scholarly journals Cell death during complete metamorphosis

2019 ◽  
Vol 374 (1783) ◽  
pp. 20190065 ◽  
Author(s):  
Gianluca Tettamanti ◽  
Morena Casartelli
Keyword(s):  
Cell Death ◽  
Body Structure ◽  
Theme Issue ◽  
Tissue Remodelling ◽  
Regulatory Pathways ◽  
Adult Transition ◽  
Similarities And Differences ◽  
Cell Death Mechanisms ◽  
Complete Metamorphosis

In insects that undergo complete metamorphosis, cell death is essential for reshaping or removing larval tissues and organs, thus contributing to formation of the adult's body structure. In the last few decades, the study of metamorphosis in Lepidoptera and Diptera has provided broad information on the tissue remodelling processes that occur during larva–pupa–adult transition and made it possible to unravel the underlying regulatory pathways. This review summarizes recent knowledge on cell death mechanisms in Lepidoptera and other holometabolous insects, highlighting similarities and differences with Drosophila melanogaster , and discusses the role of apoptosis and autophagy in this developmental setting. This article is part of the theme issue ‘The evolution of complete metamorphosis'.

scholarly journals Mitochondrion-Dependent Cell Death in TDP-43 Proteinopathies

Biomedicines ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 376
Author(s):  
Chantal B. Lucini ◽  
Ralf J. Braun
Keyword(s):  
Cell Death ◽  
Oxygen Species ◽  
In Vivo Models ◽  
Dependent Cell ◽  
Cell Death Mechanisms ◽  
Sting Pathway ◽  
Mitochondrial Membrane Permeabilization

In the last decade, pieces of evidence for TDP-43-mediated mitochondrial dysfunction in neurodegenerative diseases have accumulated. In patient samples, in vitro and in vivo models have shown mitochondrial accumulation of TDP-43, concomitantly with hallmarks of mitochondrial destabilization, such as increased production of reactive oxygen species (ROS), reduced level of oxidative phosphorylation (OXPHOS), and mitochondrial membrane permeabilization. Incidences of TDP-43-dependent cell death, which depends on mitochondrial DNA (mtDNA) content, is increased upon ageing. However, the molecular pathways behind mitochondrion-dependent cell death in TDP-43 proteinopathies remained unclear. In this review, we discuss the role of TDP-43 in mitochondria, as well as in mitochondrion-dependent cell death. This review includes the recent discovery of the TDP-43-dependent activation of the innate immunity cyclic GMP-AMP synthase/stimulator of interferon genes (cGAS/STING) pathway. Unravelling cell death mechanisms upon TDP-43 accumulation in mitochondria may open up new opportunities in TDP-43 proteinopathy research.

scholarly journals Primary and Secondary Cone Cell Death Mechanisms in Inherited Retinal Diseases and Potential Treatment Options

2022 ◽  
Vol 23 (2) ◽  
pp. 726
Author(s):  
Alicia A. Brunet ◽  
Alan R. Harvey ◽  
Livia S. Carvalho
Keyword(s):  
Quality Of Life ◽  
Cell Death ◽  
Effective Treatment ◽  
Treatment Options ◽  
Retinal Diseases ◽  
Potential Treatment ◽  
Cone Cell ◽  
Similarities And Differences ◽  
Cell Death Mechanisms

Inherited retinal diseases (IRDs) are a leading cause of blindness. To date, 260 disease-causing genes have been identified, but there is currently a lack of available and effective treatment options. Cone photoreceptors are responsible for daylight vision but are highly susceptible to disease progression, the loss of cone-mediated vision having the highest impact on the quality of life of IRD patients. Cone degeneration can occur either directly via mutations in cone-specific genes (primary cone death), or indirectly via the primary degeneration of rods followed by subsequent degeneration of cones (secondary cone death). How cones degenerate as a result of pathological mutations remains unclear, hindering the development of effective therapies for IRDs. This review aims to highlight similarities and differences between primary and secondary cone cell death in inherited retinal diseases in order to better define cone death mechanisms and further identify potential treatment options.

scholarly journals The Nucleus/Mitochondria-Shuttling LncRNAs Function as New Epigenetic Regulators of Mitophagy in Cancer

2021 ◽  
Vol 9 ◽  
Author(s):  
Yan Li ◽  
Wei Li ◽  
Andrew R. Hoffman ◽  
Jiuwei Cui ◽  
Ji-Fan Hu
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Cancer Cells ◽  
Recent Progress ◽  
Regulatory Pathways ◽  
Tumor Cell Survival ◽  
Non Coding Rnas ◽  
Epigenetic Regulators ◽  
Malignant Behavior

Mitophagy is a specialized autophagic pathway responsible for the selective removal of damaged or dysfunctional mitochondria by targeting them to the autophagosome in order to maintain mitochondria quality. The role of mitophagy in tumorigenesis has been conflicting, with the process both supporting tumor cell survival and promoting cell death. Cancer cells may utilize the mitophagy pathway to augment their metabolic requirements and resistance to cell death, thereby leading to increased cell proliferation and invasiveness. This review highlights major regulatory pathways of mitophagy involved in cancer. In particular, we summarize recent progress regarding how nuclear-encoded long non-coding RNAs (lncRNAs) function as novel epigenetic players in the mitochondria of cancer cells, affecting the malignant behavior of tumors by regulating mitophagy. Finally, we discuss the potential application of regulating mitophagy as a new target for cancer therapy.

Macrophage recruitment during limb development and wound healing in the embryonic and foetal mouse

1994 ◽  
Vol 107 (5) ◽  
pp. 1159-1167 ◽  
Author(s):  
J. Hopkinson-Woolley ◽  
D. Hughes ◽  
S. Gordon ◽  
P. Martin
Keyword(s):  
Wound Healing ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Limb Development ◽  
Close Association ◽  
Active Role ◽  
Tissue Remodelling ◽  
Fibroblastic Cells ◽  
Made In

Macrophages play a pivotal role in the adult inflammatory response to wounding. They are directly responsible for cellular debridement and, by providing a source of growth factors and cytokines, they recruit other inflammatory and fibroblastic cells and influence cell proliferation and tissue remodelling. In this paper we investigate the role of macrophages in clearing areas of programmed cell death in the developing embryo and also their role in embryonic and foetal wound healing. Immunocytochemistry using the monocyte/macrophage-specific monoclonal antibody, F4/80, reveals a close association between areas of programmed cell death in the remodelling interdigital regions of the mouse footplate and of F4/80-positive cells, suggesting that monocyte-derived macrophages, and not locally recruited fibroblastic cells, as previously believed, are responsible for phagocytosing and clearing areas of interdigital apoptosis. Our studies of wound healing reveal that macrophages are not recruited to, and therefore cannot be playing an active role in the healing of, excisional wounds made in the mouse embryo at any stage up until E14.5. Beyond this transition stage we see a significant recruitment of macrophages within 12 hours of wounding. We find that macrophages can be attracted to wounds in earlier embryos if the wound results in significant cell death such as after burning.

scholarly journals The Role of Neutrophil NETosis in Organ Injury: Novel Inflammatory Cell Death Mechanisms

Inflammation ◽  
2020 ◽  
Vol 43 (6) ◽  
pp. 2021-2032 ◽  
Author(s):  
Zhen Cahilog ◽  
Hailin Zhao ◽  
Lingzhi Wu ◽  
Azeem Alam ◽  
Shiori Eguchi ◽  
...  
Keyword(s):  
Cell Death ◽  
Organ Injury ◽  
Microbial Function ◽  
Regulated Cell Death ◽  
Therapeutic Measures ◽  
Unexplored Area ◽  
Decondensed Chromatin ◽  
Cell Death Mechanisms ◽  
The Brain

Abstract NETosis is a type of regulated cell death dependent on the formation of neutrophil extracellular traps (NET), where net-like structures of decondensed chromatin and proteases are produced by polymorphonuclear (PMN) granulocytes. These structures immobilise pathogens and restrict them with antimicrobial molecules, thus preventing their spread. Whilst NETs possess a fundamental anti-microbial function within the innate immune system under physiological circumstances, increasing evidence also indicates that NETosis occurs in the pathogenic process of other disease type, including but not limited to atherosclerosis, airway inflammation, Alzheimer’s and stroke. Here, we reviewed the role of NETosis in the development of organ injury, including injury to the brain, lung, heart, kidney, musculoskeletal system, gut and reproductive system, whilst therapeutic agents in blocking injuries induced by NETosis in its primitive stages were also discussed. This review provides novel insights into the involvement of NETosis in different organ injuries, and whilst potential therapeutic measures targeting NETosis remain a largely unexplored area, these warrant further investigation.

scholarly journals Complete metamorphosis of insects

2019 ◽  
Vol 374 (1783) ◽  
pp. 20190063 ◽  
Author(s):  
Jens Rolff ◽  
Paul R. Johnston ◽  
Stuart Reynolds
Keyword(s):  
Adult Stage ◽  
Pupal Stage ◽  
Life Stages ◽  
Micro Ct ◽  
Larval Form ◽  
Theme Issue ◽  
The Cost ◽  
Ephemeral Resources ◽  
Complete Metamorphosis

The majority of described hexapod species are holometabolous insects, undergoing an extreme form of metamorphosis with an intercalated pupal stage between the larva and adult, in which organs and tissues are extensively remodelled and in some cases completely rebuilt. Here, we review how and why this developmental strategy has evolved. While there are many theories explaining the evolution of metamorphosis, many of which fit under the hypothesis of decoupling of life stages, there are few clear adaptive hypotheses on why complete metamorphosis evolved. We propose that the main adaptive benefit of complete metamorphosis is decoupling between growth and differentiation. This facilitates the exploitation of ephemeral resources and enhances the probability of the metamorphic transition escaping developmental size thresholds. The evolution of complete metamorphosis comes at the cost of exposure to predators, parasites and pathogens during pupal life and requires specific adaptations of the immune system at this time. Moreover, metamorphosis poses a challenge for the maintenance of symbionts and the gut microbiota, although it may also offer the benefit of allowing an extensive change in microbiota between the larval and adult stages. The regulation of metamorphosis by two main players, ecdysone and juvenile hormone, and the related signalling cascades are now relatively well understood. The mechanics of metamorphosis have recently been studied in detail because of the advent of micro-CT and research into the role of cell death in remodelling tissues and organs. We support the argument that the adult stage must necessarily have preceded the larval form of the insect. We do not resolve the still contentious question of whether the larva of insects in general originated through the modification of existing preadult forms or through heterochrony as a modified embryonic stage (pronymph), nor whether the holometabolous pupa arose as a modified hemimetabolous final stage larva. This article is part of the theme issue ‘The evolution of complete metamorphosis’.

scholarly journals Reactive Oxygen Species (ROS) Regulates Different Types of Cell Death by Acting as a Rheostat

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Gloria E. Villalpando-Rodriguez ◽  
Spencer B. Gibson
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cellular Signaling ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Regulatory Pathways ◽  
Disease States ◽  
Different Types ◽  
Response To Stress ◽  
Cell Death Mechanisms

Reactive oxygen species (ROS) are essential for cellular signaling and response to stress. The level of ROS and the type of ROS determine the ability of cells to undergo cell death. Furthermore, dysregulation of the antioxidant pathways is associated with many diseases. It has become apparent that cell death can occur through different mechanisms leading to the classifications of different types of cell death such as apoptosis, ferroptosis, and necroptosis. ROS play essential roles in all forms of cell death, but it is only now coming into focus that ROS control and determine the type of cell death that occurs in any given cell. Indeed, ROS may act as a rheostat allowing different cell death mechanisms to be engaged and crosstalk with different cell death types. In this review, we will describe the ROS regulatory pathways and how they control different types of cell death under normal and disease states. We will also propose how ROS could provide a mechanism of crosstalk between cell death mechanisms and act as a rheostat determining the type of cell death.

Abstract TMP32: Ischemic Stroke Causes Vascular Regression in Type-II Diabetic Male Rats: Potential Role of Regulated Cell Death Mechanisms

Stroke ◽  
2018 ◽  
Vol 49 (Suppl_1) ◽  
Author(s):  
Yasir Abdul ◽  
Weiguo Li ◽  
Rebecca Ward ◽  
Sherif Hafez ◽  
Mohammed Abdelsaid ◽  
...  
Keyword(s):  
Cell Death ◽  
Ischemic Stroke ◽  
Potential Role ◽  
Male Rats ◽  
Type Ii ◽  
Regulated Cell Death ◽  
Cell Death Mechanisms
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