Platelet‐rich plasma inhibits osteoblast apoptosis and actin cytoskeleton disruption induced by gingipains through upregulating integrin β1

2020 ◽  
Vol 44 (10) ◽  
pp. 2120-2130 ◽  
Author(s):  
Weiyan Mo ◽  
Juan Wu ◽  
Qihong Qiu ◽  
Fuping Zhang ◽  
Haoyuan Luo ◽  
...  
Keyword(s):  
Actin Cytoskeleton ◽  
Platelet Rich Plasma ◽  
Integrin Β1 ◽  
Osteoblast Apoptosis ◽  
Cytoskeleton Disruption

scholarly journals Farnesylated RhoB Prevents Cell Cycle Arrest and Actin Cytoskeleton Disruption Caused by the Geranylgeranyltransferase I Inhibitor GGTI-298

Cell Cycle ◽  
2002 ◽  
Vol 1 (6) ◽  
pp. 430-437 ◽  
Author(s):  
Cuider Allal ◽  
Anne Pradines ◽  
Andrew D. Hamilton ◽  
Said M. Sebti ◽  
Gilles FAVRE
Keyword(s):  
Cell Cycle ◽  
Actin Cytoskeleton ◽  
Cell Cycle Arrest ◽  
Cycle Arrest ◽  
Geranylgeranyltransferase I ◽  
Cytoskeleton Disruption

scholarly journals Cytochalasin E alters the cytoskeleton and decreases ENaC activity in Xenopus 2F3 cells

2014 ◽  
Vol 307 (1) ◽  
pp. F86-F95 ◽  
Author(s):  
Matthew S. Reifenberger ◽  
Ling Yu ◽  
Hui-Fang Bao ◽  
Billie Jeanne Duke ◽  
Bing-Chen Liu ◽  
...  
Keyword(s):  
Actin Cytoskeleton ◽  
Single Channel ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Open Probability ◽  
Kinase Substrate ◽  
Substrate Complex ◽  
Associated Proteins ◽  
Cytochalasin E ◽  
Cytoskeleton Disruption

Numerous reports have linked cytoskeleton-associated proteins with the regulation of epithelial Na+ channel (ENaC) activity. The purpose of the present study was to determine the effect of actin cytoskeleton disruption by cytochalasin E on ENaC activity in Xenopus 2F3 cells. Here, we show that cytochalasin E treatment for 60 min can disrupt the integrity of the actin cytoskeleton in cultured Xenopus 2F3 cells. We show using single channel patch-clamp experiments and measurements of short-circuit current that ENaC activity, but not its density, is altered by cytochalasin E-induced disruption of the cytoskeleton. In nontreated cells, 8 of 33 patches (24%) had no measurable ENaC activity, whereas in cytochalasin E-treated cells, 17 of 32 patches (53%) had no activity. Analysis of those patches that did contain ENaC activity showed channel open probability significantly decreased from 0.081 ± 0.01 in nontreated cells to 0.043 ± 0.01 in cells treated with cytochalasin E. Transepithelial current from mpkCCD cells treated with cytochalasin E, cytochalasin D, or latrunculin B for 60 min was decreased compared with vehicle-treated cells. The subcellular expression of fodrin changed significantly, and several protein elements of the cytoskeleton decreased at least twofold after 60 min of cytochalasin E treatment. Cytochalasin E treatment disrupted the association between ENaC and myristoylated alanine-rich C-kinase substrate. The results presented here suggest disruption of the actin cytoskeleton by different compounds can attenuate ENaC activity through a mechanism involving changes in the subcellular expression of fodrin, several elements of the cytoskeleton, and destabilization of the ENaC-myristoylated alanine-rich C-kinase substrate complex.

scholarly journals Disruption of the Actin Cytoskeleton Can Complement the Ability of Nef To Enhance Human Immunodeficiency Virus Type 1 Infectivity

2004 ◽  
Vol 78 (11) ◽  
pp. 5745-5755 ◽  
Author(s):  
Edward M. Campbell ◽  
Rafael Nunez ◽  
Thomas J. Hope
Keyword(s):  
Human Immunodeficiency Virus ◽  
Actin Cytoskeleton ◽  
Leukemia Virus ◽  
Actin Network ◽  
Cortical Actin ◽  
Immunodeficiency Virus ◽  
Cytoskeleton Disruption ◽  
Amphotropic Envelope ◽  
Cytoskeleton Rearrangements

ABSTRACT The human immunodeficiency virus (HIV) protein Nef has been shown to increase the infectivity of HIV at an early point during infection. Since Nef is known to interact with proteins involved in actin cytoskeleton rearrangements, we tested the possibility that Nef may enhance HIV infectivity via a mechanism that involves the actin cytoskeleton. We find that disruption of the actin cytoskeleton complements the Nef infectivity defect. The ability of disruption of the actin cytoskeleton to complement the Nef defect was specific to envelopes that fuse at the cell surface, including a variety of HIV envelopes and the murine leukemia virus amphotropic envelope. In contrast, the infectivity of HIV virions pseudotyped to enter cells via endocytosis, which is known to complement the HIV Nef infectivity defect and can naturally penetrate the cortical actin barrier, was not altered by actin cytoskeleton disruption. The results presented here suggest that Nef functions to allow the HIV genome to penetrate the cortical actin network, a known barrier for intracellular parasitic organisms.

Small silica nanoparticles transiently modulate the intestinal permeability by actin cytoskeleton disruption in both Caco-2 and Caco-2/HT29-MTX models

2020 ◽  
Vol 94 (4) ◽  
pp. 1191-1202 ◽  
Author(s):  
Raphaël Cornu ◽  
Claire Chrétien ◽  
Yann Pellequer ◽  
Hélène Martin ◽  
Arnaud Béduneau
Keyword(s):  
Actin Cytoskeleton ◽  
Silica Nanoparticles ◽  
Intestinal Permeability ◽  
Cytoskeleton Disruption

scholarly journals scribble abrogation induces tumor growth through JNK-Wnt pathways depending on cellular-microenvironment in Drosophila wing imaginal tissue

2019 ◽  
Author(s):  
Amarish Kumar Yadav ◽  
Roshan Fatima ◽  
Saripella Srikrishna
Keyword(s):  
Tumor Growth ◽  
Actin Cytoskeleton ◽  
Tumor Progression ◽  
Cell Polarity ◽  
Cancer Progression ◽  
Wing Disc ◽  
Cellular Microenvironment ◽  
Large Area ◽  
Wnt Pathways ◽  
Cytoskeleton Disruption

Abstractscribble (scrib) is a cell-polarity determinant in Drosophila and human. Cell polarity plays a crucial role in the maintenance of tissue homeostasis and its disruption leads to neoplastic cancer progression. However, the underlying mechanisms by which loss of cell-polarity regulators drives cancer progression are poorly known. In this study, we have explored the tumor progression mechanisms upon scrib knockdown in Drosophila wing imaginal disc using UASRNAi-GAL4 approach. We have found that scrib knockdown in wing disc leads to tumor growth with disrupted actin cytoskeleton, loss of cell-polarity and elevated JNK signalling, resulting in absolute early pupal lethality. Further, scrib abrogated cells in a large area of the disc are capable of invading the surrounding wild type cells and inducing apoptosis along with compensatory proliferation through JNK-Wnt pathways. Moreover, JNK pathway upstream candidate hep (JNKK) knockdown in scrib abrogated cells rescues the cell polarity defects, actin cytoskeleton disruption and tumor growth, while constitutive hep activation further aggravates the tumor phenotype. Interestingly, generation of undead cells by apoptosis inhibition in these hep knockdown cells by p35 expression further leads to tumor development. Hence, we conclude that scrib knockdown in a large area of wing disc might have a ‘group-protection’ and ‘undead-cells’ microenvironment that modulates the action of JNK signalling resulting in tumor formation. Furthermore, JNK dependent activation of Wnt/Ca2+ signalling also supports the tumor growth and actin cytoskeleton disruption. Thus, our results importantly highlight the role of JNK signalling in tumor progression upon scrib loss of function depending on cellular-microenvironment.

scholarly journals Perturbation of actin dynamics induces NF-κB activation in myelomonocytic cells through an NADPH oxidase-dependent pathway

2005 ◽  
Vol 387 (2) ◽  
pp. 531-540 ◽  
Author(s):  
Gaelle KUSTERMANS ◽  
Jamel EL BENNA ◽  
Jacques PIETTE ◽  
Sylvie LEGRAND-POELS
Keyword(s):  
Nadph Oxidase ◽  
Actin Cytoskeleton ◽  
Nuclear Factor Κb ◽  
Cytochalasin D ◽  
Actin Dynamics ◽  
Cellular Attachment ◽  
Cyclic Shifts ◽  
Myelomonocytic Cells ◽  
Cytoskeleton Disruption ◽  
Dependent Pathway

Although several reports showed the effect of compounds disrupting microtubules on NF-κB (nuclear factor κB) activation, nothing is known about agents perturbing actin dynamics. In the present study, we have shown that actin cytoskeleton disruption induced by actin-depolymerizing agents such as cytochalasin D and latrunculin B and actin-polymerizing compounds such as jasplakinolide induced NF-κB activation in myelomonocytic cells. The transduction pathway involved the IκB (inhibitory κB) kinase complex and a degradation of IκBα. We have shown that NF-κB activation in response to the perturbation of actin dynamics required reactive oxygen species, as demonstrated by the effect of antioxidants. Actin cytoskeleton disruption by cytochalasin D induced O2− release from human monocytes, through the activation of the NADPH oxidase, as confirmed by the phosphorylation and by the membrane translocation of p47phox. NF-κB activation after actin cytoskeleton disruption could be physiologically relevant during monocyte activation and/or recruitment into injured tissues, where cellular attachment, migration and phagocytosis result in cyclic shifts in cytoskeletal organization and disorganization.

Effect of actin cytoskeleton disruption on electric pulse-induced apoptosis and electroporation in tumour cells

2011 ◽  
Vol 35 (2) ◽  
pp. 99-104 ◽  
Author(s):  
Deyou Xiao ◽  
Liling Tang ◽  
Chao Zeng ◽  
Jianfei Wang ◽  
Xiao Luo ◽  
...  
Keyword(s):  
Actin Cytoskeleton ◽  
Electric Pulse ◽  
Tumour Cells ◽  
Cytoskeleton Disruption ◽  
Induced Apoptosis

Effects of Actin Cytoskeleton Disruption on Electroporation In Vitro

2020 ◽  
Vol 191 (4) ◽  
pp. 1545-1561 ◽  
Author(s):  
Hong Bae Kim ◽  
Seho Lee ◽  
Jong Hoon Chung ◽  
Seong Nam Kim ◽  
Chang Kyu Sung ◽  
...  
Keyword(s):  
Actin Cytoskeleton ◽  
Cytoskeleton Disruption
Sign in / Sign up

Export Citation Format

Share Document