scholarly journals Nanocellulose-Based Inks for 3D Bioprinting: Key Aspects in Research Development and Challenging Perspectives in Applications—A Mini Review

2020 ◽  
Vol 7 (2) ◽  
pp. 40 ◽  
Author(s):  
Xiaoju Wang ◽  
Qingbo Wang ◽  
Chunlin Xu

Nanocelluloses have emerged as a catalogue of renewable nanomaterials for bioink formulation in service of 3D bioprinting, thanks to their structural similarity to extracellular matrices and excellent biocompatibility of supporting crucial cellular activities. From a material scientist’s viewpoint, this mini-review presents the key research aspects of the development of the nanocellulose-based bioinks in 3D (bio)printing. The nanomaterial properties of various types of nanocelluloses, including bacterial nanocellulose, cellulose nanofibers, and cellulose nanocrystals, are reviewed with respect to their origins and preparation methods. Different cross-linking strategies to integrate into multicomponent nanocellulose-based bioinks are discussed in terms of regulating ink fidelity in direct ink writing as well as tuning the mechanical stiffness as a bioactive cue in the printed hydrogel construct. Furthermore, the impact of surface charge and functional groups on nanocellulose surface on the crucial cellular activities (e.g., cell survival, attachment, and proliferation) is discussed with the cell–matrix interactions in focus. Aiming at a sustainable and cost-effective alternative for end-users in biomedical and pharmaceutical fields, challenging aspects such as biodegradability and potential nanotoxicity of nanocelluloses call for more fundamental comprehension of the cell–matrix interactions and further validation in in vivo models.

1979 ◽  
Vol 38 (1) ◽  
pp. 267-281
Author(s):  
S.L. Schor ◽  
J. Court

The attachment of cells to collagen has been reported previously to require the presence of serum and the particular serum protein involved in this process, variously known as CIG, CAP or fibronectin, has been isolated. This conclusion that cell attachment to collagen requires serum (or more precisely, fibronectin) is based on experiments measuring the kinetics of cell attachment to films of collagen. We have measured the kinetics of attachment of HeLa and attachment to films of collagen-containing substrata under a variety of experimental conditions and present evidence that the serum-dependent mechanism of cell attachment described by others is actually only the case for films of denatured collagen, while cell attachment to native collagen fibres occurs by a different, serum-independent, mechanism. The possible relevance of these findings to cell-matrix interactions in vivo is discussed.


2000 ◽  
Vol 20 (14) ◽  
pp. 5208-5215 ◽  
Author(s):  
X. Z. Huang ◽  
J. F. Wu ◽  
R. Ferrando ◽  
J. H. Lee ◽  
Y. L. Wang ◽  
...  

ABSTRACT Members of the integrin family of adhesion receptors mediate both cell-cell and cell-matrix interactions and have been shown to play vital roles in embryonic development, wound healing, metastasis, and other biological processes. The integrin α9β1 is a receptor for the extracellular matrix proteins osteopontin and tenacsin C and the cell surface immunoglobulin vascular cell adhesion molecule-1. This receptor is widely expressed in smooth muscle, hepatocytes, and some epithelia. To examine the in vivo function of α9β1, we have generated mice lacking expression of the α9 subunit. Mice homozygous for a null mutation in the α9 subunit gene appear normal at birth but develop respiratory failure and die between 6 and 12 days of age. The respiratory failure is caused by an accumulation of large volumes of pleural fluid which is rich in triglyceride, cholesterol, and lymphocytes. α9 −/− mice also develop edema and lymphocytic infiltration in the chest wall that appears to originate around lymphatics. α9 protein is transiently expressed in the developing thoracic duct at embryonic day 14, but expression is rapidly lost during later stages of development. Our results suggest that the α9 integrin is required for the normal development of the lymphatic system, including the thoracic duct, and that α9 deficiency could be one cause of congenital chylothorax.


1998 ◽  
Vol 143 (4) ◽  
pp. 1113-1128 ◽  
Author(s):  
Shinji Imai ◽  
Marko Kaksonen ◽  
Erkki Raulo ◽  
Tarja Kinnunen ◽  
Carole Fages ◽  
...  

Bone has an enormous capacity for growth, regeneration, and remodeling. This capacity is largely due to induction of osteoblasts that are recruited to the site of bone formation. The recruitment of osteoblasts has not been fully elucidated, though the immediate environment of the cells is likely to play a role via cell– matrix interactions. We show here that heparin-binding growth-associated molecule (HB-GAM), an extracellular matrix–associated protein that enhances migratory responses in neurons, is prominently expressed in the cell matrices that act as target substrates for bone formation. Intriguingly, N-syndecan, which acts as a receptor for HB-GAM, is expressed by osteoblasts/osteoblast precursors, whose ultrastructural phenotypes suggest active cell motility. The hypothesis that HB-GAM/N-syndecan interaction mediates osteoblast recruitment, as inferred from developmental studies, was tested using osteoblast-type cells that express N-syndecan abundantly. These cells migrate rapidly to HB-GAM in a haptotactic transfilter assay and in a migration assay where HB-GAM patterns were created on culture wells. The mechanism of migration is similar to that previously described for the HB-GAM–induced migratory response of neurons. Our hypothesis that HB-GAM/N-syndecan interaction participates in regulation of osteoblast recruitment was tested using two different in vivo models: an adjuvant-induced arthritic model and a transgenic model. In the adjuvant-induced injury model, the expression of HB-GAM and of N-syndecan is strongly upregulated in the periosteum accompanying the regenerative response of bone. In the transgenic model, the HB-GAM expression is maintained in mesenchymal tissues with the highest expression in the periosteum. The HB-GAM transgenic mice develop a phenotype characterized by an increased bone thickness. HB-GAM may thus play an important role in bone formation, probably by mediating recruitment and attachment of osteoblasts/osteoblast precursors to the appropriate substrates for deposition of new bone.


2002 ◽  
Vol 223 (4) ◽  
pp. 497-516 ◽  
Author(s):  
Janine M. Prince ◽  
Teresa C.M. Klinowska ◽  
Emma Marshman ◽  
Emma T. Lowe ◽  
Ulrike Mayer ◽  
...  

2020 ◽  
Author(s):  
Edi Meco ◽  
W. Sharon Zheng ◽  
Anahita H. Sharma ◽  
Kyle J. Lampe

AbstractDemyelinating injuries and diseases, like multiple sclerosis, affect millions of people worldwide. Oligodendrocyte precursor cells (OPCs) have the potential to repair demyelinated tissue because they can both self-renew and differentiate into oligodendrocytes (OLs), the myelin producing cells of the central nervous system (CNS). Cell-matrix interactions impact OPC differentiation into OLs, but the process is not fully understood. Biomaterial hydrogel systems help to elucidate cell-matrix interactions because they can mimic specific properties of native CNS tissue in an in vitro setting. We investigated whether OPC maturation into OLs is influenced by interacting with a urokinase plasminogen activator (uPA) degradable extracellular matrix (ECM). uPA is a proteolytic enzyme that is transiently upregulated in the developing rat brain, with peak uPA expression correlating with an increase in myelin production in vivo. OPC-like cells isolated through the Mosaic Analysis with Double Marker technique (MADM OPCs) produced low molecular weight uPA in culture. MADM OPCs were encapsulated into two otherwise similar elastin-like protein (ELP) hydrogel systems: one that was uPA degradable and one that was non-degradable. Encapsulated MADM OPCs had similar viability, proliferation, and metabolic activity in uPA degradable and non-degradable ELP hydrogels. Expression of OPC maturation-associated genes, however, indicated that uPA degradable ELP hydrogels promoted MADM OPC maturation although not sufficiently for these cells to differentiate into OLs.Graphical Abstract – For table of contents only


Oncogene ◽  
2003 ◽  
Vol 22 (24) ◽  
pp. 3680-3684 ◽  
Author(s):  
Vincenzo M Varallo ◽  
Bing Siang Gan ◽  
Shannon Seney ◽  
Douglas C Ross ◽  
James H Roth ◽  
...  

2014 ◽  
Vol 6 (6) ◽  
pp. 618-626 ◽  
Author(s):  
Jonathan J. Campbell ◽  
Laur-Alexandru Botos ◽  
Timothy J. Sargeant ◽  
Natalia Davidenko ◽  
Ruth E. Cameron ◽  
...  

An in vitro model of mammary gland supporting 3D cell–cell and cell–matrix interactions demonstrates complete in vivo-like neo-tissue formation and remodelling processes (involution) under hormonal control.


Cancers ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2014
Author(s):  
Silvia Pietrobono ◽  
Barbara Stecca

Sialylation is an integral part of cellular function, governing many biological processes including cellular recognition, adhesion, molecular trafficking, signal transduction and endocytosis. Sialylation is controlled by the levels and the activities of sialyltransferases on glycoproteins and lipids. Altered gene expression of these enzymes in cancer yields to cancer-specific alterations of glycoprotein sialylation. Mounting evidence indicate that hypersialylation is closely associated with cancer progression and metastatic spread, and can be of prognostic significance in human cancer. Aberrant sialylation is not only a result of cancer, but also a driver of malignant phenotype, directly impacting key processes such as tumor cell dissociation and invasion, cell-cell and cell-matrix interactions, angiogenesis, resistance to apoptosis, and evasion of immune destruction. In this review we provide insights on the impact of sialylation in tumor progression, and outline the possible application of sialyltransferases as cancer biomarkers. We also summarize the most promising findings on the development of sialyltransferase inhibitors as potential anti-cancer treatments.


2017 ◽  
Vol 14 (127) ◽  
pp. 20160877 ◽  
Author(s):  
X. Cui ◽  
Y. Hartanto ◽  
H. Zhang

Three-dimensional multicellular spheroids (MCSs) have a complex architectural structure, dynamic cell–cell/cell–matrix interactions and bio-mimicking in vivo microenvironment. As a fundamental building block for tissue reconstruction, MCSs have emerged as a powerful tool to narrow down the gap between the in vitro and in vivo model. In this review paper, we discussed the structure and biology of MCSs and detailed fabricating methods. Among these methods, the approach in microfluidics with hydrogel support for MCS formation is promising because it allows essential cell–cell/cell–matrix interactions in a confined space.


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