scholarly journals Mitochondria as a target and central hub of energy division during cold stress in insects

2022 ◽  
Vol 19 (1) ◽  
Author(s):  
Jan Lubawy ◽  
Szymon Chowański ◽  
Zbigniew Adamski ◽  
Małgorzata Słocińska
Keyword(s):  
Cold Stress ◽  
Current Knowledge ◽  
Mitochondrial Gene ◽  
Mitochondrial Pathway ◽  
Cellular Level ◽  
Insect Species ◽  
Experimental Conditions ◽  
Mitochondrial Homeostasis ◽  
Stress Injuries ◽  
Important Player

AbstractTemperature stress is one of the crucial factors determining geographical distribution of insect species. Most of them are active in moderate temperatures, however some are capable of surviving in extremely high as well as low temperatures, including freezing. The tolerance of cold stress is a result of various adaptation strategies, among others the mitochondria are an important player. They supply cells with the most prominent energy carrier—ATP, needed for their life processes, but also take part in many other processes like growth, aging, protection against stress injuries or cell death. Under cold stress, the mitochondria activity changes in various manner, partially to minimize the damages caused by the cold stress, partially because of the decline in mitochondrial homeostasis by chill injuries. In the response to low temperature, modifications in mitochondrial gene expression, mtDNA amount or phosphorylation efficiency can be observed. So far study also showed an increase or decrease in mitochondria number, their shape and mitochondrial membrane permeability. Some of the changes are a trigger for apoptosis induced via mitochondrial pathway, that protects the whole organism against chill injuries occurring on the cellular level. In many cases, the observed modifications are not unequivocal and depend strongly on many factors including cold acclimation, duration and severity of cold stress or environmental conditions. In the presented article, we summarize the current knowledge about insect response to cold stress focusing on the role of mitochondria in that process considering differences in results obtained in different experimental conditions, as well as depending on insect species. These differentiated observations clearly indicate that it is still much to explore. Graphical Abstract

scholarly journals Effects of Sex and 17 β-Estradiol on Cardiac Fibroblast Morphology and Signaling Activities In Vitro

Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2564
Author(s):  
Kelsey Watts ◽  
William J. Richardson
Keyword(s):  
Cardiac Fibrosis ◽  
Cardiac Fibroblasts ◽  
Cellular Level ◽  
Cellular Morphology ◽  
Structural Level ◽  
Experimental Conditions ◽  
Male And Female ◽  
Protein Protein Interaction ◽  
Complex Signaling

Several studies have demonstrated estrogen’s cardioprotective abilities in decreasing the fibrotic response of cardiac fibroblasts (CFs). However, the majority of these studies are not sex-specific, and those at the cellular level utilize tissue culture plastic, a substrate with a much higher stiffness than physiological conditions. Understanding the intrinsic differences between male and female CFs under more physiologically “healthy” conditions will help to elucidate the divergences in their complex signaling networks. We aimed to do this by conducting a sex-disaggregated analysis of changes in cellular morphology and relative levels of profibrotic signaling proteins in CFs cultured on 8 kPa stiffness plates with and without 17 β-estradiol (E2). Cyclic immunofluorescent analysis indicated that there was a negligible change in cellular morphology due to sex and E2 treatment and that the differences between male and female CFs occur at a biochemical rather than structural level. Several proteins corresponding to profibrotic activity had various sex-specific responses with and without E2 treatment. Single-cell correlation analysis exhibited varied protein–protein interaction across experimental conditions. These findings demonstrate the need for further research into the dimorphisms of male and female CFs to develop better tailored sex-informed prevention and treatment interventions of cardiac fibrosis.

scholarly journals Mitochondrial Quality Control Mechanisms and the PHB (Prohibitin) Complex

Cells ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 238 ◽  
Author(s):  
Blanca Hernando-Rodríguez ◽  
Marta Artal-Sanz
Keyword(s):  
Quality Control ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Stress Responses ◽  
Membrane Lipids ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Gene ◽  
Control Mechanisms ◽  
Mitochondrial Homeostasis ◽  
Mitochondrial Functions

Mitochondrial functions are essential for life, critical for development, maintenance of stem cells, adaptation to physiological changes, responses to stress, and aging. The complexity of mitochondrial biogenesis requires coordinated nuclear and mitochondrial gene expression, owing to the need of stoichiometrically assemble the oxidative phosphorylation (OXPHOS) system for ATP production. It requires, in addition, the import of a large number of proteins from the cytosol to keep optimal mitochondrial function and metabolism. Moreover, mitochondria require lipid supply for membrane biogenesis, while it is itself essential for the synthesis of membrane lipids. To achieve mitochondrial homeostasis, multiple mechanisms of quality control have evolved to ensure that mitochondrial function meets cell, tissue, and organismal demands. Herein, we give an overview of mitochondrial mechanisms that are activated in response to stress, including mitochondrial dynamics, mitophagy and the mitochondrial unfolded protein response (UPRmt). We then discuss the role of these stress responses in aging, with particular focus on Caenorhabditis elegans. Finally, we review observations that point to the mitochondrial prohibitin (PHB) complex as a key player in mitochondrial homeostasis, being essential for mitochondrial biogenesis and degradation, and responding to mitochondrial stress. Understanding how mitochondria responds to stress and how such responses are regulated is pivotal to combat aging and disease.

scholarly journals Acute Myeloid Leukemia Stem Cells: The Challenges of Phenotypic Heterogeneity

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3742
Author(s):  
Marlon Arnone ◽  
Martina Konantz ◽  
Pauline Hanns ◽  
Anna M. Paczulla Stanger ◽  
Sarah Bertels ◽  
...  
Keyword(s):  
Stem Cells ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Current Knowledge ◽  
Phenotypic Variability ◽  
Cellular Level ◽  
Patient Specific ◽  
Heterogeneous Landscape ◽  
Cells Of Origin ◽  
Acute Myeloid

Patients suffering from acute myeloid leukemia (AML) show highly heterogeneous clinical outcomes. Next to variabilities in patient-specific parameters influencing treatment decisions and outcome, this is due to differences in AML biology. In fact, different genetic drivers may transform variable cells of origin and co-exist with additional genetic lesions (e.g., as observed in clonal hematopoiesis) in a variety of leukemic (sub)clones. Moreover, AML cells are hierarchically organized and contain subpopulations of more immature cells called leukemic stem cells (LSC), which on the cellular level constitute the driver of the disease and may evolve during therapy. This genetic and hierarchical complexity results in a pronounced phenotypic variability, which is observed among AML cells of different patients as well as among the leukemic blasts of individual patients, at diagnosis and during the course of the disease. Here, we review the current knowledge on the heterogeneous landscape of AML surface markers with particular focus on those identifying LSC, and discuss why identification and targeting of this important cellular subpopulation in AML remains challenging.

The Role of Free Radicals in Traumatic Brain Injury

2012 ◽  
Vol 15 (3) ◽  
pp. 253-263 ◽  
Author(s):  
Karen M. O’Connell ◽  
Marguerite T. Littleton-Kearney
Keyword(s):  
Traumatic Brain Injury ◽  
Free Radicals ◽  
Free Radical ◽  
Brain Injury ◽  
Current Knowledge ◽  
Cellular Level ◽  
Secondary Brain Injury ◽  
Secondary Injury ◽  
The Military

Traumatic brain injury (TBI) is a significant cause of death and disability in both the civilian and the military populations. The primary impact causes initial tissue damage, which initiates biochemical cascades, known as secondary injury, that expand the damage. Free radicals are implicated as major contributors to the secondary injury. Our review of recent rodent and human research reveals the prominent role of the free radicals superoxide anion, nitric oxide, and peroxynitrite in secondary brain injury. Much of our current knowledge is based on rodent studies, and the authors identified a gap in the translation of findings from rodent to human TBI. Rodent models are an effective method for elucidating specific mechanisms of free radical-induced injury at the cellular level in a well-controlled environment. However, human TBI does not occur in a vacuum, and variables controlled in the laboratory may affect the injury progression. Additionally, multiple experimental TBI models are accepted in rodent research, and no one model fully reproduces the heterogeneous injury seen in humans. Free radical levels are measured indirectly in human studies based on assumptions from the findings from rodent studies that use direct free radical measurements. Further study in humans should be directed toward large samples to validate the findings in rodent studies. Data obtained from these studies may lead to more targeted treatment to interrupt the secondary injury cascades.

scholarly journals Impact of Salmonella enterica Type III Secretion System Effectors on the Eukaryotic Host Cell

2012 ◽  
Vol 2012 ◽  
pp. 1-36 ◽  
Author(s):  
Francisco Ramos-Morales
Keyword(s):  
Type Iii Secretion ◽  
Salmonella Enterica ◽  
Current Knowledge ◽  
Cellular Level ◽  
Host Cells ◽  
Secretion Systems ◽  
Type Iii ◽  
Cellular Processes ◽  
Type Iii Secretion Systems ◽  
Near Future

Type III secretion systems are molecular machines used by many Gram-negative bacterial pathogens to inject proteins, known as effectors, directly into eukaryotic host cells. These proteins manipulate host signal transduction pathways and cellular processes to the pathogen’s advantage. Salmonella enterica possesses two virulence-related type III secretion systems that deliver more than forty effectors. This paper reviews our current knowledge about the functions, biochemical activities, host targets, and impact on host cells of these effectors. First, the concerted action of effectors at the cellular level in relevant aspects of the interaction between Salmonella and its hosts is analyzed. Then, particular issues that will drive research in the field in the near future are discussed. Finally, detailed information about each individual effector is provided.

scholarly journals Mitochondrial Heterogeneity in the Brain at the Cellular Level

1998 ◽  
Vol 18 (3) ◽  
pp. 231-237 ◽  
Author(s):  
Ursula Sonnewald ◽  
Leif Hertz ◽  
Arne Schousboe
Keyword(s):  
Amino Acid ◽  
Current Knowledge ◽  
Cell Types ◽  
Cellular Level ◽  
Mitochondrial Structure ◽  
Cell Type Specific ◽  
Mitochondrial Heterogeneity ◽  
Specific Tissue ◽  
And Function ◽  
The Brain

Classically, compartmentation of glutamate metabolism in the brain is associated with the fact that neurons and glia exhibit distinct differences with regard to metabolism of this amino acid. The recent use of 13C-labeled compounds to study this metabolism in conjunction with the availability of cell type-specific tissue culture modes has led to the notion that such compartmentation may even be present in individual cell types, neurons as well as glia. To better understand and explain this, it is proposed that mitochondrial heterogeneity may exist resulting in tricarboxylic acid cycles with different properties regarding cycling rates and ratio as well as coupling to amino acid biosynthesis, primarily involving glutamate and aspartate. These hypotheses are evaluated in the light of current knowledge about mitochondrial structure and function.

scholarly journals Effects of Sex and 17β-Estradiol on Cardiac Fibroblast Morphology and Signaling Activities in vitro

2021 ◽  
Author(s):  
Kelsey Watts ◽  
Will Richardson
Keyword(s):  
Cardiac Fibrosis ◽  
Cardiac Fibroblasts ◽  
Cellular Level ◽  
Cellular Morphology ◽  
Structural Level ◽  
Experimental Conditions ◽  
Male And Female ◽  
Protein Protein Interaction ◽  
Complex Signaling

Several studies have demonstrated estrogen’s cardioprotective abilities in decreasing the fibrotic response of cardiac fibroblasts (CFs). However, the majority of these studies are not sex-specific, and those at the cellular level utilize tissue culture plastic, a substrate that has a stiffness much higher than physiological conditions. Understanding the intrinsic differences between male and female CFs under more physiologically “healthy” conditions will help to elucidate the divergences in their complex signaling networks. We aimed to do this by conducting sex-disaggregated analysis of changes in cellular morphology and relative concentrations of profibrotic signaling proteins in CFs cultured on 8kPa stiffness plates with and without 17-β estradiol (E2). Cyclic immunofluorescent analysis indicated that there is a negligible change in cellular morphology due to sex and E2 treatment and that the differences between male and female CFs are occurring at a biochemical rather than structural level. Several proteins corresponding to profibrotic activity had various sex-specific responses with and without E2 treatment. Single-cell correlation analysis exhibited varied protein-protein interaction across experimental conditions. These findings demonstrate the need for further research into the dimorphisms of male and female CFs to develop better tailored, sex-informed prevention and treatment interventions of cardiac fibrosis.

scholarly journals Mitochondrial Protein PGAM5 Emerges as a New Regulator in Neurological Diseases

2021 ◽  
Vol 14 ◽  
Author(s):  
Min-Zong Liang ◽  
Ting-Ling Ke ◽  
Linyi Chen
Keyword(s):  
Current Knowledge ◽  
Neurological Diseases ◽  
Mitochondrial Protein ◽  
Phosphoglycerate Mutase ◽  
Future Perspectives ◽  
Cellular Physiology ◽  
Mitochondrial Regulation ◽  
Mitochondrial Homeostasis ◽  
Neuronal Tissues ◽  
External Stimuli

As mitochondrial dysfunction has increasingly been implicated in neurological diseases, much of the investigation focuses on the response of the mitochondria. It appears that mitochondria can respond to external stimuli speedy fast, in seconds. Understanding how mitochondria sense the signal and communicate with cytosolic pathways are keys to understand mitochondrial regulation in diseases or in response to trauma. It was not until recently that a novel mitochondrial protein, phosphoglycerate mutase family member 5 (PGAM5) has emerged to be a new regulator of mitochondrial homeostasis. Although controversial results reveal beneficial as well as detrimental roles of PGAM5 in cancers, these findings also suggest PGAM5 may have diverse regulation on cellular physiology. Roles of PGAM5 in neuronal tissues remain to be uncovered. This review discusses current knowledge of PGAM5 in neurological diseases and provides future perspectives.

scholarly journals Tuning the Cell and Biological Tissue Environment through Magneto-Active Materials

2021 ◽  
Vol 11 (18) ◽  
pp. 8746
Author(s):  
Jorge Gonzalez-Rico ◽  
Emanuel Nunez-Sardinha ◽  
Leticia Valencia ◽  
Angel Arias ◽  
Arrate Muñoz-Barrutia ◽  
...  
Keyword(s):  
Smart Materials ◽  
Current Knowledge ◽  
Bone Development ◽  
Polymeric Materials ◽  
Cellular Level ◽  
Special Focus ◽  
Collective Cell Migration ◽  
Biological Processes ◽  
Novel Applications ◽  
Cell Collective

This review focuses on novel applications based on multifunctional materials to actuate biological processes. The first section of the work revisits the current knowledge on mechanically dependent biological processes across several scales from subcellular and cellular level to the cell-collective scale (continuum approaches). This analysis presents a wide variety of mechanically dependent biological processes on nervous system behaviour; bone development and healing; collective cell migration. In the second section, this review presents recent advances in smart materials suitable for use as cell substrates or scaffolds, with a special focus on magneto-active polymers (MAPs). Throughout the manuscript, both experimental and computational methodologies applied to the different treated topics are reviewed. Finally, the use of smart polymeric materials in bioengineering applications is discussed.

scholarly journals Involvement of Mitochondrial Dynamics and Mitophagy in Sevoflurane-Induced Cell Toxicity

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Ming Li ◽  
Jiguang Guo ◽  
Hongjie Wang ◽  
Yuzhen Li
Keyword(s):  
Pediatric Surgery ◽  
Cell Function ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Pathway ◽  
Cell Toxicity ◽  
Mitochondrial Homeostasis ◽  
Unpleasant Odor ◽  
Inhalational Anesthetic ◽  
Indispensable Tool ◽  
The Stability

General anesthesia is a powerful and indispensable tool to ensure the accomplishment of surgical procedures or clinical examinations. Sevoflurane as an inhalational anesthetic without unpleasant odor is commonly used in clinical practice, especially for pediatric surgery. However, the toxicity caused by sevoflurane has gained growing attention. Mitochondria play a key role in maintaining cellular metabolism and survival. To maintain the stability of mitochondrial homeostasis, they are constantly going through fusion and fission. Also, damaged mitochondria need to be degraded by autophagy, termed as mitophagy. Accumulating evidence proves that sevoflurane exposure in young age could lead to cell toxicity by triggering the mitochondrial pathway of apoptosis, inducing the abnormalities of mitochondrial dynamics and mitophagy. In the present review, we focus on the current understanding of mitochondrial apoptosis, dynamics and mitophagy in cell function, the implications for cell toxicity in response to sevoflurane, and their underlying potential mechanisms.

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