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 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 Intramuscular VEGF activates an SDF1-dependent progenitor cell cascade and an SDF1-independent muscle paracrine cascade for cardiac repair

2011 ◽  
Vol 301 (6) ◽  
pp. H2422-H2432 ◽  
Author(s):  
David Zisa ◽  
Arsalan Shabbir ◽  
Michalis Mastri ◽  
Tyler Taylor ◽  
Ilija Aleksic ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Progenitor Cells ◽  
Progenitor Cell ◽  
Cardiac Repair ◽  
Trophic Factors ◽  
Therapeutic Modality ◽  
Ability To Regenerate ◽  
Organ Repair ◽  
Hamster Heart ◽  
And Function

The skeletal muscle is endowed with an impressive ability to regenerate after injury, and this ability is coupled to paracrine production of many trophic factors possessing cardiovascular benefits. Taking advantage of this humoral capacity of the muscle, we recently demonstrated an extracardiac therapeutic regimen based on intramuscular delivery of VEGF-A165 for repair of the failing hamster heart. This distal organ repair mechanism activates production from the injected hamstring of many trophic factors, among which stromal-derived factor-1 (SDF1) prominently mobilized multi-lineage progenitor cells expressing CXCR4 and their recruitment to the heart. The mobilized bone marrow progenitor cells express the cardiac transcription factors myocyte enhancer factor 2c and GATA4 and several major trophic factors, most notably IGF1 and VEGF. SDF1 blockade abrogated myocardial recruitment of CXCR4+ and c-kit+ progenitor cells with an insignificant effect on the hematopoietic progenitor lineage. The knockdown of cardiac progenitor cells led to deprivation of myocardial trophic factors, resulting in compromised cardiomyogenesis and angiogenesis. However, the VEGF-injected hamstring continued to synthesize cardioprotective factors, contributing to moderate myocardial tissue viability and function even in the presence of SDF1 blockade. These findings thus uncover two distinct but synergistic cardiac therapeutic mechanisms activated by intramuscular VEGF. Whereas the SDF1/CXCR4 axis activates the progenitor cell cascade and its trophic support of cardiomyogenesis intramuscularly, VEGF amplifies the skeletal muscle paracrine cascade capable of directly promoting myocardial survival independent of SDF1. Given that recent clinical trials of cardiac repair based on the use of marrow-mobilizing agents have been disappointing, the proposed dual therapeutic modality warrants further investigation.

Establishing a model to demonstrate physical and mathematical properties of chromatin fibres in fission yeast cells - Research in the Molecular Biophysics Lab at Hiroshima University

Impact ◽  
2018 ◽  
Vol 2018 (3) ◽  
pp. 89-91
Author(s):  
Shin-ichi Tate
Keyword(s):  
Molecular Biology ◽  
Yeast Cells ◽  
Molecular Architecture ◽  
Ministry Of Education ◽  
Cellular Functions ◽  
Sports Science ◽  
Cellular Events ◽  
And Function ◽  
Education Culture ◽  
Open The Doors

The field of molecular biology has provided great insights into the structure and function of key molecules. Thanks to this area of research, we can now grasp the biological details of DNA and have characterised an enormous number of molecules in massive data bases. These 'biological periodic tables' have allowed scientists to connect molecules to particular cellular events, furthering scientific understanding of biological processes. However, molecular biology has yet to answer questions regarding 'higher-order' molecular architecture, such as that of chromatin. Chromatin is the molecular material that serves as the building block for chromosomes, the structures that carry an organism's genetic information inside of the cell's nucleus. Understanding the physical properties of chromatin is crucial in developing a more thorough picture of how chromatin's structure relate to its key cellular functions. Moreover, by establishing a physical model of chromatin, scientists will be able to open the doors into the true inner workings of the cell nucleus. Professor Shin-ichi Tate and his team of researchers at Hiroshima University's Research Center for the Mathematics on Chromatin Live Dynamics (RcMcD), are attempting to do just that. Through a five-year grant funded by the Platform for Dynamic Approaches to Living Systems from the Ministry of Education, Culture, Sports, Science and Technology, Tate is aiming to gain a clearer understanding of the structure and dynamics of chromatin.

scholarly journals Sialic Acid—Modified Nanoparticles—New Approaches in the Glioma Management—Perspective Review

2021 ◽  
Vol 22 (14) ◽  
pp. 7494
Author(s):  
Przemyslaw Wielgat ◽  
Katarzyna Niemirowicz-Laskowska ◽  
Agnieszka Z. Wilczewska ◽  
Halina Car
Keyword(s):  
Sialic Acid ◽  
Clinical Observation ◽  
Malignant Cell ◽  
Cellular Heterogeneity ◽  
Molecular Processes ◽  
Management Perspective ◽  
Therapeutic Tools ◽  
And Function ◽  
Worse Prognosis

The cell surface is covered by a dense and complex network of glycans attached to the membrane proteins and lipids. In gliomas, the aberrant sialylation, as the final stage of glycosylation, is an important regulatory mechanism of malignant cell behavior and correlates with worse prognosis. Better understanding of the role of sialylation in cellular and molecular processes opens a new way in the development of therapeutic tools for human brain tumors. According to the recent clinical observation, the cellular heterogeneity, activity of brain cancer stem cells (BCSCs), immune evasion, and function of the blood–brain barrier (BBB) are attractive targets for new therapeutic strategies. In this review, we summarize the importance of sialic acid-modified nanoparticles in brain tumor progression.

Progenitor Cells: Megakaryocyte Development and Function.

Science ◽  
1987 ◽  
Vol 235 (4784) ◽  
pp. 96a-96a
Author(s):  
D. G. NATHAN
Keyword(s):  
Progenitor Cells ◽  
And Function

scholarly journals Quantitative and functional evaluation of endothelial progenitor cells in patients with cardiac amyloidosis

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
O Itzhaki Ben Zadok ◽  
D Leshem-Lev ◽  
T Ben-Gal ◽  
A Hamdan ◽  
N Schamroth-Pravda ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Mtt Assay ◽  
Cardiac Amyloidosis ◽  
Microvascular Dysfunction ◽  
Functional Evaluation ◽  
Endothelial Progenitor ◽  
Colony Forming Units ◽  
Study Population ◽  
And Function

Abstract Background Endothelial microvascular dysfunction is a known mechanism of injury in cardiac amyloidosis (CA), but evidence regarding the level and function of endothelial progenitor cells (EPCs) in patients with CA is lacking. Methods Study population included patients with light-chain or transthyretin (ATTR) CA. Patients with diagnosed heart failure and preserved ejection fraction (HFpEF) without monoclonal gammopathy and a 99mTc-DPD scan incompatible with TTR were used as controls. Blood circulating EPCs were assessed quantitatively by the expression of VEGFR-2(+), CD34(+) and CD133(+) using flow cytometry, and functionally by the formation of colony forming units (CFUs). MTT assay was used to demonstrate cell viability. Tests were repeated 3 months following the initiation of amyloid-suppressive therapies (either ATTR-stabilizer or targeted chemotherapy) in CA patients. Results Our preliminary cohort included 14 CA patients (median age 74 years, 62% ATTR CA). Patients with CA vs. patients with HFpEF (n=8) demonstrated lower expression of CD34(+)/VEGFR-2(+) cells [0.51% (IQR 0.4, 0.7) vs. 1.03% (IQR 0.6, 1.4), P=0.043] and CD133(+)/VEGFR-2(+) cells [0.35% (IQR 0.23, 0.52) to 1.07% (IQR 0.6, 1.5), P=0.003]. Functionally, no differences were noted between groups. Following the initiation of amyloid-suppressive therapies in CA patients, we observed the up-regulation of CD34(+)/VEGFR-2(+) cells [2.47% (IQR 2.1, 2.7), P<0.001] and CD133(+)/VEGFR-2(+) cells [1.38% (IQR 1.1, 1.7), P=0.003]. Moreover, functionally, active EPCs were evident microscopically by their ability to form colonies (from 0.5 CFUs [IQR 0, 1.5) to 2 CFUs (IQR 1, 3.5), P=0.023]. EPCs' viability was demonstrated by an MTT assay [0.12 (IQR 0.04, 0.12) to 0.24 (IQR 0.16, 0.3), p=0.014]. Conclusions These preliminary results demonstrate reduced EPCs levels in CA patients indicating significant microvascular impairment. Amyloid-targeted therapies induce the activation of EPCs, thus possibly promoting endothelial regeneration. These findings may represent a novel mechanism of action of amyloid-suppressive therapies EPCs in CA patients and during therapy Funding Acknowledgement Type of funding source: None

3008 – OXYGEN TENSION REGULATES CALCIUM SIGNALING AND FUNCTION IN HEMATOPOIETIC STEM AND PROGENITOR CELLS

2020 ◽  
Vol 88 ◽  
pp. S40
Author(s):  
Paige Dausinas ◽  
Jacob Slack ◽  
Christopher Basile ◽  
Anish Karlapudi ◽  
Heather O'Leary
Keyword(s):  
Calcium Signaling ◽  
Progenitor Cells ◽  
Oxygen Tension ◽  
Hematopoietic Stem ◽  
Stem And Progenitor Cells ◽  
And Function

Fetal Human Liver Progenitor Cells: A Potential Immune-Privileged Cellular Source from Non Heart Beating Donors

Placenta ◽  
2011 ◽  
Vol 32 ◽  
pp. S337
Author(s):  
G. Pietrosi ◽  
G.B. Vizzini ◽  
P.G. Conaldi ◽  
M. D'Amato ◽  
A. Giandomenico ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Human Liver ◽  
Heart Beating ◽  
Cellular Source
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