scholarly journals A primer on regeneration

2015 ◽  
Author(s):  
Labib Rouhana ◽  
Junichi Tasaki
Keyword(s):  
Cell Activation ◽  
Single Cells ◽  
Leading Edge ◽  
Significant Heterogeneity ◽  
Diverse Range ◽  
Differentiated Cells ◽  
Ability To Regenerate ◽  
Cellular Source ◽  
And Migration ◽  
And Function

Centuries of observation have uncovered a diverse range of organisms capable of overcoming loss of tissue. The act of restoring lost anatomy and function is known as regeneration, and it is broadly represented in both plant and animal kingdoms. Cumulative studies have identified a series of events that take place during regeneration of complex animal structures. First, the organism recognizes damage and undergoes wound healing. Then, programmed cell death in the vicinity of the damaged tissue precedes proliferation and migration of cells that foster the development of replacement tissue. Finally, rearrangement of pre-existing tissue and integration with newly differentiated cells take place to restore the function and proportionality displayed previous to damage . Although the ability to regenerate is believed to be ancestrally common and lost throughout evolution, there is significant heterogeneity of some basic mechanisms displayed during regeneration in different animal species. Perhaps one of the most noticeable differences is the cellular source contributing to formation of the new tissue during regeneration. Organisms such as planarians and Hydra rely on active reservoirs of somatic pluripotent stem cells abundantly distributed throughout their bodies and maintained throughout their life. On the other hand, vertebrates rely mostly on progenitor cell activation and dedifferentiation, to regenerate cells with limited potential to regenerate specific structures. However, not all regenerative events rely on cellular replacement. Leading edge research has begun to uncover mechanisms involved in autonomous repair and functional regeneration of single cells – be it neurons or ciliated protozoa. The fact that organisms can achieve regeneration through diverse cellular sources is remarkable, but just as remarkable is the possibility that conserved molecular pathways could be activated to achieve regeneration in different species. Analysis of these pathways will contribute to understanding human development and potential avenues for regenerative medicine.

scholarly journals A primer on regeneration

2015 ◽  
Author(s):  
Labib Rouhana ◽  
Junichi Tasaki
Keyword(s):  
Cell Activation ◽  
Single Cells ◽  
Leading Edge ◽  
Significant Heterogeneity ◽  
Diverse Range ◽  
Differentiated Cells ◽  
Ability To Regenerate ◽  
Cellular Source ◽  
And Migration ◽  
And Function

Centuries of observation have uncovered a diverse range of organisms capable of overcoming loss of tissue. The act of restoring lost anatomy and function is known as regeneration, and it is broadly represented in both plant and animal kingdoms. Cumulative studies have identified a series of events that take place during regeneration of complex animal structures. First, the organism recognizes damage and undergoes wound healing. Then, programmed cell death in the vicinity of the damaged tissue precedes proliferation and migration of cells that foster the development of replacement tissue. Finally, rearrangement of pre-existing tissue and integration with newly differentiated cells take place to restore the function and proportionality displayed previous to damage . Although the ability to regenerate is believed to be ancestrally common and lost throughout evolution, there is significant heterogeneity of some basic mechanisms displayed during regeneration in different animal species. Perhaps one of the most noticeable differences is the cellular source contributing to formation of the new tissue during regeneration. Organisms such as planarians and Hydra rely on active reservoirs of somatic pluripotent stem cells abundantly distributed throughout their bodies and maintained throughout their life. On the other hand, vertebrates rely mostly on progenitor cell activation and dedifferentiation, to regenerate cells with limited potential to regenerate specific structures. However, not all regenerative events rely on cellular replacement. Leading edge research has begun to uncover mechanisms involved in autonomous repair and functional regeneration of single cells – be it neurons or ciliated protozoa. The fact that organisms can achieve regeneration through diverse cellular sources is remarkable, but just as remarkable is the possibility that conserved molecular pathways could be activated to achieve regeneration in different species. Analysis of these pathways will contribute to understanding human development and potential avenues for regenerative medicine.

scholarly journals Epigenetics and Shared Molecular Processes in the Regeneration of Complex Structures

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Labib Rouhana ◽  
Junichi Tasaki
Keyword(s):  
Progenitor Cells ◽  
Structural Damage ◽  
Complex Structures ◽  
Molecular Processes ◽  
Differentiated Cells ◽  
Cellular Events ◽  
Ability To Regenerate ◽  
Cellular Source ◽  
And Function ◽  
Regeneration Blastema

The ability to regenerate complex structures is broadly represented in both plant and animal kingdoms. Although regenerative abilities vary significantly amongst metazoans, cumulative studies have identified cellular events that are broadly observed during regenerative events. For example, structural damage is recognized and wound healing initiated upon injury, which is followed by programmed cell death in the vicinity of damaged tissue and a burst in proliferation of progenitor cells. Sustained proliferation and localization of progenitor cells to site of injury give rise to an assembly of differentiating cells known as the regeneration blastema, which fosters the development of new tissue. Finally, preexisting tissue rearranges and integrates with newly differentiated cells to restore proportionality and function. While heterogeneity exists in the basic processes displayed during regenerative events in different species—most notably the cellular source contributing to formation of new tissue—activation of conserved molecular pathways is imperative for proper regulation of cells during regeneration. Perhaps the most fundamental of such molecular processes entails chromatin rearrangements, which prime large changes in gene expression required for differentiation and/or dedifferentiation of progenitor cells. This review provides an overview of known contributions to regenerative processes by noncoding RNAs and chromatin-modifying enzymes involved in epigenetic regulation.

scholarly journals AIF-1 expression regulates endothelial cell activation, signal transduction, and vasculogenesis

2009 ◽  
Vol 296 (2) ◽  
pp. C256-C266 ◽  
Author(s):  
Ying Tian ◽  
Surbhi Jain ◽  
Sheri E. Kelemen ◽  
Michael V. Autieri
Keyword(s):  
Signal Transduction ◽  
Endothelial Cell ◽  
Calcium Binding ◽  
Cell Activation ◽  
Strong Association ◽  
Mitogen Activated Protein Kinase ◽  
Inflammatory Factor ◽  
And Migration ◽  
And Function ◽  
Proliferation And Migration

Endothelial cell (EC) activation plays a key role in vascular inflammation, thrombosis, and angiogenesis. Allograft inflammatory factor-1 (AIF-1) is a cytoplasmic, calcium-binding, inflammation-responsive scaffold protein that has been implicated in the regulation of inflammation. The expression and function of AIF-1 in EC is uncharacterized, and the purpose of this study was to characterize AIF-1 expression and function in ECs. AIF-1 expression colocalized with CD31-positive ECs in neointima of inflamed human arteries but not normal arteries. AIF-1 is detected at low levels in unstimulated EC, but expression can be increased in response to serum and soluble factors. Stable transfection of AIF-1 small interfering RNA (siRNA) in ECs reduced AIF-1 protein expression by 73% and significantly reduced EC proliferation and migration ( P < 0.05 and 0.001). Rescue of AIF-1 expression restored both proliferation and migration of siRNA-expressing ECs, and AIF-1 overexpression enhanced both of these activities, suggesting a strong association between AIF-1 expression and EC activation. Activation of mitogen-activated protein kinase p44/42 and PAK1 was significantly reduced in siRNA ECs challenged with inflammatory stimuli. Reduction of AIF-1 expression did not decrease EC tube-like structure or microvessel formation from aortic rings, but overexpression of AIF-1 did significantly increase the number and complexity of these structures. These data indicate that AIF-1 expression plays an important role in signal transduction and activation of ECs and may also participate in new vessel formation.

L-selectin stimulation enhances functional expression of surface CXCR4 in lymphocytes: implications for cellular activation during adhesion and migration

Blood ◽  
2003 ◽  
Vol 101 (11) ◽  
pp. 4245-4252 ◽  
Author(s):  
Ziqiang Ding ◽  
Thomas B. Issekutz ◽  
Gregory P. Downey ◽  
Thomas K. Waddell
Keyword(s):  
Actin Polymerization ◽  
Cell Activation ◽  
Kinase Inhibitors ◽  
Leukocyte Adhesion ◽  
Cxcr4 Expression ◽  
Receptor Expression ◽  
Leukocyte Activation ◽  
Β2 Integrin ◽  
And Migration ◽  
And Function

Abstract L-selectin mediates leukocyte tethering and rolling, the first step in a sequential process of leukocyte adhesion and migration. Additionally, L-selectin has important signaling roles perhaps contributing to leukocyte activation and integrin-mediated adhesion. Because chemokines are critically involved in leukocyte activation, we questioned whether L-selectin signaling affects chemokine receptor expression and function. We observed that whereas only 5% to 15% of freshly isolated lymphocytes expressed CXCR4 on the cell surface, intracellular CXCR4 was detectable in all cells. Engagement of L-selectin by antibody cross-linking or the L-selectin ligands fucoidan or sulfatide mobilized intracellular CXCR4 to significantly increase surface CXCR4 expression but did not affect CCR5, CCR7, or β2-integrin expression. L-selectin stimulation also inhibited stromal-derived factor 1 (SDF-1)–induced CXCR4 internalization. The combined effects of L-selectin on CXCR4 trafficking are likely important in markedly enhancing cell activation by SDF-1. Blockade of SDF-1–induced CXCR4 internalization resulted in enhanced actin polymerization on subsequent exposure to SDF-1. Physiologically more important, L-selectin stimulation increased SDF-1–induced lymphocyte adhesion and transendothelial migration, which were inhibited by anti–leukocyte function-associated antigen 1 antibodies, tyrosine kinase inhibitors, and pertussis toxin. To further corroborate the additive stimulating effects, L-selectin signaling and SDF-1 increased β2-integrin activation. Taken together, L-selectin–mediated signals specifically enhance CXCR4 expression and function, suggesting a novel mechanism for the modulation of lymphocyte activation during cell adhesion and transmigration.

CD38 as an immunomodulator in cancer

2020 ◽  
Vol 16 (34) ◽  
pp. 2853-2861
Author(s):  
Yanli Li ◽  
Rui Yang ◽  
Limo Chen ◽  
Sufang Wu
Keyword(s):  
Multiple Myeloma ◽  
Cell Activation ◽  
Human Tissues ◽  
Transmembrane Glycoprotein ◽  
Cell Activation Marker ◽  
Research Findings ◽  
A Cell ◽  
And Function ◽  
Human Molecule

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.

scholarly journals Climate Mobility and Development Cooperation

2021 ◽  
Author(s):  
Robert Stojanov ◽  
Sarah Rosengaertner ◽  
Alex de Sherbinin ◽  
Raphael Nawrotzki
Keyword(s):  
Climate Adaptation ◽  
Human Mobility ◽  
Climate Impacts ◽  
Development Cooperation ◽  
Climate Variability And Change ◽  
Policy Frameworks ◽  
And Migration ◽  
And Function ◽  
Role And Function

AbstractDevelopment cooperation actors have been addressing climate change as a cross-cutting issue and investing in climate adaptation projects since the early 2000s. More recently, as concern has risen about the potential impacts of climate variability and change on human mobility, development cooperation actors have begun to design projects that intentionally address the drivers of migration, including climate impacts on livelihoods. However, to date, we know little about the development cooperation’s role and function in responding to climate related mobility and migration. As such, the main aim of this paper is to outline the policy frameworks and approaches shaping development cooperation actors’ engagement and to identify areas for further exploration and investment. First, we frame the concept of climate mobility and migration and discuss some applicable policy frameworks that govern the issue from various perspectives; secondly, we review the toolbox of approaches that development cooperation actors bring to climate mobility; and third, we discuss the implications of the current Covid-19 pandemic and identify avenues for the way forward. We conclude that ensuring safe and orderly mobility and the decent reception and long-term inclusion of migrants and displaced persons under conditions of more severe climate hazards, and in the context of rising nationalism and xenophobia, poses significant challenges. Integrated approaches across multiple policy sectors and levels of governance are needed. In addition to resources, development cooperation actors can bring data to help empower the most affected communities and regions and leverage their convening power to foster more coordinated approaches within and across countries.

scholarly journals Morphodynamic signatures of MDA-MB-231 single cells and cell doublets undergoing invasion in confined microenvironments

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xingjian Zhang ◽  
Trevor Chan ◽  
Michael Mak
Keyword(s):  
Single Cell ◽  
Single Cells ◽  
Leading Edge ◽  
Cell Group ◽  
Collective State ◽  
Long Term Effects ◽  
Cell Metastasis ◽  
Geometric Confinement ◽  
Short And Long Term ◽  
The Impact

AbstractCancer cell metastasis is a major factor in cancer-related mortality. During the process of metastasis, cancer cells exhibit migratory phenotypes and invade through pores in the dense extracellular matrix. However, the characterization of morphological and subcellular features of cells in similar migratory phenotypes and the effects of geometric confinement on cell morphodynamics are not well understood. Here, we investigate the phenotypes of highly aggressive MDA-MB-231 cells in single cell and cell doublet (an initial and simplified collective state) forms in confined microenvironments. We group phenotypically similar single cells and cell doublets and characterize related morphological and subcellular features. We further detect two distinct migratory phenotypes, fluctuating and non-fluctuating, within the fast migrating single cell group. In addition, we demonstrate an increase in the number of protrusions formed at the leading edge of cells after invasion through geometric confinement. Finally, we track the short and long term effects of varied degrees of confinement on protrusion formation. Overall, our findings elucidate the underlying morphological and subcellular features associated with different single cell and cell doublet phenotypes and the impact of invasion through confined geometry on cell behavior.

scholarly journals EMT Participates in the Regulation of Exosomes Secretion and Function in Esophageal Cancer Cells

2021 ◽  
Vol 20 ◽  
pp. 153303382110330
Author(s):  
Chuangui Chen ◽  
Zhao Ma ◽  
Hongjing Jiang
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Promoting Effect ◽  
Migration Ability ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration ◽  
And Function ◽  
Esophageal Cancer Cells

Epithelial-mesenchymal transition (EMT) is a key step in tumor invasion and distant metastasis. Abundant evidence has documented that exosomes can mediate EMT of tumor cells and endow them with the ability of invasion and migration. However, there are few studies focusing on whether EMT can reverse the secretion of exosomes. In this study, 2 esophageal cancer cells (FLO-1 and SK-GT-4) were selected to compare the migration ability and EMT activation, and to further analyze the secretion ability of exosomes of the 2 cell lines. According to the results, inhibited activation of EMT in FLO-1 cells with relatively high migration ability could effectively reduce the secretion of exosomes. Besides, in SK-GT-4 cells, EMT activation induced by TGF-β could promote the secretion of exosomes. FLO-1 cell derived exosomes exhibited a paracrine effect of promoting the migration of SK-GT-4 cells, and the use of EMT inhibitors could weaken this ability. Furthermore, inhibition of EMT could change the relative content of some miRNAs in exosomes, with a particularly significant downregulation in the expression of miR-196-5p, miR-21-5p and miR-194-5p. Significantly, artificial transfection of the 3 miRNAs into exosomes by electroporation resulted in the recovery of migration-promoting effect of exosomes. Subsequent experiments further revealed that the effect of EMT on these miRNAs could be explained by the intracellular transcription level or the specific sorting mechanism of exosomes. To sum up, our study undoubtedly reveals that EMT has a regulatory effect on exosomes in the quantity and contents in esophageal cancer cells. Significantly, findings in our study provide experimental evidence for the interaction of EMT with the secretion and sorting pathway of exosomes, and also give a new direction for the further study of tumor metastasis.

A widespread pathway for substitution of adenine by diaminopurine in phage genomes

Science ◽  
2021 ◽  
Vol 372 (6541) ◽  
pp. 512-516
Author(s):  
Yan Zhou ◽  
Xuexia Xu ◽  
Yifeng Wei ◽  
Yu Cheng ◽  
Yu Guo ◽  
...  
Keyword(s):  
Large Scale ◽  
Restriction Enzymes ◽  
Diverse Range ◽  
Host Restriction ◽  
Form And Function ◽  
Multienzyme System ◽  
Dna Modifications ◽  
Dna Production ◽  
And Function

DNA modifications vary in form and function but generally do not alter Watson-Crick base pairing. Diaminopurine (Z) is an exception because it completely replaces adenine and forms three hydrogen bonds with thymine in cyanophage S-2L genomic DNA. However, the biosynthesis, prevalence, and importance of Z genomes remain unexplored. Here, we report a multienzyme system that supports Z-genome synthesis. We identified dozens of globally widespread phages harboring such enzymes, and we further verified the Z genome in one of these phages, Acinetobacter phage SH-Ab 15497, by using liquid chromatography with ultraviolet and mass spectrometry. The Z genome endows phages with evolutionary advantages for evading the attack of host restriction enzymes, and the characterization of its biosynthetic pathway enables Z-DNA production on a large scale for a diverse range of applications.

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