Role of Extracellular Adenosine Triphosphate in Human Skin

2004 ◽  
Vol 8 (2) ◽  
pp. 90-96 ◽  
Author(s):  
Aton M. Holzer ◽  
Richard D. Granstein
Keyword(s):  
Human Skin ◽  
Adenosine Triphosphate ◽  
Current Knowledge ◽  
Extracellular Atp ◽  
Cell Type ◽  
Skin Injury ◽  
Direct Role ◽  
Extracellular Adenosine ◽  
Proliferation And Apoptosis

Background: The nucleotide adenosine triphosphate (ATP) has long been known to drive and participate in countless intracellular processes. Extracellular ATP and its metabolite adenosine have also been shown to exert a variety of effects on nearly every cell type in human skin. Knowledge of the sources and effects of extracellular ATP in human skin may help shape new therapies for skin injury, inflammation, and numerous other cutaneous disorders. Objective: The objective of this review is to introduce the reader to current knowledge regarding the sources and effects of extracellular ATP in human skin and to outline areas in which further research is necessary to clarify the nature and mechanism of these effects. Conclusion: Extracellular ATP seems to play a direct role in triggering skin inflammatory, regenerative, and fibrotic responses to mechanical injury, an indirect role in melanocyte proliferation and apoptosis, and a complex role in Langerhans cell-directed adaptive immunity.

scholarly journals The Intricate Role of p53 in Adipocyte Differentiation and Function

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2621
Author(s):  
Yun Kyung Lee ◽  
Yu Seong Chung ◽  
Ji Hye Lee ◽  
Jin Mi Chun ◽  
Jun Hong Park
Keyword(s):  
Adipocyte Differentiation ◽  
Metabolic Diseases ◽  
Metabolic Stress ◽  
Health Concern ◽  
Metabolic Dysfunction ◽  
Direct Role ◽  
Proliferation And Apoptosis ◽  
Response To Stress ◽  
And Function

For more than three decades, numerous studies have demonstrated the function of p53 in cell cycle, cellular senescence, autophagy, apoptosis, and metabolism. Among diverse functions, the essential role of p53 is to maintain cellular homeostatic response to stress by regulating proliferation and apoptosis. Recently, adipocytes have been studied with increasing intensity owing to the increased prevalence of metabolic diseases posing a serious public health concern and because metabolic dysfunction can directly induce tumorigenesis. The prevalence of metabolic diseases has steadily increased worldwide, and a growing interest in these diseases has led to the focus on the role of p53 in metabolism and adipocyte differentiation with or without metabolic stress. However, our collective understanding of the direct role of p53 in adipocyte differentiation and function remains insufficient. Therefore, this review focuses on the newly discovered roles of p53 in adipocyte differentiation and function.

scholarly journals Extracellular adenosine triphosphate increases cation permeability of chronic lymphocytic leukemic lymphocytes

Blood ◽  
1989 ◽  
Vol 73 (5) ◽  
pp. 1316-1323 ◽  
Author(s):  
JS Wiley ◽  
GR Dubyak
Keyword(s):  
Adenosine Triphosphate ◽  
Fold Increase ◽  
Normal Subjects ◽  
Peripheral Blood Lymphocytes ◽  
Extracellular Atp ◽  
Total Cell ◽  
Lymphocytic Leukemia ◽  
Maximal Response ◽  
Extracellular Adenosine ◽  
Cation Permeability

Abstract Extracellular adenosine triphosphate (ATP) is known to reversibly increase the cation permeability of a variety of freshly isolated and cultured cell types. In this study the effects of extracellular ATP were studied using peripheral blood lymphocytes (PBL) isolated from both normal subjects and from patients with chronic lymphocytic leukemia (CLL). Changes in the permeability to Na+, Rb+, and Li+ ions were measured using conventional isotope and flame photometry techniques. In addition, changes in cytosolic (Ca2+) were fluorimetrically monitored to assess possible changes in net Ca2+ influx. ATP produced a 12-fold increase in 22Na+ influx into CLL cells but only a 3.5-fold increase in this flux in PBL cells. A maximal response was produced by 0.1 mmol/L ATP in the absence of Mg2+, while a twofold molar excess of Mg2+ over ATP abolished the response. ATP had no effect on the passive (ouabain-insensitive) 86Rb+ influx into PBL cells but stimulated this flux by fivefold in the CLL cells. Li+ influx into CLL cells was also stimulated threefold by ATP. Under these same conditions ATP also produced a net increase in total cell Na and a decrease in total cell K in the CLL cells. Exclusion of two normally impermeable dyes, trypan blue and ethidium bromide, was not altered in the ATP-treated CLL cells. Finally, extracellular ATP (3 mmol/L) produced no significant change in the cytosolic (Ca2+) of normal, monocyte-depleted populations of PBL. Conversely, this same concentration of ATP produced a very rapid (complete within 30 seconds) and a significant (an average threefold peak change) increase in the cytosolic (Ca2+) of cell preparations derived from five out of nine CLL patients. In these latter CLL cells, the ATP-induced elevation in cytosolic (Ca2+) appeared to be due to a net increase in Ca2+ influx, since no elevations were observed when the extracellular (Ca2+) was reduced to less than 0.1 mmol/L. These actions of ATP were specific in that equimolar concentrations of other nucleotides were without effect. These data indicate that treatment of CLL lymphocytes with extracellular ATP4 produces large increases in cation permeability. In contrast, there is less or no ATP-induced permeabilization of normal PBL.

The Role of Extracellular Adenosine Triphosphate in Ischemic Organ Injury

2016 ◽  
Vol 44 (5) ◽  
pp. 1000-1012 ◽  
Author(s):  
Hailin Zhao ◽  
Susan Kilgas ◽  
Azeem Alam ◽  
Shiori Eguchi ◽  
Daqing Ma
Keyword(s):  
Adenosine Triphosphate ◽  
Organ Injury ◽  
Extracellular Adenosine

scholarly journals Pleiotropic Role of Notch Signaling in Human Skin Diseases

2020 ◽  
Vol 21 (12) ◽  
pp. 4214 ◽  
Author(s):  
Rossella Gratton ◽  
Paola Maura Tricarico ◽  
Chiara Moltrasio ◽  
Ana Sofia Lima Estevão de Oliveira ◽  
Lucas Brandão ◽  
...  
Keyword(s):  
Notch Signaling ◽  
Human Skin ◽  
Hidradenitis Suppurativa ◽  
Target Genes ◽  
Skin Diseases ◽  
Current Knowledge ◽  
Cellular Mechanisms ◽  
Degos Disease ◽  
Cellular Pathways

Notch signaling orchestrates the regulation of cell proliferation, differentiation, migration and apoptosis of epidermal cells by strictly interacting with other cellular pathways. Any disruption of Notch signaling, either due to direct mutations or to an aberrant regulation of genes involved in the signaling route, might lead to both hyper- or hypo-activation of Notch signaling molecules and of target genes, ultimately inducing the onset of skin diseases. The mechanisms through which Notch contributes to the pathogenesis of skin diseases are multiple and still not fully understood. So far, Notch signaling alterations have been reported for five human skin diseases, suggesting the involvement of Notch in their pathogenesis: Hidradenitis Suppurativa, Dowling Degos Disease, Adams–Oliver Syndrome, Psoriasis and Atopic Dermatitis. In this review, we aim at describing the role of Notch signaling in the skin, particularly focusing on the principal consequences associated with its alterations in these five human skin diseases, in order to reorganize the current knowledge and to identify potential cellular mechanisms in common between these pathologies.

scholarly journals The Human Carbonic Anhydrase II in Platelets: An Underestimated Field of Its Activity

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Maciej Jakubowski ◽  
Ewa Szahidewicz-Krupska ◽  
Adrian Doroszko
Keyword(s):  
Carbonic Anhydrase ◽  
Current Knowledge ◽  
Short Review ◽  
Carbonic Anhydrase Ii ◽  
Carbonic Anhydrases ◽  
Direct Role ◽  
Novel Strategy ◽  
The Impact ◽  
First Time

Carbonic anhydrases constitute a group of enzymes that catalyse reversible hydration of carbon dioxide leading to the formation of bicarbonate and proton. The platelet carbonic anhydrase II (CAII) was described for the first time in the '80s of the last century. Nevertheless, its direct role in platelet physiology and pathology still remains poorly understood. The modulation of platelet CAII action as a therapeutic approach holds promise as a novel strategy to reduce the impact of cardiovascular diseases. This short review paper summarises the current knowledge regarding the role of human CAII in regulating platelet function. The potential future directions considering this enzyme as a potential drug target and important pathophysiological chain in platelet-related disorders are described.

scholarly journals MicroRNAs as Novel Regulators of Neuroinflammation

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Dominika Justyna Ksiazek-Winiarek ◽  
Magdalena Justyna Kacperska ◽  
Andrzej Glabinski
Keyword(s):  
Multiple Sclerosis ◽  
Current Knowledge ◽  
Neurological Diseases ◽  
Small Noncoding Rnas ◽  
Cellular Processes ◽  
Proliferation And Apoptosis ◽  
Genetic And Environmental Factors ◽  
Ms Pathogenesis ◽  
Fine Tune

MicroRNAs are relatively recently discovered class of small noncoding RNAs, which function as important regulators of gene expression. They fine-tune protein expression either by translational inhibition or mRNA degradation. MicroRNAs act as regulators of diverse cellular processes, such as cell differentiation, proliferation, and apoptosis. Their defective biogenesis or function has been identified in various pathological conditions, like inflammation, neurodegeneration, or autoimmunity. Multiple sclerosis is one of the predominated debilitating neurological diseases affecting mainly young adults. It is a multifactorial disorder of as yet unknown aetiology. As far, it is suggested that interplay between genetic and environmental factors is responsible for MS pathogenesis. The role of microRNAs in this pathology is now extensively studied. Here, we want to review the current knowledge of microRNAs role in multiple sclerosis.

scholarly journals Modulation of platelet function by extracellular adenosine triphosphate

Blood ◽  
1989 ◽  
Vol 74 (3) ◽  
pp. 984-993 ◽  
Author(s):  
G Soslau ◽  
J Parker
Keyword(s):  
Platelet Aggregation ◽  
Adenosine Triphosphate ◽  
Platelet Function ◽  
Surface Membrane ◽  
Adenosine Diphosphate ◽  
Extracellular Atp ◽  
Surface Proteins ◽  
Intracellular Camp ◽  
Extracellular Adenosine ◽  
Camp Levels

Abstract A potential physiologic role of extracellular adenosine triphosphate (ATP) on platelet function is proposed in this report. It is widely accepted that ATP competitively inhibits adenosine diphosphate (ADP)- induced platelet aggregation. Our observations of platelet aggregation with the agonists, collagen, epinephrine, and ADP in the presence of 180 mumol/L ATP could support this competitive nature of ATP. However, the disaggregation of maximally aggregated platelets induced by ATP, theophylline, or ATP plus theophylline indicates that additional mechanisms of ATP action may be present. Extracellular gamma-32P-ATP (7 pmol) labels surface-membrane proteins in intact platelets as demonstrated by several criteria. The reaction is Ca++-dependent. Stimulation by calcium occurs in the physiologic range of 1 to 5 mmol/L. Significant levels of phosphorylation occur within one minute with near maximal levels reached by five minutes. Platelet cyclic AMP (cAMP) levels were elevated in a dose-dependent fashion in cells incubated for four minutes with increasing amounts of extracellular ATP (18 to 540 nmol). The addition of ATP plus theophylline resulted in a synergistic stimulation of cAMP levels. ATP was not being hydrolyzed to adenosine by plasma nucleotidases, as demonstrated by the lack of effect of ten U of adenosine deaminase. The phosphorylation of surface proteins by extracellular ATP released from activated platelets may modulate platelet responsiveness to agonists at distances removed from the site of vascular injury. Phosphorylation may also play a role in signal transduction to regulate the levels of intracellular cAMP, which further inhibits platelet activation.

scholarly journals Molecular Background of miRNA Role in Asthma and COPD: An Updated Insight

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Izabela Szymczak ◽  
Joanna Wieczfinska ◽  
Rafal Pawliczak
Keyword(s):  
Gene Expression Regulation ◽  
Current Knowledge ◽  
Airway Remodeling ◽  
Chronic Obstructive ◽  
Cell Type ◽  
Obstructive Pulmonary Disease ◽  
Airway Diseases ◽  
Antigen Presenting ◽  
Significant Health

Inflammatory airway diseases are a significant health problems requiring new approaches to the existing therapies and addressing fundamental issues. Difficulties in developing effective therapeutic strategies might be caused by lack of understanding of their exact molecular mechanism. MicroRNAs (miRNAs) are a class of regulators that already revolutionized the view of gene expression regulation. A cumulating number of investigations show a pivotal role of miRNAs in the pathogenesis of asthma, chronic obstructive pulmonary disease (COPD), or airway remodeling through the regulation of many pathways involved in their pathogenesis. Expression changes of several miRNAs have also been found to play a role in the development and/or improvement in asthma or COPD. Still, relatively little is known about the role of miRNAs in inflammatory disorders. The microRNA profiles may differ depending on the cell type or antigen-presenting cell. Based on the newest literature, this review discusses the current knowledge concerning miRNA contribution and influence on lung inflammation and chosen inflammatory airway diseases: asthma and COPD.

Staphylococcus epidermidis: A Potential New Player in the Physiopathology of Acne?

Dermatology ◽  
2019 ◽  
Vol 235 (4) ◽  
pp. 287-294 ◽  
Author(s):  
Jean-Paul Claudel ◽  
Nicole Auffret ◽  
Marie-Thérèse Leccia ◽  
Florence Poli ◽  
Stéphane Corvec ◽  
...  
Keyword(s):  
Human Skin ◽  
Staphylococcus Epidermidis ◽  
Skin Disease ◽  
Potential Role ◽  
Current Knowledge ◽  
Treatment Options ◽  
Skin Microbiome ◽  
Cutibacterium Acnes ◽  
Skin Commensals

Background: Cutibacterium acnes has been identified as one of the main triggers of acne. However, increasing knowledge of the human skin microbiome raises questions about the role of other skin commensals, such as Staphylococcus epidermidis, in the physiopathology of this skin disease. Summary: This review provides an overview of current knowledge of the potential role of S. epidermidis in the physiopathology of acne. Recent research indicates that acne might be the result of an unbalanced equilibrium between C. acnes and S. epidermidis,according to dedicated interactions. Current treatments act on C. acnesonly. Other treatment options may be considered, such as probiotics derived from S. epidermidis to restore the naturally balanced microbiota or through targeting the regulation of the host’s AMP mediators. Key Messages: Research seems to confirm the beneficial role of S. epidermidis in acne by limiting C. acnes over-colonisation and inflammation.

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