scholarly journals Protocadherin-19 and N-cadherin interact to control cell movements during anterior neurulation

2010 ◽  
Vol 191 (5) ◽  
pp. 1029-1041 ◽  
Author(s):  
Sayantanee Biswas ◽  
Michelle R. Emond ◽  
James D. Jontes
Keyword(s):  
Cell Adhesion ◽  
Control Cell ◽  
Time Lapse ◽  
Image Sequences ◽  
Cell Movements ◽  
Calcium Dependent ◽  
Two Photon ◽  
Cadherin Superfamily

The protocadherins comprise the largest subgroup within the cadherin superfamily, yet their cellular and developmental functions are not well understood. In this study, we demonstrate that pcdh19 (protocadherin 19) acts synergistically with n-cadherin (ncad) during anterior neurulation in zebrafish. In addition, Pcdh19 and Ncad interact directly, forming a protein–protein complex both in vitro and in vivo. Although both molecules are required for calcium-dependent adhesion in a zebrafish cell line, the extracellular domain of Pcdh19 does not exhibit adhesive activity, suggesting that the involvement of Pcdh19 in cell adhesion is indirect. Quantitative analysis of in vivo two-photon time-lapse image sequences reveals that loss of either pcdh19 or ncad impairs cell movements during neurulation, disrupting both the directedness of cell movements and the coherence of movements among neighboring cells. Our results suggest that Pcdh19 and Ncad function together to regulate cell adhesion and to mediate morphogenetic movements during brain development.

scholarly journals DSCAM promotes self-avoidance in the developing mouse retina by masking the functions of cadherin superfamily members

2018 ◽  
Vol 115 (43) ◽  
pp. E10216-E10224 ◽  
Author(s):  
Andrew M. Garrett ◽  
Andre Khalil ◽  
David O. Walton ◽  
Robert W. Burgess
Keyword(s):  
Cell Adhesion ◽  
Neural Development ◽  
Individual Cell ◽  
Cell Types ◽  
Mouse Retina ◽  
Cell Level ◽  
The Individual ◽  
Cadherin Superfamily

During neural development, self-avoidance ensures that a neuron’s processes arborize to evenly fill a particular spatial domain. At the individual cell level, self-avoidance is promoted by genes encoding cell-surface molecules capable of generating thousands of diverse isoforms, such as Dscam1 (Down syndrome cell adhesion molecule 1) in Drosophila. Isoform choice differs between neighboring cells, allowing neurons to distinguish “self” from “nonself”. In the mouse retina, Dscam promotes self-avoidance at the level of cell types, but without extreme isoform diversity. Therefore, we hypothesize that DSCAM is a general self-avoidance cue that “masks” other cell type-specific adhesion systems to prevent overly exuberant adhesion. Here, we provide in vivo and in vitro evidence that DSCAM masks the functions of members of the cadherin superfamily, supporting this hypothesis. Thus, unlike the isoform-rich molecules tasked with self-avoidance at the individual cell level, here the diversity resides on the adhesive side, positioning DSCAM as a generalized modulator of cell adhesion during neural development.

scholarly journals Recent advance in surface modification for regulating cell adhesion and behaviors

2020 ◽  
Vol 9 (1) ◽  
pp. 971-989
Author(s):  
Shuxiang Cai ◽  
Chuanxiang Wu ◽  
Wenguang Yang ◽  
Wenfeng Liang ◽  
Haibo Yu ◽  
...  
Keyword(s):  
Tissue Engineering ◽  
Cell Adhesion ◽  
Control Cell ◽  
Biochemical Properties ◽  
Cell Behavior ◽  
Factors Affecting ◽  
Artificial Surfaces ◽  
The Matrix

AbstractCell adhesion is a basic requirement for anchorage-dependent cells to survive on the matrix. It is the first step in a series of cell activities, such as cell diffusion, migration, proliferation, and differentiation. In vivo, cells are surrounded by extracellular matrix (ECM), whose physical and biochemical properties and micromorphology may affect and regulate the function and behavior of cells, causing cell reactions. Cell adhesion is also the basis of communication between cells and the external environment and plays an important role in tissue development. Therefore, the significance of studying cell adhesion in vitro has become increasingly prominent. For instance, in the field of tissue engineering and regenerative medicine, researchers have used artificial surfaces of different materials to simulate the properties of natural ECM, aiming to regulate the behavior of cell adhesion. Understanding the factors that affect cell behavior and how to control cell behavior, including cell adhesion, orientation, migration, and differentiation on artificial surfaces, is essential for materials and life sciences, such as advanced biomedical engineering and tissue engineering. This article reviews various factors affecting cell adhesion as well as the methods and materials often used in investigating cell adhesion.

scholarly journals Oxysterols and EBI2 promote osteoclast precursor migration to bone surfaces and regulate bone mass homeostasis

2015 ◽  
Vol 212 (11) ◽  
pp. 1931-1946 ◽  
Author(s):  
Erin Nevius ◽  
Flavia Pinho ◽  
Meera Dhodapkar ◽  
Huiyan Jin ◽  
Kristina Nadrah ◽  
...  
Keyword(s):  
Bone Mass ◽  
Therapeutic Potential ◽  
Time Lapse ◽  
Two Photon Microscopy ◽  
Two Photon ◽  
Time Lapse Microscopy ◽  
Necessary And Sufficient ◽  
Gαi Protein

Bone surfaces attract hematopoietic and nonhematopoietic cells, such as osteoclasts (OCs) and osteoblasts (OBs), and are targeted by bone metastatic cancers. However, the mechanisms guiding cells toward bone surfaces are essentially unknown. Here, we show that the Gαi protein–coupled receptor (GPCR) EBI2 is expressed in mouse monocyte/OC precursors (OCPs) and its oxysterol ligand 7α,25-dihydroxycholesterol (7α,25-OHC) is secreted abundantly by OBs. Using in vitro time-lapse microscopy and intravital two-photon microscopy, we show that EBI2 enhances the development of large OCs by promoting OCP motility, thus facilitating cell–cell interactions and fusion in vitro and in vivo. EBI2 is also necessary and sufficient for guiding OCPs toward bone surfaces. Interestingly, OCPs also secrete 7α,25-OHC, which promotes autocrine EBI2 signaling and reduces OCP migration toward bone surfaces in vivo. Defective EBI2 signaling led to increased bone mass in male mice and protected female mice from age- and estrogen deficiency–induced osteoporosis. This study identifies a novel pathway involved in OCP homing to the bone surface that may have significant therapeutic potential.

Evidence for endogenous proteases, mRNA level and insulin as multiple mechanisms of N-cadherin down-regulation during retinal development

Development ◽  
1992 ◽  
Vol 114 (4) ◽  
pp. 973-984 ◽  
Author(s):  
E.F. Roark ◽  
N.E. Paradies ◽  
L.A. Lagunowich ◽  
G.B. Grunwald
Keyword(s):  
Cell Adhesion ◽  
Organ Culture ◽  
Retinal Development ◽  
Mrna Level ◽  
Down Regulation ◽  
Regulation Of Expression ◽  
Calcium Dependent ◽  
Endogenous Proteases

Our previous studies of the role of cell adhesion in retinal development have focused on the expression and function of N-cadherin, the predominant calcium-dependent intercellular adhesion protein of neural tissues. During the course of retinal development, N-cadherin expression undergoes significant qualitative and quantitative changes in its pattern of expression, most prominently a sharp down-regulation of expression throughout most of the retina. The present studies were directed at investigating the epigenetic mechanisms that could mediate this loss of N-cadherin from the retina. Using an in vitro intact retinal organ culture system, results were obtained which suggest that insulin enhances the down-regulation of N-cadherin expression in a protein-synthesis-dependent fashion. Furthermore, the metalloprotease inhibitor 1,10-phenanthroline inhibits the loss of N-cadherin from the retina. While N-cadherin is down-regulated in organ culture, other cell adhesion molecules, which are not down-regulated in vivo, are also not down-regulated in organ culture. The defined organ culture medium conditioned by the retina accumulates both a soluble 90 × 10(3) M(r) N-terminal fragment of N-cadherin as well as a number of secreted proteases. Both of these components are also shown to be present in vivo in the vitreous humor. Northern blot analysis indicates a single mRNA encoding N-cadherin in the retina and no evidence for a second message that could encode the 90 × 10(3) M(r) fragment. However, the amount of N-cadherin mRNA detectable on northern blots decreases during development. The results reported here suggest that the down-regulation of N-cadherin that occurs during retinal development is possibly mediated by multiple mechanisms, which include turnover at the cell surface mediated by endogenous proteolysis, reduced levels of N-cadherin mRNA and modulation by growth factors.

Measurement of Cell Adhesion and Migration on Protein-Coated Surfaces

1991 ◽  
Vol 252 ◽  
Author(s):  
Paul A. DiMilla ◽  
Julie A. Stone ◽  
Steven M. Albelda ◽  
Douglas A. Lauffenburger ◽  
John A. Quinn
Keyword(s):  
Cell Adhesion ◽  
Critical Shear Stress ◽  
Cell Movement ◽  
Time Lapse ◽  
Tissue Cell ◽  
Cell Adhesion And Migration ◽  
And Migration ◽  
Coated Surfaces

ABSTRACTThe performance of biomaterials forin vivoandin vitroapplications can depend critically on tissue cell adhesion and migration. We have been investigating the role that specific reversible interactions between cell adhesion receptors and complementary substratum-bound ligands play in the regulation of cell adhesion and migration. With an axisymmetric radial flow detachment assay (RFDA) [1] we measured cell-substratum adhesive strength for human smooth muscle cells (HSMCs) on surfaces coated with type IV collagen (CIV). We found that the critical shear stress for detachment increased linearly with increasing CIV coating concentration. Using time-lapse videomicroscopy and image analysis we tracked the movement of individual HSMCs over similar CIV-coated surfaces. Cell speed and persistence were determined for variations in CIV coating concentration by applying a persistent random walk model for individual cell movement. Cell speed reached a maximum at an intermediate concentration of CIV, supporting the hypothesis that an optimal cell-substratum adhesiveness exists for HSMC movement. This combination of techniques for measuring adhesion and motility provides a valuable tool to examine the role of cell-biomaterial interactions on cell behavior.

Ultrastructure of melanocyte-keratinocyte interactions and pigment transfer in vitro

1978 ◽  
Vol 36 (2) ◽  
pp. 650-651
Author(s):  
Raul I. Garcia ◽  
Evelyn A. Flynn ◽  
George Szabo
Keyword(s):  
Direct Injection ◽  
Skin Pigmentation ◽  
Freeze Fracture ◽  
Pigment Granule ◽  
Time Lapse ◽  
Ultrastructural Level ◽  
Lanthanum Tracer ◽  
A Cell

Skin pigmentation in mammals involves the interaction of epidermal melanocytes and keratinocytes in the structural and functional unit known as the Epidermal Melanin Unit. Melanocytes(M) synthesize melanin within specialized membrane-bound organelles, the melanosome or pigment granule. These are subsequently transferred by way of M dendrites to keratinocytes(K) by a mechanism still to be clearly defined. Three different, though not necessarily mutually exclusive, mechanisms of melanosome transfer have been proposed: cytophagocytosis by K of M dendrite tips containing melanosomes, direct injection of melanosomes into the K cytoplasm through a cell-to-cell pore or communicating channel formed by localized fusion of M and K cell membranes, release of melanosomes into the extracellular space(ECS) by exocytosis followed by K uptake using conventional phagocytosis. Variability in methods of transfer has been noted both in vivo and in vitro and there is evidence in support of each transfer mechanism. We Have previously studied M-K interactions in vitro using time-lapse cinemicrography and in vivo at the ultrastructural level using lanthanum tracer and freeze-fracture.

iTSP-PseAAC: Identify Tumor Suppressor Proteins by Using Fully Connected Neural Network and PseAAC

2021 ◽  
Vol 15 ◽  
Author(s):  
Muhammad Awais ◽  
Waqar Hussain ◽  
Nouman Rasool ◽  
Yaser Daanial Khan
Keyword(s):  
Tumor Suppressor ◽  
Cross Validation ◽  
Control Cell ◽  
Normal Function ◽  
In Vivo Studies ◽  
Tumor Suppressor Proteins ◽  
Proposed Model ◽  
Self Consistency

Background: The uncontrolled growth due to accumulation of genetic and epigenetic changes as a result of loss or reduction in the normal function of Tumor Suppressor Genes (TSGs) and Pro-oncogenes is known as cancer. TSGs control cell division and growth by repairing of DNA mistakes during replication and restrict the unwanted proliferation of a cell or activities, those are the part of tumor production. Objectives: This study aims to propose a novel, accurate, user-friendly model to predict tumor suppressor proteins, which would be freely available to experimental molecular biologists to assist them using in vitro and in vivo studies. Methods: The predictor model has used the input feature vector (IFV) calculated from the physicochemical properties of proteins based on FCNN to compute the accuracy, sensitivity, specificity, and MCC. The proposed model was validated against different exhaustive validation techniques i.e. self-consistency and cross-validation. Results: Using self-consistency, the accuracy is 99%, for cross-validation and independent testing has 99.80% and 100% accuracy respectively. The overall accuracy of the proposed model is 99%, sensitivity value 98% and specificity 99% and F1-score was 0.99. Conclusion: It concludes, the proposed model for prediction of the tumor suppressor proteins can predict the tumor suppressor proteins efficiently, but it still has space for improvements in computational ways as the protein sequences may rapidly increase, day by day.

scholarly journals Eap1p, an Adhesin That Mediates Candida albicans Biofilm Formation In Vitro and In Vivo

2007 ◽  
Vol 6 (6) ◽  
pp. 931-939 ◽  
Author(s):  
Fang Li ◽  
Michael J. Svarovsky ◽  
Amy J. Karlsson ◽  
Joel P. Wagner ◽  
Karen Marchillo ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Cell Adhesion ◽  
Biofilm Formation ◽  
Fungal Infections ◽  
Gene Dosage ◽  
Venous Catheter ◽  
Flow Chamber ◽  
Dependent Manner

ABSTRACT Candida albicans is the leading cause of systemic fungal infections in immunocompromised humans. The ability to form biofilms on surfaces in the host or on implanted medical devices enhances C. albicans virulence, leading to antimicrobial resistance and providing a reservoir for infection. Biofilm formation is a complex multicellular process consisting of cell adhesion, cell growth, morphogenic switching between yeast form and filamentous states, and quorum sensing. Here we describe the role of the C. albicans EAP1 gene, which encodes a glycosylphosphatidylinositol-anchored, glucan-cross-linked cell wall protein, in adhesion and biofilm formation in vitro and in vivo. Deleting EAP1 reduced cell adhesion to polystyrene and epithelial cells in a gene dosage-dependent manner. Furthermore, EAP1 expression was required for C. albicans biofilm formation in an in vitro parallel plate flow chamber model and in an in vivo rat central venous catheter model. EAP1 expression was upregulated in biofilm-associated cells in vitro and in vivo. Our results illustrate an association between Eap1p-mediated adhesion and biofilm formation in vitro and in vivo.

scholarly journals Persistence of intramyocardially transplanted murine induced pluripotent stem cell-derived cardiomyocytes from different developmental stages

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Gabriel Peinkofer ◽  
Martina Maass ◽  
Kurt Pfannkuche ◽  
Agapios Sachinidis ◽  
Stephan Baldus ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Stem Cell ◽  
Cell Adhesion ◽  
Developmental Stage ◽  
Pluripotent Stem Cell ◽  
Induced Pluripotent Stem Cell ◽  
Induced Pluripotent

Abstract Background Induced pluripotent stem cell-derived cardiomyocytes (iPSC-CM) are regarded as promising cell type for cardiac cell replacement therapy, but it is not known whether the developmental stage influences their persistence and functional integration in the host tissue, which are crucial for a long-term therapeutic benefit. To investigate this, we first tested the cell adhesion capability of murine iPSC-CM in vitro at three different time points during the differentiation process and then examined cell persistence and quality of electrical integration in the infarcted myocardium in vivo. Methods To test cell adhesion capabilities in vitro, iPSC-CM were seeded on fibronectin-coated cell culture dishes and decellularized ventricular extracellular matrix (ECM) scaffolds. After fixed periods of time, stably attached cells were quantified. For in vivo experiments, murine iPSC-CM expressing enhanced green fluorescent protein was injected into infarcted hearts of adult mice. After 6–7 days, viable ventricular tissue slices were prepared to enable action potential (AP) recordings in transplanted iPSC-CM and surrounding host cardiomyocytes. Afterwards, slices were lysed, and genomic DNA was prepared, which was then used for quantitative real-time PCR to evaluate grafted iPSC-CM count. Results The in vitro results indicated differences in cell adhesion capabilities between day 14, day 16, and day 18 iPSC-CM with day 14 iPSC-CM showing the largest number of attached cells on ECM scaffolds. After intramyocardial injection, day 14 iPSC-CM showed a significant higher cell count compared to day 16 iPSC-CM. AP measurements revealed no significant difference in the quality of electrical integration and only minor differences in AP properties between d14 and d16 iPSC-CM. Conclusion The results of the present study demonstrate that the developmental stage at the time of transplantation is crucial for the persistence of transplanted iPSC-CM. iPSC-CM at day 14 of differentiation showed the highest persistence after transplantation in vivo, which may be explained by a higher capability to adhere to the extracellular matrix.

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