scholarly journals From Cell Death to Regeneration: Rebuilding After Injury

2021 ◽  
Vol 9 ◽  
Author(s):  
Dylan J. Guerin ◽  
Cindy X. Kha ◽  
Kelly Ai-Sun Tseng
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Normal Development ◽  
Tissue Remodeling ◽  
Cell Number ◽  
The Body ◽  
Apoptosis Induction ◽  
New Knowledge ◽  
And Function

The ability to regrow lost or damaged tissues is widespread, but highly variable among animals. Understanding this variation remains a challenge in regeneration biology. Numerous studies from Hydra to mouse have shown that apoptosis acts as a potent and necessary mechanism in regeneration. Much is known about the involvement of apoptosis during normal development in regulating the number and type of cells in the body. In the context of regeneration, apoptosis also regulates cell number and proliferation in tissue remodeling. Apoptosis acts both early in the process to stimulate regeneration and later to regulate regenerative patterning. Multiple studies indicate that apoptosis acts as a signal to stimulate proliferation within the regenerative tissues, producing the cells needed for full regeneration. The conservation of apoptosis as a regenerative mechanism demonstrated across species highlights its importance and motivates the continued investigation of this important facet of programmed cell death. This review summarizes what is known about the roles of apoptosis during regeneration, and compares regenerative apoptosis with the mechanisms and function of apoptosis in development. Defining the complexity of regenerative apoptosis will contribute to new knowledge and perspectives for understanding mechanisms of apoptosis induction and regulation.

scholarly journals THE INFLUENCE OF PARENTS' ATTITUDES IN PROVIDING EDUCATION AT HOME TOWARD THE DEVELOPMENT OF CHILDREN AGED 5-6 YEARS IN BULUSARI VILLAGE, GEMPOL SUB-DISTRICT, PASURUAN DISTRICT

2019 ◽  
Vol 8 (1) ◽  
pp. 56-61
Author(s):  
Siti Fithrotul Umami ◽  
Titiek Idayanti
Keyword(s):  
Normal Development ◽  
Health Workers ◽  
The Body ◽  
Family Education ◽  
Exact Test ◽  
Parents And Children ◽  
Preliminary Study ◽  
Individual Evaluation ◽  
And Function ◽  
At Home

Background: Development is increasing ability (skill) in the structure and function of the body that is more complex in a regular pattern and can be predicted as a result, from the results of maturation. attitude is an individual evaluation in the form of a tendency (Inclination) towards various elements outside of him. Based on the results of a preliminary study of 10 children aged 5-6 years, it was found that 5 children had normal development, 2 children doubted, and 3 children developed abnormally. While for family education conducted by parents, it was found that 7 parents supported (favorabel), and 3 parents were not supportive (unfavorable).Objectives: The study aimed to determine the influence of parents' attitudes in providing education at home toward the development of children aged 5-6 years in Bulusari Village, Gempol Sub-District, Pasuruan District.Methods: The research design was analytical design using purposive sampling with a sample of 45 parents and children in Bulusari Village, Gempol Sub-District, Pasuruan District. The measuring instrument used was a questionnaire for parents and KPSP for child development. This research is presented in the form of the Fisher's Exact Test.Results: The results showed that of 38 parents (84.45%) who supported having normal development children as many as 35 children (77.78%). Based on the results of the Fisher's Exact Test statistical test, it was found that the value of p <α, which is 0.001022 <0.05, which means that there is an influence from the provision of family education conducted by parents to the development of children aged 5-6 years.Conclusion: Based on the results of this study, it is expected that efforts from health workers to increase counseling to parents so that they have a role and have an obligation to help, assist children, teach children to actively learn, give love, develop creativity and socialization of children. Kata kunci : Parent’s attitude, development of 5-6 years, giving education in houses.

scholarly journals Have necrohormones a role in embryogenesis?

2014 ◽  
Vol 65 (1-2) ◽  
pp. 7-9 ◽  
Author(s):  
P. R. Bell
Keyword(s):  
Cell Death ◽  
Somatic Embryogenesis ◽  
Programmed Cell Death ◽  
Picea Abies ◽  
Recent Work ◽  
Normal Development ◽  
Living Cells ◽  
Embryogenic Cultures ◽  
Conflicting Evidence ◽  
Apomictic Reproduction

The recognition of apoptosis (programmed cell death) as an accompaniment of normal development, the products released by the protoplasts undergoing self-destruction being utilized by adjacent living cells, stimulates renewed interest in Haberlandt's concept of "necrohormones" playing a role in apomictic reproduction. Recent work on somatic embryogenesis in carrot shows that regular death of certain cells in embryogenic cultures satifies the criteria of apoptosis. Similar observations have been made with embryogenic cultures of <em>Picea abies</em>. Haberlandt's claim that cell death induced by injury adjacent to an ovule in <em>Oenothera</em> could lead to parthenogenesis, despite conflicting evidence from later experimenters, is worthy of reexamination.

scholarly journals Myocardial Damage by SARS-CoV-2: Emerging Mechanisms and Therapies

Viruses ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 1880
Author(s):  
Huyen Tran Ho ◽  
Stefan Peischard ◽  
Nathalie Strutz-Seebohm ◽  
Karin Klingel ◽  
Guiscard Seebohm
Keyword(s):  
Immune Response ◽  
Cell Death ◽  
Energy Metabolism ◽  
Programmed Cell Death ◽  
Viral Replication ◽  
Ion Homeostasis ◽  
Membrane Vesicles ◽  
Cardiac Cells ◽  
The Body ◽  
Double Membrane

Evidence is emerging that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can infect various organs of the body, including cardiomyocytes and cardiac endothelial cells in the heart. This review focuses on the effects of SARS-CoV-2 in the heart after direct infection that can lead to myocarditis and an outline of potential treatment options. The main points are: (1) Viral entry: SARS-CoV-2 uses specific receptors and proteases for docking and priming in cardiac cells. Thus, different receptors or protease inhibitors might be effective in SARS-CoV-2-infected cardiac cells. (2) Viral replication: SARS-CoV-2 uses RNA-dependent RNA polymerase for replication. Drugs acting against ssRNA(+) viral replication for cardiac cells can be effective. (3) Autophagy and double-membrane vesicles: SARS-CoV-2 manipulates autophagy to inhibit viral clearance and promote SARS-CoV-2 replication by creating double-membrane vesicles as replication sites. (4) Immune response: Host immune response is manipulated to evade host cell attacks against SARS-CoV-2 and increased inflammation by dysregulating immune cells. Efficiency of immunosuppressive therapy must be elucidated. (5) Programmed cell death: SARS-CoV-2 inhibits programmed cell death in early stages and induces apoptosis, necroptosis, and pyroptosis in later stages. (6) Energy metabolism: SARS-CoV-2 infection leads to disturbed energy metabolism that in turn leads to a decrease in ATP production and ROS production. (7) Viroporins: SARS-CoV-2 creates viroporins that lead to an imbalance of ion homeostasis. This causes apoptosis, altered action potential, and arrhythmia.

Apoptosis in Degenerative Diseases of the Basal Ganglia

1998 ◽  
Vol 4 (4) ◽  
pp. 301-311 ◽  
Author(s):  
Robert E. Burke
Keyword(s):  
Cell Death ◽  
Basal Ganglia ◽  
Programmed Cell Death ◽  
Direct Evidence ◽  
Normal Development ◽  
Dopamine Neurons ◽  
Degenerative Diseases ◽  
Morphological Markers ◽  
Degenerative Disorders ◽  
New Hypothesis

Degenerative disorders of the basal ganglia are characterized by disturbances of motor control. Prototypic examples are Parkinson's disease, which is caused by degeneration of dopamine neurons of the substantia nigra, and Huntington's disease, which is caused by degeneration of neurons of the striatum. In recent years, it has been postulated that some of these disorders may be caused by programmed cell death or apoptosis, a genetically regulated form of cell death. There is clear evidence that apoptosis occurs in neurons of the basal ganglia during normal development, that it can be regulated, and that it can be induced in some animal models of these disorders. Although there is some suggestive direct evidence that apoptosis may occur in the human brain in these disorders, the evidence to date is partial and not yet compelling. Nevertheless, programmed cell death is an important new hypothesis for the pathogenesis of these disorders and warrants vigorous further investigation, particularly with molecular markers in addition to classic morphological markers. The concept of programmed cell death is relevant not only to the pathogenesis of these diseases but also to therapeutic issues, such as transplantation approaches.

scholarly journals Normal development, oncogenesis and programmed cell death

Oncogene ◽  
1998 ◽  
Vol 17 (10) ◽  
pp. 1189-1194 ◽  
Author(s):  
Dan A Liebermann
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Normal Development

scholarly journals Programmed Cell Death-1 Receptor (PD-1)-Mediated Regulation of Innate Lymphoid Cells

2019 ◽  
Vol 20 (11) ◽  
pp. 2836 ◽  
Author(s):  
Grace Mallett ◽  
Arian Laurence ◽  
Shoba Amarnath
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Cell Surface Receptor ◽  
Programmed Cell Death 1 ◽  
Surface Receptor ◽  
A Cell ◽  
And Function

Programmed cell death-1 (PD-1) is a cell surface receptor that dampens adaptive immune responses. PD-1 is activated by the engagement of its ligands PDL-1 or PDL-2. This results in the inhibition of T cell proliferation, differentiation, cytokine secretion, and cytolytic function. Although a great deal is known about PD-1 mediated regulation of CD4+ and CD8+ T cells, its expression and function in innate lymphoid cells (ILCs) are yet to be fully deciphered. This review summarizes the role of PD-1 in (1) modulating ILC development, (2) ILC function, and (3) PD-1 signaling in ILC. Finally, we explore how PD-1 based immunotherapies may be beneficial in boosting ILC responses in cancer, infections, and other immune-related disorders.

scholarly journals Expression and function of Fas (APO-1/CD95) in patient myeloma cells and myeloma cell lines

Blood ◽  
1995 ◽  
Vol 85 (12) ◽  
pp. 3566-3576 ◽  
Author(s):  
JJ Westendorf ◽  
JM Lammert ◽  
DF Jelinek
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Cell Lines ◽  
Protective Factor ◽  
Plasma Cells ◽  
Myeloma Cell ◽  
Color Flow ◽  
Fas Antigen ◽  
Myeloma Cells ◽  
And Function

Cross-linkage of the Fas antigen induces programmed cell death in many normal and malignant lymphoid cells by a process known as apoptosis. In this study, we examined the sensitivity of myeloma cell lines and patient plasma cells to a cytolytic anti-Fas monoclonal antibody (MoAb). Eight of 10 myeloma cell lines were induced to undergo programmed cell death by anti-Fas MoAb as determined by DNA fragmentation and morphologic changes. Of the two myeloma cell lines that were resistant to anti-Fas treatment, one did not express the Fas antigen. Only the U266 cell line expressed Fas, but was not killed by the anti0Fas MoAb. To extend these studies, we have examined the expression and function of Fas in freshly isolated CD38hiCD45neg-int plasma cells from patients with multiple myeloma (MM), monoclonal gammopathy of undetermined significance (MGUS), and primary amyloidosis (AL). By three-color flow cytometry, we found Fas expression in CD38hiCD45neg-int plasma cells from all patient groups to be variable, as Fas was expressed in 15 of 28 MM, 3 of 6 MGUS, and 2 of 7 AL patients. In morphologic studies of apoptosis, Fas-positive myeloma cells in patient bone marrow mononuclear cell (MNC) cultures appeared to be resistant to anti-Fas-mediated apoptosis. By contrast, purified myeloma cells from the same patient were sensitive to anti-Fas treatment, suggesting the presence of a protective factor(s) in unseparated MNC cultures that may inhibit Fas-induced apoptosis of plasma cells. Of interest, serum from normal individuals and myeloma patients also protected myeloma cell lines from undergoing Fas-mediated apoptosis. These studies show that Fas expression in myeloma cell lines and CD38hiCD45neg-int patient plasma cells is variable and may reflect a variance in the maturation status of the various plasma cell populations. Moreover, Fas-mediated killing of patient cells and myeloma cell lines was also variable, which may be influenced, in part, by the presence of a soluble protective factor.

scholarly journals The Reaper-Binding Protein Scythe Modulates Apoptosis and Proliferation during Mammalian Development

2005 ◽  
Vol 25 (23) ◽  
pp. 10329-10337 ◽  
Author(s):  
Fabienne Desmots ◽  
Helen R. Russell ◽  
Youngsoo Lee ◽  
Kelli Boyd ◽  
Peter J. McKinnon
Keyword(s):  
Cell Death ◽  
Drosophila Melanogaster ◽  
Programmed Cell Death ◽  
Xenopus Laevis ◽  
Cellular Proliferation ◽  
Nuclear Protein ◽  
Normal Development ◽  
Mammalian Development ◽  
Developmental Defects ◽  
Cell Extracts

ABSTRACT Scythe (BAT3 [HLA-B-associated transcript 3]) is a nuclear protein that has been implicated in apoptosis, as it can modulate Reaper, a central apoptotic regulator in Drosophila melanogaster. While Scythe can markedly affect Reaper-dependent apoptosis in Xenopus laevis cell extracts, the function of Scythe in mammals is unknown. Here, we report that inactivation of Scythe in the mouse results in lethality associated with pronounced developmental defects in the lung, kidney, and brain. In all cases, these developmental defects were associated with dysregulation of apoptosis and cellular proliferation. Scythe − / − cells were also more resistant to apoptosis induced by menadione and thapsigargin. These data show that Scythe is critical for viability and normal development, probably via regulation of programmed cell death and cellular proliferation.

scholarly journals Calpain inhibition preserves myocardial structure and function following myocardial infarction

2009 ◽  
Vol 297 (5) ◽  
pp. H1744-H1751 ◽  
Author(s):  
Santhosh K. Mani ◽  
Sundaravadivel Balasubramanian ◽  
Juozas A. Zavadzkas ◽  
Laura B. Jeffords ◽  
William T. Rivers ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Left Ventricular ◽  
Structure And Function ◽  
Left Ventricular Ejection ◽  
Tunel Staining ◽  
Ventricular Ejection Fraction ◽  
Myocardial Structure ◽  
And Function

Cardiac pathology, such as myocardial infarction (MI), activates intracellular proteases that often trigger programmed cell death and contribute to maladaptive changes in myocardial structure and function. To test whether inhibition of calpain, a Ca2+-dependent cysteine protease, would prevent these changes, we used a mouse MI model. Calpeptin, an aldehydic inhibitor of calpain, was intravenously administered at 0.5 mg/kg body wt before MI induction and then at the same dose subcutaneously once per day. Both calpeptin-treated ( n = 6) and untreated ( n = 6) MI mice were used to study changes in myocardial structure and function after 4 days of MI, where end-diastolic volume (EDV) and left ventricular ejection fraction (EF) were measured by echocardiography. Calpain activation and programmed cell death were measured by immunohistochemistry, Western blotting, and TdT-mediated dUTP nick-end labeling (TUNEL). In MI mice, calpeptin treatment resulted in a significant improvement in EF [EF decreased from 67 ± 2% pre-MI to 30 ± 4% with MI only vs. 41 ± 2% with MI + calpeptin] and attenuated the increase in EDV [EDV increased from 42 ± 2 μl pre-MI to 73 ± 4 μl with MI only vs. 55 ± 4 μl with MI + calpeptin]. Furthermore, calpeptin treatment resulted in marked reduction in calpain- and caspase-3-associated changes and TUNEL staining. These studies indicate that calpain contributes to MI-induced alterations in myocardial structure and function and that it could be a potential therapeutic target in treating MI patients.

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