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Platelet Interactions in Thrombosis
IUBMB Life - Tập 56 Số 1 - Trang 13-18 - 2004
Robert K. Andrews, Elizabeth E. Gardiner, Yang Shen, Michael C. Berndt
Abstract

Patho/physiological platelet aggregate (thrombus) formation is initiated by engagement of platelet surface receptors, glycoprotein (GP)Ib‐IX‐V and GPVI that bind von Willebrand factor or collagen. Although beneficial in response to vascular injury by preventing blood loss (haemostasis), platelet aggregation in a sclerotic coronary artery or other diseased blood vessel (thrombosis) can cause thrombotic diseases like heart attack and stroke. At the molecular level, ligand interactions with GPIb‐IX‐V or GPVI trigger signalling responses, including elevation of cytosolic Ca2 +, dissociation of calmodulin from their cytoplasmic domains, cytoskeletal actin‐filament rearrangements, activation of src‐family kinases or PI 3‐kinase, and 'inside‐out' activation of the integrin, αIIbβ3 (GPIIb‐IIIa), that binds von Willebrand factor or fibrinogen and mediates platelet aggregation. Furthermore, emerging evidence supports a topographical co‐association of these receptors of the leucine‐rich repeat family (GPIb‐IX‐V) and immunoglobulin superfamily (GPVI) in an adhesive cluster or 'adhesosome'. This arrangement may underlie common mechanisms of initiating thrombus formation in haemostasis or thrombotic disease. IUBMB Life, 56: 13‐18, 2004

The Mitochondrial Potassium Cycle
IUBMB Life - Tập 52 Số 3-5 - Trang 153-158 - 2001
Keith Garlid, Petr Pauček
Abstract

The mitochondrial K + cycle consists of influx and efflux pathways for K + and anions. Net movement of K + salts across the inner membrane causes changes of matrix volume, so regulation of the cycle is vital for maintaining the structural integrity of the organelle. The mitochondrial K + cycle also appears to play important roles in cellular pathophysiology in vivo. Opening the mitochondrial ATP‐sensitive K + channel (mitoK ATP ) prior to ischemia protects the heart from ischemia‐reperfusion injury. MitoK ATP is an important player in the cell signaling pathways for ischemic protection and also for gene transcription, roles that appear to depend on the ability of mitoK ATP opening to trigger increased mitochondrial production of reactive oxygen species. MitoK ATP opening during both ischemia and reperfusion and during the high work state is found to preserve the structure of the intermembrane space and thereby maintains the normally low outer membrane permeability to adenine nucleotides. This review discusses the properties of the mitochondrial K + cycle that help to understand the basis of these effects.

Sphingosine 1‐Phosphate Activates Erk‐1/‐2 by Transactivating Epidermal Growth Factor Receptor in Rat‐2 Cells
IUBMB Life - Tập 50 Số 2 - Trang 119-124 - 2000
Joo‐Hee Kim, Jung Hee Kim, Woo Keun Song, Jae‐Hong Kim, Jang‐Soo Chun
Abstract

We investigated a signaling pathway leading to activation of extracellular signal‐regulated protein kinase (Erk) 1 and 2 in Rat‐2 cells stimulated with sphingosine 1‐phosphate (S1P). S1P treatment transiently activated Erk‐1/‐2 in a dose‐dependent manner, and its activation was blocked by pertussis toxin, expression of RasN17, or inhibition of Raf or MEK‐1/‐2. S1P‐induced activation of Erk‐1/‐2 was also suppressed by the inhibition of epidermal growth factor (EGF) receptor tyrosine kinase with the specific inhibitor AG1478, suggesting that activation of EGF receptor tyrosine kinase was involved in the signaling pathway. S1P‐induced Erk‐1/‐2 activation was enhanced up to 2‐fold by inhibiting protein kinase C (PKC) with GF109203X, and PKC inhibition in the absence of S1P treatment also activated Erk‐1/‐2. The stimulatory effects of Erk‐1/‐2 activation by PKC inhibition was blocked by treating cells with AG1478, suggesting the involvement of PKC in the regulation of EGF receptor tyrosine kinase activation that leads to Erk‐1/‐2 activation. Together, these results suggest that S1P activates the EGF receptor through a PKC‐dependent pathway that links Ras signaling to the activation of Erk‐1/‐2 in Rat‐2 cells.

Fluorescent proteins for live cell imaging: Opportunities, limitations, and challenges
IUBMB Life - Tập 61 Số 11 - Trang 1029-1042 - 2009
Jörg Wiedenmann, Franz Oswald, G. Ulrich Nienhaus
Abstract

The green fluorescent protein (GFP) from the jellyfish Aequorea victoria can be used as a genetically encoded fluorescence marker due to its autocatalytic formation of the chromophore. In recent years, numerous GFP‐like proteins with emission colors ranging from cyan to red were discovered in marine organisms. Their diverse molecular properties enabled novel approaches in live cell imaging but also impose certain limitations on their applicability as markers. In this review, we give an overview of key structural and functional properties of fluorescent proteins that should be considered when selecting a marker protein for a particular application and also discuss challenges that lie ahead in the further optimization of the glowing probes. © 2009 IUBMB IUBMB Life, 61(11): 1029–1042, 2009

Geldanamycin Induces Cell Cycle Arrest in K562 Erythroleukemic Cells
IUBMB Life - Tập 48 Số 4 - Trang 425-428 - 1999
Hong Ro Kim, Chang Hoon Lee, Yung Hyun Choi, Ho Sung Kang, Han Do Kim
Abstract

Geldanamycin (GA), a benzoquinone ansamycin, is one of the specific inhibitors of 90‐kDa heat shock protein and induces growth inhibition and apoptosis in certain cancer cell lines. We have investigated the mechanism of GA‐induced growth inhibition in K562 erythroleukemic cells. DNA flow‐cytometric analysis indicated that GA‐induced growth arrest was associated with G2/M phase arrest of the cell cycle. GA treatment down‐regulated the expression of cyclin B1 and inhibited phosphorylation of Cdc2 protein, both key regulatory proteins at the G2/M boundary. GA also markedly inhibited the Cdc2 kinase activity, which may be in part a result of up‐regulation of p27KIP1 by GA. The present results suggest a novel mechanism that p27KIP1 could be involved in the regulation of G2 to M phase transition.

Geldanamycin Induces Heat Shock Protein Expression Through Activation of HSF1 in K562 Erythroleukemic Cells
IUBMB Life - Tập 48 Số 4 - Trang 429-433 - 1999
Hong Ro Kim, Ho Sung Kang, Han Do Kim
Abstract

HSP90 is one of the most abundant heat shock proteins (HSPs) in eukaryotic cells and is found in complex with several regulatory proteins such as kinases and transcription factors. Geldanamycin (GA), a benzoquinone ansamycin, specifically binds to HSP90 and disrupts the interaction of HSP90 and target proteins. Thus, GA has been used as a specific inhibitor of HSP90. In this study, we examined whether GA could affect protein synthesis and gene expression in the human erythroleukemic cell line K562. Treatment with GA, but not herbimycin A (another benzoquinone ansamycin), highly induced a 70‐kDa protein, which was revealed to be HSP70 by immunoblotting and immunoprecipitation with anti‐HSP70 antibody. The expression of HSP28 was also enhanced by GA. Furthermore, GA induced the activation of heat shock factor 1 (HSF1), but not HSF2, as determined by electromobility shift and electromobility supershift assay. In addition, similar to heat shock treatment, GA induced the phosphorylation of HSF1. Heat shock element‐binding activity and phosphorylation of HSF1 were attenuated 3 h after GA treatment. These results indicate that the functional inactivation of HSP90 by GA potentially stimulates the expression of heat shock proteins through activation of HSF1.

Đường đi Kennedy—Tổng hợp De novo của phosphatidylethanolamine và phosphatidylcholine Dịch bởi AI
IUBMB Life - Tập 62 Số 6 - Trang 414-428 - 2010
Federica Gibellini, Terry Smith
Tóm tắt

Các glycerophospholipid phosphatidylcholine (PC) và phosphatidylethanolamine (PE) chiếm hơn 50% tổng số loài phospholipid trong màng eukaryote và do đó đóng vai trò quan trọng trong cấu trúc và chức năng của các màng này. Trong hầu hết các tế bào eukaryote, PC và PE được tổng hợp thông qua phản ứng aminocoholphosphotransferase, sử dụng sn‐1,2‐diradylglycerol và CDP‐choline hoặc CDP‐ethanolamine, tương ứng. Đây là bước cuối cùng trong một con đường sinh tổng hợp được gọi là đường đi Kennedy, được đặt tên theo Eugene Kennedy, người đã làm sáng tỏ nó hơn 50 năm trước. Bài viết này sẽ đề cập đến nhiều khía cạnh của đường đi Kennedy bao gồm: từng bước trong quá trình sinh tổng hợp, các chức năng và vai trò của các sản phẩm phospholipid PC và PE, và cách mà đường đi Kennedy có khả năng trở thành một mục tiêu hóa trị liệu chống lại ung thư và các bệnh nhiễm trùng khác nhau. © 2010 IUBMB IUBMB Life, 62(6): 414–428, 2010

The Central Role of Perilipin A in Lipid Metabolism and Adipocyte Lipolysis
IUBMB Life - Tập 56 Số 7 - Trang 379-385 - 2004
John T. Tansey, Carole Sztalryd, Erica M. Hlavin, Alan R. Kimmel, Constantine Londos
Abstract

The related disorders of obesity and diabetes are increasing to epidemic proportions. The role of neutral lipid storage and hydrolysis, and hence the adipocyte, is central to understanding this phenomenon. The adipocyte holds the major source of stored energy in the body in the form of triacylglycerols (TAG). It has been known for over 35 years that the breakdown of TAG and release of free (unesterified) fatty acids and glycerol from fat tissue can be regulated by a cAMP‐mediated process. However, beyond the initial signaling cascade, the mechanistic details of this lipolytic reaction have remained unclear. Work in recent years has revealed that both hormone‐sensitive lipase (HSL), generally thought to be the rate‐limiting enzyme, and perilipin, a lipid droplet surface protein, are required for optimal lipid storage and fatty acid release. There are multiple perilipin proteins encoded by mRNA splice variants of a single perilipin gene. The perilipin proteins are polyphosphorylated by protein kinase A and phosphorylation is necessary for translocation of HSL to the lipid droplet and enhanced lipolysis. Hence, the surface of the lipid storage droplet has emerged as a central site of regulation of lipolysis. This review will focus on adipocyte lipolysis with emphasis on hormone signal transduction, lipolytic enzymes, the lipid storage droplet, and fatty acid release from the adipocyte. IUBMB Life, 56: 379‐385, 2004

Modulation of hepatic lipid metabolism by olive oil and its phenols in nonalcoholic fatty liver disease
IUBMB Life - Tập 67 Số 1 - Trang 9-17 - 2015
Paola Priore, Alessandro Cavallo, Antonio Gnoni, Fabrizio Damiano, Gabriele V. Gnoni, Luisa Siculella
Abstract

Nonalcoholic fatty liver disease (NAFLD) represents the most common chronic liver disease in western countries, being considered the hepatic manifestation of metabolic syndrome. Cumulative lines of evidence suggest that olive oil, used as primary source of fat by Mediterranean populations, may play a key role in the observed health benefits on NAFLD. In this review, we summarize the state of the art of the knowledge on the protective role of both major and minor components of olive oil on lipid metabolism during NAFLD. In particular, the biochemical mechanisms responsible for the increase or decrease in hepatic lipid content are critically analyzed, taking into account that several studies have often provided different and/or conflicting results in animal models fed on olive oil‐enriched diet. In addition, new findings that highlight the hypolipidemic and the antisteatotic actions of olive oil phenols are presented. As mitochondrial dysfunction plays a key role in the pathogenesis of NAFLD, the targeting of these organelles with olive oil phenols as a powerful therapeutic approach is also discussed. © 2015 IUBMB Life, 67(1):9–17, 2015

Exenatide ameliorates inflammatory response in human rheumatoid arthritis fibroblast‐like synoviocytes
IUBMB Life - Tập 71 Số 7 - Trang 969-977 - 2019
Yunxia Tao, Gaoran Ge, Qing Wang, Wei Wang, Wenhao Zhang, Jiaxiang Bai, Jiayi Lin, Jining Shen, Xiaobin Guo, Yaozeng Xu, Dechun Geng
Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease of unknown etiology characterized by degradation of cartilage and bone, accompanied by unimpeded proliferation of synoviocytes of altered phenotype. In the present study, we investigated the involvement of the glucagon‐like peptide 1 (GLP‐1) receptor on human fibroblast‐like synoviocytes (FLS) in the pathogenesis of RA using the selective GLP‐1 agonist exenatide, a licensed drug used for the treatment of type 2 diabetes. Our results indicate that exenatide may play a role in regulating tumor necrosis factor‐α‐induced mitochondrial dysfunction by increasing mitochondrial membrane potential, oxidative stress by reducing the production of reactive oxygen species, the expression of NADPH oxidase 4, expression of matrix metalloproteinase (MMP)‐3 and MMP‐13, release of proinflammatory cytokines including interleukin‐1β (IL‐1β), IL‐6, monocyte chemoattractant protein‐1, and high‐mobility group protein 1, as well as activation of the p38/nuclear factor of κ light polypeptide gene enhancer in B‐cells inhibitor, α/nuclear factor κB signaling pathway in primary human RA FLS. These positive results indicate that exenatide may have potential as a therapeutic agent for the treatment and prevention of RA. © 2019 IUBMB Life, 9999(9999):1–9, 2019

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