Effect of Substratum Morphology on Animal Cell Adhesion and Behavior

1991 ◽  
Vol 252 ◽  
Author(s):  
Rahul Singhvi ◽  
Gregory N. Stephanopoulos ◽  
Daniel I. C. Wang

ABSTRACTGlass surfaces with well defined surface morphologies have been prepared using photolithography to study the effect of surface morphology on cell adhesion and function. Using a transformed recombinant cell-line, AtT-20, as a model of shear sensitive cell, we have shown that cell-substratum adhesion strength is enhanced using a surface with uniform grooves without any loss in cellular function. Furthermore, using primary hepatocytes as a model for a cell whose function is sensitive to its shape, we have shown that surface morphology can modulate cell shape as well as its function.


1995 ◽  
Vol 17 (3-4) ◽  
pp. 229-244 ◽  
Author(s):  
Suzanne M. Watt ◽  
Steve E. Gschmeissner ◽  
Paul A. Bates


Fluids ◽  
2020 ◽  
Vol 5 (2) ◽  
pp. 60
Author(s):  
Zachary Wagner ◽  
John H. Costello ◽  
Sean P. Colin

The feeding current of scyphomedusae entrains and transports surrounding fluids and prey through trailing tentacles to initiate encounters with prey. After contact, most prey are retained for ingestion. However, the probability that a contact will occur depends on several factors including capture surface morphology, prey size and behavior. We examined how hydrodynamics, capture surface morphology and prey behavior affect the capture probability of copepods. To do this, we documented medusa-copepod interactions of four species of scyphomedusae (two semeostomes and two rhizostomes) possessing different capture surface morphologies. We tracked the movement and behavior of entrained copepods throughout the feeding process to quantify prey behavior effects upon capture efficiency (# captures/# encounters). The feeding currents generated by all the medusan species generated fluid shear deformation rates well above the detection limits of copepods. Despite strong hydrodynamic signals, copepod behavior was highly variable and only 58% of the copepods reacted to entrainment within feeding currents. Furthermore, copepod behavior (categorized as no reaction, escape jump or adjustment jump) did not significantly affect the capture efficiency. The scale and complexity of the feeding current generated by scyphomedusae may help explain the poor ability of copepods to avoid capture.



2019 ◽  
Author(s):  
Julia Obergasteiger ◽  
Giulia Frapporti ◽  
Giulia Lamonaca ◽  
Sara Pizzi ◽  
Anne Picard ◽  
...  

AbstractThe Parkinson’s disease (PD)-associated kinase Leucine-Rich Repeat Kinase 2 (LRRK2) is a potent modulator of autophagy and impacts on lysosome biology and function, but unclarity exists on the precise mechanics of its role and the direction of this modulation. LRRK2 is also involved in the degradation of pathological alpha-synuclein, with pathogenic mutations precipitating neuropathology in cellular and animal models of PD, and most LRRK2 familial cases manifesting with Lewy neuropathology. Defects in autophagic processing and lysosomal degradation of alpha-synuclein have been postulated to underlie its accumulation and onset of neuropathology. Thus, it is critical to reconcile these independent pieces of information to obtain a comprehensive knowledge on LRRK2-associated pathology that could also be generalized to the idiopathic disease.Here, we report a focused investigation on the role of PD-causing G2019S-LRRK2 in the autophagy-lysosome pathway in a recombinant cell line model. Initially, we evaluated the effect of LRRK2 expression on autophagy-related transcriptome. Then, we found that G2019S-LRRK2 leads to accumulation of autophagosomes with no net effect on autophagy induction. This is linked to abnormalities in lysosome morphology and proteolytic activity that are associated with a decrease in the successful formation of autolysosomes. Despite some of these features being shared by WT-LRRK2, alpha-synuclein intracellular inclusions are specifically found in G2019S-LRRK2 cells. Pharmacological kinase inhibition is capable of rescuing defects in the autophagy-lysosome pathway and reducing the number of inclusions. Notably, this effect is prevented by upstream blockade of autophagosome-lysosome fusion events, highlighting this step of the process as critical for alpha-synuclein clearance.



2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Neah Likhite ◽  
Vikas Yadav ◽  
Eric J. Milliman ◽  
Danesh H. Sopariwala ◽  
Sabina Lorca ◽  
...  

ABSTRACT Estrogen-related receptors (ERRs) have emerged as major metabolic regulators in various tissues. However, their expression and function in the vasculature remains unknown. Here, we report the transcriptional program and cellular function of ERRα in endothelial cells (ECs), a cell type with a multifaceted role in vasculature. Of the three ERR subtypes, ECs exclusively express ERRα. Gene expression profiling of ECs lacking ERRα revealed that ERRα predominantly acts as a transcriptional repressor, targeting genes linked with angiogenesis, cell migration, and cell adhesion. ERRα-deficient ECs exhibit decreased proliferation but increased migration and tube formation. ERRα depletion increased basal as well as vascular endothelial growth factor A (VEGFA)- and ANG1/2-stimulated angiogenic sprouting in endothelial spheroids. Moreover, retinal angiogenesis is enhanced in ERRα knockout mice compared to that in wild-type mice. Surprisingly, ERRα is dispensable for the regulation of its classic targets, such as metabolism, mitochondrial biogenesis, and cellular respiration in the ECs. ERRα is enriched at the promoters of angiogenic, migratory, and cell adhesion genes. Further, VEGFA increased ERRα recruitment to angiogenesis-associated genes and simultaneously decreased their expression. Despite increasing its gene occupancy, proangiogenic stimuli decrease ERRα expression in ECs. Our work shows that endothelial ERRα plays a repressive role in angiogenesis and potentially fine-tunes growth factor-mediated angiogenesis.



2003 ◽  
Vol 163 (6) ◽  
pp. 1351-1362 ◽  
Author(s):  
Nibedita Chattopadhyay ◽  
Zemin Wang ◽  
Leonie K. Ashman ◽  
Susann M. Brady-Kalnay ◽  
Jordan A. Kreidberg

The β1 family of integrins has been primarily studied as a set of receptors for the extracellular matrix. In this paper, we define a novel role for α3β1 integrin in association with the tetraspanin CD151 as a component of a cell–cell adhesion complex in epithelial cells that directly stimulates cadherin-mediated adhesion. The integrin–tetraspanin complex affects epithelial cell–cell adhesion at the level of gene expression both by regulating expression of PTPμ and by organizing a multimolecular complex containing PKCβII, RACK1, PTPμ, β-catenin, and E-cadherin. These findings demonstrate how integrin-based signaling can regulate complex biological responses at multiple levels to determine cell morphology and behavior.



Author(s):  
R H Dixon ◽  
P Kidd ◽  
P J Goodhew

Thick relaxed InGaAs layers grown epitaxially on GaAs are potentially useful substrates for growing high indium percentage strained layers. It is important that these relaxed layers are defect free and have a good surface morphology for the subsequent growth of device structures.3μm relaxed layers of InxGa1-xAs were grown on semi - insulating GaAs substrates by Molecular Beam Epitaxy (MBE), where the indium composition ranged from x=0.1 to 1.0. The interface, bulk and surface of the layers have been examined in planar view and cross-section by Transmission Electron Microscopy (TEM). The surface morphologies have been characterised by Scanning Electron Microscopy (SEM), and the bulk lattice perfection of the layers assessed using Double Crystal X-ray Diffraction (DCXRD).The surface morphology has been found to correlate with the growth conditions, with the type of defects grown-in to the layer (e.g. stacking faults, microtwins), and with the nature and density of dislocations in the interface.





2020 ◽  
Vol 16 (34) ◽  
pp. 2853-2861
Author(s):  
Yanli Li ◽  
Rui Yang ◽  
Limo Chen ◽  
Sufang Wu

CD38 is a transmembrane glycoprotein that is widely expressed in a variety of human tissues and cells, especially those in the immune system. CD38 protein was previously considered as a cell activation marker, and today monoclonal antibodies targeting CD38 have witnessed great achievements in multiple myeloma and promoted researchers to conduct research on other tumors. In this review, we provide a wide-ranging review of the biology and function of the human molecule outside the field of myeloma. We focus mainly on current research findings to summarize and update the findings gathered from diverse areas of study. Based on these findings, we attempt to extend the role of CD38 in the context of therapy of solid tumors and expand the role of the molecule from a simple marker to an immunomodulator.



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