scholarly journals miR-34/449 control apical actin network formation during multiciliogenesis through small GTPase pathways

2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Benoît Chevalier ◽  
Anna Adamiok ◽  
Olivier Mercey ◽  
Diego R. Revinski ◽  
Laure-Emmanuelle Zaragosi ◽  
...  
Keyword(s):  
Network Formation ◽  
Small Gtpase ◽  
Actin Network

Endothelial k-RasV12 Expression Induces Capillary Deficiency Attributable to Marked Tube Network Expansion Coupled to Reduced Pericytes and Basement Membranes

2021 ◽  
Author(s):  
Zheying Sun ◽  
Scott S. Kemp ◽  
Prisca K. Lin ◽  
Kalia N. Aguera ◽  
George E. Davis
Keyword(s):  
Protein Kinase ◽  
Basement Membrane ◽  
Arteriovenous Malformations ◽  
Network Formation ◽  
Tube Formation ◽  
Small Gtpase ◽  
Basement Membranes ◽  
Formation Mechanisms ◽  
Lumen Formation ◽  
The Impact

Objective: We sought to determine how endothelial cell (EC) expression of the activating k-Ras mutation, k-RasV12, affects their ability to form lumens and tubes and interact with pericytes during capillary assembly Approach and Results: Using defined bioassays where human ECs undergo observable tubulogenesis, sprouting behavior, pericyte recruitment to EC-lined tubes, and pericyte-induced EC basement membrane deposition, we assessed the impact of EC k-RasV12 expression on these critical processes that are necessary for proper capillary network formation. This mutation, which is frequently seen in human ECs within brain arteriovenous malformations, was found to markedly accentuate EC lumen formation mechanisms, with strongly accelerated intracellular vacuole formation, vacuole fusion, and lumen expansion and with reduced sprouting behavior, leading to excessively widened tube networks compared with control ECs. These abnormal tubes demonstrate strong reductions in pericyte recruitment and pericyte-induced EC basement membranes compared with controls, with deficiencies in fibronectin, collagen type IV, and perlecan deposition. Analyses of signaling during tube formation from these k-RasV12 ECs reveals strong enhancement of Src, Pak2 (P21 [RAC1 (Rac family small GTPase 1)] activated kinase 2), b-Raf (v-raf murine sarcoma viral oncogene homolog B1), Erk (extracellular signal–related kinase), and Akt activation and increased expression of PKCε (protein kinase C epsilon), MT1-MMP (membrane-type 1 matrix metalloproteinase), acetylated tubulin and CDCP1 (CUB domain-containing protein 1; most are known EC lumen regulators). Pharmacological blockade of MT1-MMP, Src, Pak, Raf, Mek (mitogen-activated protein kinase) kinases, Cdc42 (cell division cycle 42)/Rac1, and Notch markedly interferes with lumen and tube formation from these ECs. Conclusions: Overall, this novel work demonstrates that EC expression of k-RasV12 disrupts capillary assembly due to markedly excessive lumen formation coupled with strongly reduced pericyte recruitment and basement membrane deposition, which are critical pathogenic features predisposing the vasculature to develop arteriovenous malformations.

F-actin network formation in tethers and in pseudopods stimulated by chemoattractant

1996 ◽  
Vol 35 (4) ◽  
pp. 331-344 ◽  
Author(s):  
Doncho V. Zhelev ◽  
Abdullatif M. Alteraifi ◽  
Robert M. Hochmuth
Keyword(s):  
Network Formation ◽  
Actin Network

Actin Network Formation by Unidirectional Polycation Diffusion

Langmuir ◽  
2007 ◽  
Vol 23 (11) ◽  
pp. 6257-6262 ◽  
Author(s):  
Hyuck Joon Kwon ◽  
Akira Kakugo ◽  
Takehiro Ura ◽  
Takaharu Okajima ◽  
Yoshimi Tanaka ◽  
...  
Keyword(s):  
Network Formation ◽  
Actin Network

scholarly journals Enhanced Dendritic Actin Network Formation in Extended Lamellipodia Drives Proliferation in Growth-Challenged Rac1P29S Melanoma Cells

2019 ◽  
Vol 49 (3) ◽  
pp. 444-460.e9 ◽  
Author(s):  
Ashwathi S. Mohan ◽  
Kevin M. Dean ◽  
Tadamoto Isogai ◽  
Stacy Y. Kasitinon ◽  
Vasanth S. Murali ◽  
...  
Keyword(s):  
Network Formation ◽  
Melanoma Cells ◽  
Actin Network

scholarly journals Mechanisms for Dendritic Actin Network Formation, Distributed Turnover, and Structural Remodeling

2019 ◽  
Vol 116 (3) ◽  
pp. 456a
Author(s):  
Danielle Holz ◽  
Aaron Hall ◽  
Dimitrios Vavylonis
Keyword(s):  
Network Formation ◽  
Actin Network ◽  
Structural Remodeling

scholarly journals Hydraulic resistance induces cell phenotypic transition in confinement

2021 ◽  
Vol 7 (17) ◽  
pp. eabg4934
Author(s):  
Runchen Zhao ◽  
Siqi Cui ◽  
Zhuoxu Ge ◽  
Yuqi Zhang ◽  
Kaustav Bera ◽  
...  
Keyword(s):  
Hydraulic Resistance ◽  
Focal Adhesion ◽  
Actin Filaments ◽  
Fluorescence Recovery After Photobleaching ◽  
Network Formation ◽  
Calcium Oscillations ◽  
Cell Phenotype ◽  
Actin Network ◽  
Mesenchymal Transition ◽  
Phenotypic Transition

Cells penetrating into confinement undergo mesenchymal-to-amoeboid transition. The topographical features of the microenvironment expose cells to different hydraulic resistance levels. How cells respond to hydraulic resistance is unknown. We show that the cell phenotype shifts from amoeboid to mesenchymal upon increasing resistance. By combining automated morphological tracking and wavelet analysis along with fluorescence recovery after photobleaching (FRAP), we found an oscillatory phenotypic transition that cycles from blebbing to short, medium, and long actin network formation, and back to blebbing. Elevated hydraulic resistance promotes focal adhesion maturation and long actin filaments, thereby reducing the period required for amoeboid-to-mesenchymal transition. The period becomes independent of resistance upon blocking the mechanosensor TRPM7. Mathematical modeling links intracellular calcium oscillations with actomyosin turnover and force generation and recapitulates experimental data. We identify hydraulic resistance as a critical physical cue controlling cell phenotype and present an approach for connecting fluorescent signal fluctuations to morphological oscillations.

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