The liaison between apoptotic cells and macrophages – the end programs the beginning

2009 ◽  
Vol 390 (5/6) ◽  
Author(s):  
Andreas Weigert ◽  
Carla Jennewein ◽  
Bernhard Brüne
Keyword(s):  
Cell Death ◽  
Inflammatory Disease ◽  
Regulatory Mechanism ◽  
Current Knowledge ◽  
Apoptotic Cell ◽  
Tumor Development ◽  
Tissue Homeostasis ◽  
Human Diseases ◽  
Apoptotic Cells ◽  
Resolution Of Inflammation

AbstractThe efficient execution of apoptotic cell death with the clearance of apoptotic debris by phagocytes is a key regulatory mechanism ensuring tissue homeostasis. Failure in this execution program contributes to the pathogenesis of many human diseases. In this review, we describe the current knowledge regarding the interaction of apoptotic cells with their professional ‘captors’, the macrophages, with special emphasis on the immunological outcome. Removal of apoptotic cells must be considered as a process that actively delivers signals to polarize macrophages, which are fundamental for the resolution of inflammation. However, the sculpting of macrophage responses by apoptotic cells can be misused under certain inflammatory disease conditions, including tumor development.

scholarly journals Apoptotic cell-derived extracellular vesicles: structure–function relationships

2019 ◽  
Vol 47 (2) ◽  
pp. 509-516 ◽  
Author(s):  
Lois R. Grant ◽  
Ivana Milic ◽  
Andrew Devitt
Keyword(s):  
Structure Function ◽  
Extracellular Vesicles ◽  
Current Knowledge ◽  
Apoptotic Cell ◽  
Apoptotic Cells ◽  
Phagocytic Cells ◽  
Future Directions ◽  
Resolution Of Inflammation ◽  
Ongoing Work

Abstract Apoptosis is an essential process for normal physiology and plays a key role in the resolution of inflammation. Clearance of apoptotic cells (ACs) involves complex signalling between phagocytic cells, ACs, and the extracellular vesicles (EVs) they produce. Here, we discuss apoptotic cell-derived extracellular vesicles (ACdEVs) and how their structure relates to their function in AC clearance and the control of inflammation, focussing on the ACdEV proteome. We review the current knowledge, ongoing work and future directions for research in this field.

scholarly journals Cytotoxicity, Antiproliferative Effects, and Apoptosis Induction of Methanolic Extract ofCynometra caulifloraLinn. Whole Fruit on Human Promyelocytic Leukemia HL-60 Cells

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
T-Johari S. A. Tajudin ◽  
Nashriyah Mat ◽  
Abu Bakar Siti-Aishah ◽  
A. Aziz M. Yusran ◽  
Afnani Alwi ◽  
...  
Keyword(s):  
Cell Death ◽  
Methanolic Extract ◽  
Apoptotic Cell ◽  
Mouse Fibroblast ◽  
Promyelocytic Leukemia ◽  
Apoptotic Cell Death ◽  
Apoptotic Cells ◽  
3T3 Cells ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

Methanolic extract ofCynometra cauliflorawhole fruit was assayed for cytotoxicity against the human promyelocytic leukemia HL-60 and the normal mouse fibroblast NIH/3T3 cell lines by using the MTT assay. The CD50of the extract for 72 hours was 0.9 μg/mL whereas the value for the cytotoxic drug vincristine was 0.2 μg/mL. The viability of the NIH/3T3 cells was at 80.0% when treated at 15.0 μg/mL. The extract inhibited HL-60 cell proliferation with dose dependence. AO/PI staining of HL-60 cells treated with the extract revealed that majority of cells were in the apoptotic cell death mode. Flow cytometry analysis of HL-60 cells treated at CD50of the extract showed that the early apoptotic cells were 31.0, 26.3 and 19.9% at 24, 48, and 72 hours treatment, respectively. The percentage of late apoptotic cells was increased from 62.0 at 24 hours to 64.1 and 70.2 at 48 and 72 hours, respectively. Meanwhile, percent of necrotic cells were 4.9, 6.6, and 8.5 at 24, 48, and 72 hours, respectively. This study has shown that the methanolic extract ofC. cauliflorawhole fruit was cytotoxic towards HL-60 cells and induced the cells into apoptotic cell death mode, but less cytotoxic towards NIH/3T3 cells.

scholarly journals Hydrocortisone decreases apoptosis in jejunum of horses subjected to experimental ischemia and reperfusion

2011 ◽  
Vol 31 (6) ◽  
pp. 471-476 ◽  
Author(s):  
Geraldo Eleno S. Alves ◽  
Heloisa M.F. Mendes ◽  
Tiago G.S. Alves ◽  
Rafael R. Faleiros ◽  
Anilton C. Vasconcelos ◽  
...  
Keyword(s):  
Cell Death ◽  
Time Course ◽  
Apoptotic Cell ◽  
Treated Group ◽  
Apoptotic Cell Death ◽  
Apoptotic Cells ◽  
Ischemia And Reperfusion ◽  
Beneficial Effects ◽  
Time Zero ◽  
Venous Ischemia

In order to evaluate the effect of hydrocortisone on apoptosis in the jejunum of horses subjected to ischemia and reperfusion, ten horses were paired and grouped into two groups - treated (n=5) and non treated (n=5). Segments of the jejunum were used as controls (C), or as venous ischemia (VIsc), which were subjected to 2h of ischemia followed by 2 or 12h of reperfusion. C samples were collected at time zero (prior to ischemia) and VIsc samples were collected at 2h of ischemia and at 2 and 12h of reperfusion. TUNEL positive apoptotic cells were counted in 10 microscopical fields in deep mucosa from each horse throughout the time course. After 12h of reperfusion, the number of apoptotic cells in treated group were significantly lower than in untreated animals, indicating that hydrocortisone inhibits apoptosis. These results indicate that hydrocortisone has a beneficial effects favoring the maintenance of jejunal integrity in horses with ischemia and reperfusion injuries by preventing apoptotic cell death.

Inhalation of formaldehyde and xylene induces apoptotic cell death in the lung tissue

2009 ◽  
Vol 25 (7) ◽  
pp. 455-461 ◽  
Author(s):  
M. Sandikci ◽  
K. Seyrek ◽  
H. Aksit ◽  
H. Kose
Keyword(s):  
Cell Death ◽  
Lung Tissue ◽  
Lymphoid Tissue ◽  
Apoptotic Cell ◽  
Apoptotic Cells ◽  
Sprague Dawley ◽  
Control Groups ◽  
Adult Rats ◽  
Lymphoid Follicles ◽  
Sprague Dawley Rats

The aim of this study was to determine the localization and number of apoptotic cells in lung tissue and bronchus-associated lymphoid tissue (BALT) of newborns, young, and adult rats exposed to formaldehyde (6 ppm) or technical xylene (300 ppm) for 6 weeks (8 h/day). A total of 27 female Sprague-Dawley rats were used. Apoptotic cells were mainly localized around the bronchus and bronchioles and relatively less frequently on the walls of alveoli and interalveolar septa both in control and experimental groups. In the BALT, reactive cells were localized in the area under the epithelium and distributed homogenously within the lymphoid follicles. The numbers of apoptotic cells in the lung tissue including the BALT were significantly higher in young and adult rats exposed to formaldehyde and xylene than those detected in control groups.

scholarly journals “Dead Cells Talking”: The Silent Form of Cell Death Is Not so Quiet

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Richard Jäger ◽  
Howard O. Fearnhead
Keyword(s):  
Cell Death ◽  
Cancer Therapy ◽  
Apoptotic Cell ◽  
Surrounding Tissue ◽  
Apoptotic Cells ◽  
Cancer Cell Proliferation ◽  
Loss Of Function ◽  
Molecular Events ◽  
Dying Cells

After more than twenty years of research, the molecular events of apoptotic cell death can be succinctly stated; different pathways, activated by diverse signals, increase the activity of proteases called caspases that rapidly and irreversibly dismantle condemned cell by cleaving specific substrates. In this time the ideas that apoptosis protects us from tumourigenesis and that cancer chemotherapy works by inducing apoptosis also emerged. Currently, apoptosis research is shifting away from the intracellular events within the dying cell to focus on the effect of apoptotic cells on surrounding tissues. This is producing counterintuitive data showing that our understanding of the role of apoptosis in tumourigenesis and cancer therapy is too simple, with some interesting and provocative implications. Here, we will consider evidence supporting the idea that dying cells signal their presence to the surrounding tissue and, in doing so, elicit repair and regeneration that compensates for any loss of function caused by cell death. We will discuss evidence suggesting that cancer cell proliferation may be driven by inappropriate or corrupted tissue-repair programmes that are initiated by signals from apoptotic cells and show how this may dramatically modify how we view the role of apoptosis in both tumourigenesis and cancer therapy.

scholarly journals Role of Cell Death in Cellular Processes During Odontogenesis

2021 ◽  
Vol 9 ◽  
Author(s):  
John Abramyan ◽  
Poongodi Geetha-Loganathan ◽  
Marie Šulcová ◽  
Marcela Buchtová
Keyword(s):  
Cell Death ◽  
Tooth Development ◽  
Apoptotic Cell ◽  
Tooth Germ ◽  
Oral Epithelium ◽  
Special Focus ◽  
Apoptotic Cells ◽  
Molecular Signaling ◽  
Apoptotic Pathway ◽  
Cellular Processes

The development of a tooth germ in a precise size, shape, and position in the jaw, involves meticulous regulation of cell proliferation and cell death. Apoptosis, as the most common type of programmed cell death during embryonic development, plays a number of key roles during odontogenesis, ranging from the budding of the oral epithelium during tooth initiation, to later tooth germ morphogenesis and removal of enamel knot signaling center. Here, we summarize recent knowledge about the distribution and function of apoptotic cells during odontogenesis in several vertebrate lineages, with a special focus on amniotes (mammals and reptiles). We discuss the regulatory roles that apoptosis plays on various cellular processes during odontogenesis. We also review apoptosis-associated molecular signaling during tooth development, including its relationship with the autophagic pathway. Lastly, we cover apoptotic pathway disruption, and alterations in apoptotic cell distribution in transgenic mouse models. These studies foster a deeper understanding how apoptotic cells affect cellular processes during normal odontogenesis, and how they contribute to dental disorders, which could lead to new avenues of treatment in the future.

scholarly journals Redox Regulation of STAT1 and STAT3 Signaling

2020 ◽  
Vol 21 (19) ◽  
pp. 7034
Author(s):  
Elena Butturini ◽  
Alessandra Carcereri de Prati ◽  
Sofia Mariotto
Keyword(s):  
Cell Cycle ◽  
Immune Response ◽  
Cell Death ◽  
Redox Regulation ◽  
Inflammatory Responses ◽  
Current Knowledge ◽  
Apoptotic Cell ◽  
Post Translational Modifications ◽  
Environmental Signals ◽  
Stat3 Signaling

STAT1 and STAT3 are nuclear transcription factors that regulate genes involved in cell cycle, cell survival and immune response. The cross-talk between these signaling pathways determines how cells integrate the environmental signals received ultimately translating them in transcriptional regulation of specific sets of genes. Despite being activated downstream of common cytokine and growth factors, STAT1 and STAT3 play essentially antagonistic roles and the disruption of their balance directs cells from survival to apoptotic cell death or from inflammatory to anti-inflammatory responses. Different mechanisms are proposed to explain this yin-yang relationship. Considering the redox aspect of STATs proteins, this review attempts to summarize the current knowledge of redox regulation of STAT1 and STAT3 signaling focusing the attention on the post-translational modifications that affect their activity.

Cleavage of sphingosine kinase 2 by caspase-1 provokes its release from apoptotic cells

Blood ◽  
2010 ◽  
Vol 115 (17) ◽  
pp. 3531-3540 ◽  
Author(s):  
Andreas Weigert ◽  
Sarah Cremer ◽  
Martina Victoria Schmidt ◽  
Andreas von Knethen ◽  
Carlo Angioni ◽  
...  
Keyword(s):  
Cell Death ◽  
Immune Cell ◽  
Apoptotic Cell ◽  
Sphingosine Kinase ◽  
Relevant Information ◽  
Lipid Mediator ◽  
Apoptotic Cells ◽  
Dependent Manner ◽  
Sphingosine Kinase 2 ◽  
Caspase 1

Abstract Execution of physiologic cell death known as apoptosis is tightly regulated and transfers immunologically relevant information. This ensures efficient clearance of dying cells and shapes the phenotype of their “captors” toward anti-inflammatory. Here, we identify a mechanism of sphingosine-1-phosphate production by apoptotic cells. During cell death, sphingosine kinase 2 (SphK2) is cleaved at its N-terminus in a caspase-1–dependent manner. Thereupon, a truncated but enzymatically active fragment of SphK2 is released from cells. This step is coupled to phosphatidylserine exposure, which is a hallmark of apoptosis and a crucial signal for phagocyte/apoptotic cell interaction. Our data link signaling events during apoptosis to the extracellular production of a lipid mediator that affects immune cell attraction and activation.

The final step in programmed cell death: phagocytes carry apoptotic cells to the grave

2003 ◽  
Vol 39 ◽  
pp. 105-117 ◽  
Author(s):  
Aimee M deCathelineau ◽  
Peter M Henson
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
The Body ◽  
Apoptotic Cells ◽  
Cytokines And Chemokines ◽  
Cell Clearance ◽  
And Function ◽  
Multicellular Organisms ◽  
Dying Cells ◽  
High Degree

As cells undergo apoptosis, they are recognized and removed from the body by phagocytes. This oft-overlooked yet critical final step in the cell-death programme protects tissues from exposure to the toxic contents of dying cells and also serves to prevent further tissue damage by stimulating production of anti-inflammatory cytokines and chemokines. The clearance of apoptotic-cell corpses occurs throughout the lifespan of multicellular organisms and is important for normal development during embryogenesis, the maintenance of normal tissue integrity and function, and the resolution of inflammation. Many of the signal-transduction molecules implicated in the phagocytosis of apoptotic cells appear to have a high degree of evolutionary conservation, and therefore the engulfment of apoptotic cells is likely to represent one of the most primitive forms of phagocytosis. With the realization that the signals that govern apoptotic-cell removal also serve to attenuate inflammation and the immune response, as well as initiate signals for tissue repair and remodelling in response to cell death, the study of apoptotic cell clearance is a field experiencing a dynamic increase in interest and momentum.

Apoptosis in the lung: induction, clearance and detection

2008 ◽  
Vol 294 (4) ◽  
pp. L601-L611 ◽  
Author(s):  
P. M. Henson ◽  
R. M. Tuder
Keyword(s):  
Cell Death ◽  
Tissue Repair ◽  
Alternative Explanation ◽  
Apoptotic Cell ◽  
Lung Cells ◽  
Apoptotic Cells ◽  
Local Responses ◽  
Apoptotic Cell Clearance ◽  
Cell Clearance ◽  
Dying Cells

Apoptosis and other forms of programmed cell death are important contributors to lung pathophysiology. In this brief review, we discuss some of the implications of finding apoptotic cells in the lung and methods for their detection. The balance between induction of apoptosis and the normally highly efficient clearance of such cells shows that these are highly dynamic processes and suggests that abnormalities of apoptotic cell clearance may be an alternative explanation for their detection. Because recognition of apoptotic cells by other lung cells has additional effects on inflammation, immunity, and tissue repair, local responses to the dying cells may also have important consequences in addition to the cell death itself.

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