylation of downstream proteins and modulation of gene transcription AMPK functions as a master switch of energy homeostasis in tissues with high metabolic turnover, such as the liver, skeletal muscle, and adipose tissue. Regulation of AMPK under conditions of chronic caloric oversupply emerged as substantial research target to get deeper insight into the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Evidence supporting the role of AMPK in NAFLD is mainly derived from preclinical cell culture and animal studies. Dysbalanced de novo lipogenesis has been identified as one of the key processes in NAFLD pathogenesis. Thus, the scope of this review is to provide an integrative overview of evidence, in particular from clinical studies and human samples, on the role of AMPK in the regulation of primarily de novo lipogenesis in human NAFLD.

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Mutagenicity of PFOA in Mammalian Cells: Role of Mitochondria-Dependent Reactive Oxygen Species

Environmental Science & Technology ◽

10.1021/es1026129 ◽

2011 ◽

Vol 45 (4) ◽

pp. 1638-1644 ◽

Cited By ~ 29

Author(s):

Guoping Zhao ◽

Jun Wang ◽

Xiaofei Wang ◽

Shaopeng Chen ◽

Ye Zhao ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Mammalian Cells ◽

Reactive Oxygen ◽

Oxygen Species

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Mutagenicity of ZnO nanoparticles in mammalian cells: Role of physicochemical transformations under the aging process

Nanotoxicology ◽

10.3109/17435390.2014.992816 ◽

2015 ◽

Vol 9 (8) ◽

pp. 972-982 ◽

Cited By ~ 25

Author(s):

Mei M. Wang ◽

Yi C. Wang ◽

Xi N. Wang ◽

Yun Liu ◽

Hong Zhang ◽

...

Keyword(s):

Zno Nanoparticles ◽

Mammalian Cells ◽

Aging Process

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Dietary Selenium or Zinc Supplementation Restores Brain Lipid Composition and Membrane Fluidity in Protein-Undernourished Rats

Developmental Neuroscience ◽

10.1159/000462971 ◽

2016 ◽

Vol 38 (6) ◽

pp. 397-406

Author(s):

Olusegun L. Adebayo ◽

Bamidele A. Salau ◽

Rajat Sandhir ◽

Gbenga A. Adenuga

Keyword(s):

Membrane Fluidity ◽

Lipid Composition ◽

Zinc Supplementation ◽

Protective Role ◽

Membrane Lipid ◽

Limited Information ◽

Total Lipids ◽

Major Focus ◽

Membrane Lipid Composition

Studies have shown that protein undernutrition (PU) modifies the membrane lipid composition in the intestine and liver, as well as in plasma and other areas. However, there is limited information on the effect of PU on synaptosomal membrane lipid composition and fluidity and the protective role of selenium (Se) and zinc (Zn), which is a major focus of the present study. For 10 weeks, rats were fed diets containing 16% casein, which constituted the adequate protein diet, or 5% casein, representing the PU diet. The animals were supplemented with Se and Zn at a concentration of 0.15 and 227 mg L-1, respectively, in drinking water for 3 weeks. The results showed a significant increase in total lipids, glycolipids, triglycerides, cholesterol, and the cholesterol/phospholipid (Chol/PL) ratio, and a significant reduction in phospholipids and membrane fluidity. Se and Zn supplementation to PU rats, however, significantly lowered total lipids, glycolipids, triglycerides, cholesterol, and the Chol/PL ratio, while phospholipids and membrane fluidity were significantly restored. It is concluded that a perturbed lipid composition induced by PU affects the membrane structure and fluidity, which in turn influences membrane functions. The study suggests that Se and Zn supplementation might be beneficial in restoring the lipid dyshomeostasis associated with PU.

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