scholarly journals Numerical Model for Formation and Evolution of the Bleb

2020 ◽  
Author(s):  
J. Feng ◽  
L. Tang ◽  
Z. Liu ◽  
S. Dong ◽  
L. Zhou ◽  
...  
Keyword(s):  
Cell Migration ◽  
Numerical Model ◽  
Cell Model ◽  
Viscosity Coefficient ◽  
Coupling Model ◽  
Impact Factors ◽  
Affecting Factors ◽  
A Cell ◽  
Formation And Evolution

ABSTRACTThe bleb morphology and its changes are an important mechanism of cell’s amoeboid migration. By releasing bonds between the membrane and the cortex of a cell, the formation of bleb can be observed experimentally, but the mechanism that affects the size and shape of this kind of bleb is waiting for further study. In this paper, a two-dimensional fluid-solid coupling model is established to describe a cell with membrane, cortex and cytoplasm in a solution, and a numerical solving method for the fluid-solid coupling model is developed to simulate the behaviors of cell bleb. The effects of parameters, such as the number of broken bonds, the viscosity coefficient of the cortex, and the cell’s membrane modulus on the size and the shape of the bleb were investigated. Numerical results show that the model is effective to simulate the formation and evolution of cell’s bleb, and derive the contribution of several affecting factors to the bleb shape and size clearly.SIGNIFICANCETo understand the process of cell migration with bleb pseudopods in the amoeba cell migration, it is necessary to study the formation mechanism of cells protruding bleb. In this paper, we propose a reasonable and reliable cell numerical model. With this model we successfully simulate the bleb phenomenon consistent with the experimental phenomenon by changing the key impact factors. The method in this paper is applicable to the cell model of amoeba cell migration pattern, which helps to understand the important role of blebs in the process of cell migration.

scholarly journals Numerical Model for Formation and Evolution of the Bleb

2021 ◽  
Vol 13 (01) ◽  
pp. 2150009
Author(s):  
Jiju Feng ◽  
Liqun Tang ◽  
Zejia Liu ◽  
Shoubin Dong ◽  
Licheng Zhou ◽  
...  
Keyword(s):  
Viscosity Coefficient ◽  
Coupling Model ◽  
Two Dimensional ◽  
Governing Equations ◽  
Discrete Equations ◽  
A Cell ◽  
Bleb Formation ◽  
Formation And Evolution ◽  
Mathematical Medicine ◽  
Shape And Size

The morphology of a bleb and its changes are critical to the amoeboid migration of a cell. By releasing bonds between the membrane and the cortex of a cell, the formation of a bleb can be observed experimentally, but the mechanism that affects the size and shape of a bleb during amoeboid migration requires further study. In this study, by adapting the governing equations and discrete equations of the two-dimensional fluid–solid coupling model recommended by Strychalski and Guy [2013 “A computational model of bleb formation,” Mathematical Medicine and Biology 30(2), 115–130], we overcome the defect that the bleb by traditional means is always too small compared with experimental results, and simulate the behaviors of cell blebs successfully. The effects of various parameters such as the number of broken bonds, the viscosity coefficient of the cortex, and the cell’s membrane modulus on the size and the shape of the bleb are investigated. Numerical results show that the model effectively simulates the formation and evolution of a bleb, thus, the contributions of several factors to bleb shape and size are successfully derived.

scholarly journals PapRIV, a BV-2 microglial cell activating quorum sensing peptide

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yorick Janssens ◽  
Nathan Debunne ◽  
Anton De Spiegeleer ◽  
Evelien Wynendaele ◽  
Marta Planas ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Cell Model ◽  
Dependent Manner ◽  
Communication Signals ◽  
Gram Positive Bacteria ◽  
A Cell ◽  
Gastro Intestinal Tract

AbstractQuorum sensing peptides (QSPs) are bacterial peptides produced by Gram-positive bacteria to communicate with their peers in a cell-density dependent manner. These peptides do not only act as interbacterial communication signals, but can also have effects on the host. Compelling evidence demonstrates the presence of a gut-brain axis and more specifically, the role of the gut microbiota in microglial functioning. The aim of this study is to investigate microglial activating properties of a selected QSP (PapRIV) which is produced by Bacillus cereus species. PapRIV showed in vitro activating properties of BV-2 microglia cells and was able to cross the in vitro Caco-2 cell model and reach the brain. In vivo peptide presence was also demonstrated in mouse plasma. The peptide caused induction of IL-6, TNFα and ROS expression and increased the fraction of ameboid BV-2 microglia cells in an NF-κB dependent manner. Different metabolites were identified in serum, of which the main metabolite still remained active. PapRIV is thus able to cross the gastro-intestinal tract and the blood–brain barrier and shows in vitro activating properties in BV-2 microglia cells, hereby indicating a potential role of this quorum sensing peptide in gut-brain interaction.

scholarly journals Epac increases melanoma cell migration by a heparan sulfate-related mechanism

2009 ◽  
Vol 297 (4) ◽  
pp. C802-C813 ◽  
Author(s):  
Erdene Baljinnyam ◽  
Kousaku Iwatsubo ◽  
Reiko Kurotani ◽  
Xu Wang ◽  
Coskun Ulucan ◽  
...  
Keyword(s):  
Cell Migration ◽  
Heparan Sulfate ◽  
Melanoma Cell ◽  
Translation Rate ◽  
Sulfate Production ◽  
Lung Colonization ◽  
A Cell ◽  
Interfering Rna ◽  
Kinase Pathway

Melanoma, the most malignant form of human skin cancer, has a poor prognosis due to its strong metastatic ability. It was recently demonstrated that Epac, an effector molecule of cAMP, is involved in regulating cell migration; however, the role of Epac in melanoma cell migration remains unclear. We thus examined whether Epac regulates cell migration and metastasis of melanoma. Epac activation, by either specific agonist or overexpression of Epac, increased melanoma cell migration. Deletion of endogenous Epac with small interfering RNA decreased basal melanoma cell migration. These data suggested a major role of Epac in melanoma cell migration. Epac-induced cell migration was mediated by translocation of syndecan-2, a cell-surface heparan sulfate proteoglycan, to lipid rafts. This syndecan-2 translocation was regulated by tubulin polymerization via the Epac/phosphoinositol-3 kinase pathway. Epac-induced cell migration was also regulated by the production of heparan sulfate, a major extracellular matrix. Epac-induced heparan sulfate production was attributable to the increased expression of N-deacetylase/ N-sulfotransferase-1 (NDST-1) accompanied by an increased NDST-1 translation rate. Finally, Epac overexpression enhanced lung colonization of melanoma cells in mice. Taken together, these data indicate that Epac regulates melanoma cell migration/metastasis mostly via syndecan-2 translocation and heparan sulfate production.

Computational investigation for endocytosis of CoVID-19 virus SARS-CoV-2 in cell membrane

2021 ◽  
pp. 095440622110299
Author(s):  
Soumya Mukherjee ◽  
Paritosh Mahata
Keyword(s):  
Cell Membrane ◽  
Virus Particle ◽  
Coupling Model ◽  
Lipid Exchange ◽  
Peripheral Proteins ◽  
A Cell ◽  
Anisotropic Elastic ◽  
Anisotropic Elastic Material ◽  
Infinite Reservoir

CoVID-19 virus SARS-CoV-2 follows the endocytosis process to enter inside a cell to infect it. It is important to study the endocytosis of SARS-CoV-2 in cell membrane to prevent the pandemic of CoVID-19. In this paper we develop a finite element based computational model for endocytosis of SARS-CoV-2 in cell membrane and determine curvature generation on it during the process. The virus SARS-CoV-2 is modeled as a rigid spherical particle and cell membrane as an anisotropic elastic material, while its fluidic nature due to lipid exchange with infinite reservoir is preserved using suitable conditions. With the help of a contact pair created between the virus particle and cell membrane, endocytosis process is computationally studied and the curvature of membrane is evaluated as the time progresses during the endocytosis process. At the tip of the virus particle and half-radius distance from it, the membrane follows the curvature of virus very quickly. However, it takes more time for the membrane point located at a distance equal to the radius of the virus particle. This is compensated by the cytoplasmic peripheral proteins binding onto the inside surface of the cell membrane. The role of cytoplasmic peripheral BAR proteins is investigated by using a linear curvature-coupling model with protein concentrations. It is observed that F-BAR protein is more sensitive to the curvature of virus particle in comparison to the other BAR proteins. The sensitiveness deteriorates as the curvature is increased.

scholarly journals Taraxasterol acetate targets RNF31 to inhibit RNF31/p53 axis-driven cell proliferation in colorectal cancer

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Chao-Tao Tang ◽  
Jing Yang ◽  
Zi-De Liu ◽  
Youxiang Chen ◽  
Chunyan Zeng
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Cell Model ◽  
Tissue Samples ◽  
The Third ◽  
Common Cancer ◽  
A Cell ◽  
Growth Of Tumor

AbstractColorectal cancer (CRC) is the third most common cancer worldwide. Several studies have suggested that taraxasterol acetate (TA) can inhibit the growth of tumor cells. However, to date, it remains unclear how TA inhibits cell growth and how RNF31 functions as an oncogene. We examined the expression of RNF31 in CRC tissue samples via immunohistochemistry and elucidated the function of RNF31 in CRC cells by constructing a cell model with RNF31 depletion. A cycloheximide (CHX)-chase analysis and immunofluorescence assays were conducted to demonstrate that TA can promote RNF31 degradation by activating autophagy. We used the PharmMapper website to predict targets of TA and identified RNF31. CHX-chase experiments showed that TA could facilitate RNF31 degradation, which was inhibited by the administration of chloroquine. Immunofluorescence assays showed that RNF31 protein was colocalized with LC3I/II and p62, suggesting that TA promoted RNF31 degradation by activating autophagy. We also found that CRC patients with RNF31 overexpression had poorer survival than those with low RNF31 expression. The results of the CHX-chase experiment showed that depletion of RNF31 alleviated p53 degradation, which was inhibited by MG132. A series of co-immunoprecipitation (Co-IP) assays revealed that RNF31 interacts with p53 and promotes p53 ubiquitination and degradation. A Co-IP assay performed with a truncated RNF31 plasmid showed that the PUB domain interacts with p53. Moreover, the PUB domain is the key structure in the induction of p53 ubiquitination. Our findings reveal a key role of RNF31 in CRC cell growth and indicate a mechanism through which TA inhibits cell growth.

scholarly journals Mechanisms of the effect of systemic endotoxinemia on development and course of atherosclerosis at cell, systemic and body levels

2018 ◽  
pp. 12-22
Author(s):  
Д. П. Покусаева
Keyword(s):  
Cell Model ◽  
Smooth Muscles ◽  
Developed Countries ◽  
Systemic Circulation ◽  
Population Based ◽  
Cellular Mechanisms ◽  
Atherosclerosis Progression ◽  
A Cell ◽  
Different Strains

Осложнения атеросклероза, такие, как инсульт головного мозга и инфаркт миокарда, занимают ведущее место среди причин смерти в экономически развитых странах. Существует множество гипотез атерогенеза. Анализ научных публикаций позволил проследить эволюцию представлений о патогенезе болезней атеросклеротической природы, индукции атерогенеза, рисков его прогрессирования. Абсолютизация одного из них привела к доминированию холестериновой теории атеросклероза. Появление научных фактов, свидетельствующих об участии вирусов и грамотрицательных бактерий в прогрессировании атеросклероза, позволило рассматривать атерогенез с позиции воспаления (что подтверждено многочисленными исследованиями). Рассмотрены клеточные механизмы, пути активации макрофагов, действие воспалительных цитокинов на гладкомышечные клетки стенки артерии и эндотелиоциты с позиции воспалительной теории атеросклероза. На основании современных публикаций описываются точки приложения и механизмы воздействия эндотоксина при атерогенезе, как уникального липополисахарида, способного индуцировать воспаление. Эндотоксиновая концепция атерогенеза по своей сути является современным этапом развития воспалительной теории атеросклероза. Описаны механизмы его влияния на эндотелиоцит, моноцит и гладкомышечные клетки стенки артерии. Приведены примеры новейших исследований по изучению роли эндотоксина в патологии сердечно-сосудистых заболеваний на клеточной модели с участием подкожной вены человека, на модели животных с различными линиями нокаутных мышей. Приводятся данные исследований с участием человека, включая единственное популяционное исследование Брунек. Рассмотрены возможные пути взаимосвязи липидного обмена и обмена липополисахарида за счет единых механизмов транспорта. Проанализированы трудности изучения роли эндотоксина в патологии, которые связаны с недостаточной информативностью и точностью тест систем. Приводится сравнительная характеристика различных методов анализа концентрации липополисахарида в системном кровотоке и активности антиэндотоксинового иммунитета (АЭИ), такие, как ЛАЛ-тест, микро-ЛАЛ-тест, ЛПС-тест-ИФА, ELISA, тест ЕАА, метод СОИС-ИФА, ЕNA. Complications of atherosclerosis, such as stroke and myocardial infarction, has taken a lead among causes of death in developed countries. Multiple hypotheses of atherogenesis exist. The review of 60 reports enables tracking the evolution of understanding the pathogenesis of atherosclerotic diseases, induction of atherogenesis, and risks for atherosclerosis progression. Absolutization of one of them has resulted in predomination of the cholesteric theory of atherosclerosis. Emergence of evidence for participation of viruses and gram-negative bacteria in progression of atherosclerosis allowed atherogenesis to be considered from the standpoint of inflammation (as confirmed by numerous studies). This review focuses on cellular mechanisms, ways of macrophage activation, effects of inflammatory cytokines on arterial smooth muscle cells and endotheliocytes from a position of the inflammation theory of atherosclerosis. Based on current reports, atherogenic mechanisms of endotoxin effects are described as effects of a unique lipopolysaccharide capable for induction of inflammation. The endotoxin concept of atherogenesis is essentially a current stage of the inflammation theory of atherosclerosis. The author described mechanisms of the endotoxin effect on endotheliocytes, monocytes, and arterial smooth muscles cells. Examples of recent studies demonstrated the role of endotoxin in the pathology of cardiovascular diseases on a cell model with the human saphenous vein and on different strains of knockout mice. Data from human studies are presented, including the only population-based study by Bruneck. Possible interrelations of lipid and lipopolysaccharide metabolism based on single transport mechanisms are described. Difficulties of measuring endotoxin concentration in the systemic circulation are related with insufficient informative value and accuracy of available tests. Characteristics of different tests for measuring the LPS concentration and the activity of antiendotoxin immunity were compared, including the LAL-test, micro-LAL-test, LPS-test-ELISA, EAA test, SOIS-method, and ЕNA.

scholarly journals CYFIP2 containing WAVE complexes inhibit cell migration

2020 ◽  
Author(s):  
Anna Polesskaya ◽  
Arthur Boutillon ◽  
Yanan Wang ◽  
Marc Lavielle ◽  
Sophie Vacher ◽  
...  
Keyword(s):  
Cell Migration ◽  
Mammary Epithelial Cells ◽  
Leading Edge ◽  
Good Prognosis ◽  
Mammary Epithelial ◽  
Breast Cancer Patients ◽  
Loss Of Function ◽  
A Cell ◽  
Wave Complex

ABSTRACTBranched actin networks polymerized by the Arp2/3 complex are critical for cell migration. The WAVE complex is the major Arp2/3 activator at the leading edge of migrating cells. However, multiple distinct WAVE complexes can be assembled in a cell, due to the combinatorial complexity of paralogous subunits. When systematically analyzing the contribution of each WAVE complex subunit to the metastasis-free survival of breast cancer patients, we found that overexpression of the CYFIP2 subunit was surprisingly associated with good prognosis. Gain and loss of function experiments in transformed and untransformed mammary epithelial cells revealed that cell migration was always inversely related to CYFIP2 levels. The role of CYFIP2 was systematically opposite to the role of the paralogous subunit CYFIP1 or of the NCKAP1 subunit. The specific CYFIP2 function in inhibiting cell migration was related to its unique ability to down-regulate classical pro-migratory WAVE complexes. The anti-migratory function of CYFIP2 was also revealed in migration of prechordal plate cells during gastrulation of the zebrafish embryo, indicating that the unique function of CYFIP2 is critically important in both physiological and pathophysiological migrations.

Molecular Mechanisms of EML in AML1/ETO+ AML and Its Targeting Treatments

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 5953-5953
Author(s):  
Fan Yi Meng ◽  
Ling Jiang ◽  
Qingxiu Zhong ◽  
Li Chun Wang ◽  
Guopan Yu ◽  
...  
Keyword(s):  
Cell Migration ◽  
Protein Expression ◽  
Molecular Mechanisms ◽  
Conflicts Of Interest ◽  
Cell Model ◽  
In Vitro Study ◽  
Control Group ◽  
A Cell ◽  
App Gene

Abstract Our previous study has been reported that AML1/ETO positive patients with highly expressed of APP were much easier to extramedullary infiltration, and got poor prognosis£¨followed-up median 35 ( 6-96 ) months, RFS in the high expression APP group was significantly lower than the low expression group £¬40.0% vs 80.0%£¬P = 0.001). In vitro study, we constructed a cell model kasumi-1 which was consistent with AML1/ETO positive and high expressed of APP gene. The cell migration was significantly reduced after interferce of APP expression. This study was designed to investigate the molecule mechanism of extramedullary leukemia (EML) in kasumi-1 cell model and to invent a strategy for treatment in clinic. In this study, we found p-ERK, c-Myc and MMP-2 were significantly decreased after APP expression knockdown in kasumi-1 cell. Meanwhile, we added the inhibitors to block p-ERK and c-Myc expression. The results showed that protein expression of p-ERK and c-Myc was significantly decreased after p-ERK inhibitor performance, which was proportional to the time and concentration. c-Myc and MMP-2 protein expression was significantly reduced after c-Myc inhibitor was used, but p-ERK didn't change (Fig.1B). So, we concluded that APP might regulated the AML cell migration via APP/p-ERK/c-Myc/MMP-2 pathway. Also, we found that kasumi-1 cell was resistant to adriamycin (ADM) and Ara-C, which meant APP may be related with drug resistance. So, we detected cell surviving fraction after ADM and Ara-C performance via MTT assay. The results showed that there was no difference in control group and siAPP group. But, when compared with controls groups, cell surviving fraction in siEZH2 group was significantly decreased after ADM and Ara-C performance respectively. Furthermore, we found protein expression of EZH2 was significantly reduced after LBH589 treatment in cell culture. So, we concluded that LBH589 or SiEZH2 could increase sensitivity of kasumi-1 cell to ADM and Ara-C. In sum, in AML1/ETO positive leukemia cells, we first report that APP gene regulates cell migration via APP/p-ERK/c-Myc/MMP-2 pathway and EZH2 gene induces drug resistantence. Interference or blocking of EZH2 and APP expression may be helpful in treating AML1/ETO positive leukemia. Disclosures No relevant conflicts of interest to declare.

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