Signal pathways involved in the biological effects of sulfur dioxide

2015 ◽  
Vol 764 ◽  
pp. 94-99 ◽  
Author(s):  
Xin-Bao Wang ◽  
Jun-Bao Du ◽  
Hong Cui
Keyword(s):  
Sulfur Dioxide ◽  
Biological Effects ◽  
Signal Pathways

Sulfur dioxide induces vascular relaxation through PI3K/Akt/eNOS and NO/cGMP signaling pathways in rats

2020 ◽  
Vol 39 (8) ◽  
pp. 1108-1117
Author(s):  
Q Zhang ◽  
W Lyu ◽  
M Yu ◽  
Y Niu
Keyword(s):  
Nitric Oxide ◽  
Sulfur Dioxide ◽  
Signaling Pathways ◽  
Underlying Mechanism ◽  
Cyclic Guanosine Monophosphate ◽  
Rat Aorta ◽  
Guanosine Monophosphate ◽  
Signal Pathways ◽  
Atmospheric Pollutant ◽  
Protein Levels

Sulfur dioxide (SO2) is a common exogenous atmospheric pollutant. Studies have shown that SO2 can cause vasodilation as a gas signaling molecule, but the specific signaling pathways are not well understood. This study aimed to explore the underlying mechanism behind the effects of SO2 on vasodilation of isolated rat aorta. The results showed that when the dose of SO2 was 30 μM, the vasodilation of endothelium-intact rings was partially suppressed by LY294002 and NG-nitro-l-arginine methyl ester, and the protein levels of phosphoinositide 3-kinase (PI3K), p-Akt, and p-endothelial nitric oxide synthase ( p-eNOS) were significantly increased. When the dose of SO2 was 300 μM or 1500 μM, the vasodilation of endothelium-denuded rings did not change after application of the inhibitor, but the protein levels of PI3K, p-Akt, and p-eNOS were significantly decreased, and the activity of NOS and the level of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) were significantly increased. We speculate that the mechanism of SO2-induced vasodilatation likely involved the endothelial PI3K/Akt/eNOS and NO/cGMP signal pathways. In addition, at the concentration of 1500 μM, SO2 markedly increased the level of caspase-3 and caspase-9. The results suggest that high concentrations of SO2 may cause damage to blood vessels. This study will help to further inform the etiologies of SO2-related cardiovascular disease.

Sulfur Dioxide: Endogenous Generation, Biological Effects, Detection, and Therapeutic Potential

2021 ◽  
Author(s):  
Yaqian Huang ◽  
Heng Zhang ◽  
Boyang Lv ◽  
Chaoshu Tang ◽  
Junbao Du ◽  
...  
Keyword(s):  
Sulfur Dioxide ◽  
Therapeutic Potential ◽  
Biological Effects

scholarly journals Biological effects data: Fluoride and sulfur dioxide

1975 ◽  
Author(s):  
R.L. Holton ◽  
R.J. Ulbricht ◽  
J.B. Morgan
Keyword(s):  
Sulfur Dioxide ◽  
Biological Effects

Environmental Estrogens and Their Biological Effects through GPER Mediated Signal Pathways

2021 ◽  
Vol 278 ◽  
pp. 116826
Author(s):  
Yu Qie ◽  
Weiping Qin ◽  
Keda Zhao ◽  
Chang Liu ◽  
Lixia Zhao ◽  
...  
Keyword(s):  
Biological Effects ◽  
Environmental Estrogens ◽  
Signal Pathways

scholarly journals Specificity and spatial dynamics of protein kinase A signaling organized by A-kinase-anchoring proteins

2010 ◽  
Vol 44 (5) ◽  
pp. 271-284 ◽  
Author(s):  
Guillaume Pidoux ◽  
Kjetil Taskén
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Biological Effects ◽  
Spatial Dynamics ◽  
Signal Pathways ◽  
Post Translational Modification ◽  
Anchoring Proteins ◽  
High Level ◽  
Pka Pathway ◽  
Kinase A

Protein phosphorylation is the most common post-translational modification observed in cell signaling and is controlled by the balance between protein kinase and phosphatase activities. The cAMP–protein kinase A (PKA) pathway is one of the most studied and well-known signal pathways. To maintain a high level of specificity, the cAMP–PKA pathway is tightly regulated in space and time. A-kinase-anchoring proteins (AKAPs) target PKA to specific substrates and distinct subcellular compartments providing spatial and temporal specificity in the mediation of biological effects controlled by the cAMP–PKA pathway. AKAPs also serve as scaffolding proteins that assemble PKA together with signal terminators such as phosphoprotein phosphatases and cAMP-specific phosphodiesterases as well as components of other signaling pathways into multiprotein-signaling complexes.

Localized Effects of cAMP Mediated by Distinct Routes of Protein Kinase A

2004 ◽  
Vol 84 (1) ◽  
pp. 137-167 ◽  
Author(s):  
KJETIL TASKÉN ◽  
EINAR MARTIN AANDAHL
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Biological Effects ◽  
Organ Specificity ◽  
Complex Signal ◽  
Signal Pathways ◽  
Pka Pathway ◽  
Kinase A

Taskén, Kjetil, and Einar Martin Aandahl. Localized Effects of cAMP Mediated by Distinct Routes of Protein Kinase A. Physiol Rev 84: 137–167, 2004; 10.1152/physrev.00021.2003.—More than 20% of the human genome encodes proteins involved in transmembrane and intracellular signaling pathways. The cAMP-protein kinase A (PKA) pathway is one of the most common and versatile signal pathways in eukaryotic cells and is involved in regulation of cellular functions in almost all tissues in mammals. Various extracellular signals converge on this signal pathway through ligand binding to G protein-coupled receptors, and the cAMP-PKA pathway is therefore tightly regulated at several levels to maintain specificity in the multitude of signal inputs. Ligand-induced changes in cAMP concentration vary in duration, amplitude, and extension into the cell, and cAMP microdomains are shaped by adenylyl cyclases that form cAMP as well as phosphodiesterases that degrade cAMP. Different PKA isozymes with distinct biochemical properties and cell-specific expression contribute to cell and organ specificity. A kinase anchoring proteins (AKAPs) target PKA to specific substrates and distinct subcellular compartments providing spatial and temporal specificity for mediation of biological effects channeled through the cAMP-PKA pathway. AKAPs also serve as scaffolding proteins that assemble PKA together with signal terminators such as phosphatases and cAMP-specific phosphodiesterases as well as components of other signaling pathways into multiprotein signaling complexes that serve as crossroads for different paths of cell signaling. Targeting of PKA and integration of a wide repertoire of proteins involved in signal transduction into complex signal networks further increase the specificity required for the precise regulation of numerous cellular and physiological processes.

Alkaloids exhibit a meaningful function as anticancer agents by restraining cellular signaling pathways

2021 ◽  
Vol 21 ◽  
Author(s):  
Wen Xu ◽  
Bei Wang ◽  
Yisong Gao ◽  
Yuxuan Cai ◽  
Jiali Zhang ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Signaling Pathway ◽  
Anticancer Agents ◽  
Molecular Mechanisms ◽  
Cellular Signaling ◽  
Biological Effects ◽  
Enzymatic Reaction ◽  
Mapk Signaling ◽  
Research Progress ◽  
Signal Pathways

: Alkaloids are nitrogen-containing organic compounds widely found in natural products, which play an essential role in clinical treatment. Cellular signaling pathways in tumors are a series of enzymatic reaction pathways that convert extracellular signals into intracellular signals to produce biological effects. The ordered function of cell signaling pathways is essential for tumor cell proliferation, differentiation, and programmed death. This review describes the antitumor progression mediated by various alkaloids after inhibiting classical signaling pathways; related studies are systematically retrieved and collected through PubMed. We selected the four currently most popular pathways for discussion and introduced the molecular mechanisms mediated by alkaloids in different signaling pathways, including the NF-kB signaling pathway, PI3K/AKT signaling pathway, MAPK signaling pathway, and P53 signaling pathway. The research progress of alkaloids related to tumor signal transduction pathways and the realization of alkaloids as cancer prevention drugs by targeting signal pathways remains.

scholarly journals Cytokine receptor clustering in sensory neurons with an engineered cytokine fusion protein triggers unique pain resolution pathways

2021 ◽  
Vol 118 (11) ◽  
pp. e2009647118
Author(s):  
Judith Prado ◽  
Remco H. S. Westerink ◽  
Jelena Popov-Celeketic ◽  
Cristine Steen-Louws ◽  
Aridaman Pandit ◽  
...  
Keyword(s):  
Fusion Protein ◽  
Signaling Pathways ◽  
Sensory Neurons ◽  
Inflammatory Pain ◽  
Biological Effects ◽  
Cytokine Receptor ◽  
Cytokine Receptors ◽  
Signal Pathways ◽  
Regulatory Cytokine

New therapeutic approaches to resolve persistent pain are highly needed. We tested the hypothesis that manipulation of cytokine receptors on sensory neurons by clustering regulatory cytokine receptor pairs with a fusion protein of interleukin (IL)-4 and IL-10 (IL4–10 FP) would redirect signaling pathways to optimally boost pain-resolution pathways. We demonstrate that a population of mouse sensory neurons express both receptors for the regulatory cytokines IL-4 and IL-10. This population increases during persistent inflammatory pain. Triggering these receptors with IL4–10 FP has unheralded biological effects, because it resolves inflammatory pain in both male and female mice. Knockdown of both IL4 and IL10 receptors in sensory neurons in vivo ablated the IL4–10 FP-mediated inhibition of inflammatory pain. Knockdown of either one of the receptors prevented the analgesic gain-of-function of IL4–10 FP. In vitro, IL4–10 FP inhibited inflammatory mediator-induced neuronal sensitization more effectively than the combination of cytokines, confirming its superior activity. The IL4–10 FP, contrary to the combination of IL-4 and IL-10, promoted clustering of IL-4 and IL-10 receptors in sensory neurons, leading to unique signaling, that is exemplified by activation of shifts in the cellular kinome and transcriptome. Interrogation of the potentially involved signal pathways led us to identify JAK1 as a key downstream signaling element that mediates the superior analgesic effects of IL4–10 FP. Thus, IL4–10 FP constitutes an immune-biologic that clusters regulatory cytokine receptors in sensory neurons to transduce unique signaling pathways required for full resolution of persistent inflammatory pain.

scholarly journals The effect of extracellular vesicles on the regulation of mitochondria under hypoxia

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Yaodan Zhang ◽  
Jin Tan ◽  
Yuyang Miao ◽  
Qiang Zhang
Keyword(s):  
Extracellular Vesicles ◽  
Mitochondrial Function ◽  
Biological Effects ◽  
Nuclear Gene ◽  
Signal Pathways ◽  
Receptor Cells ◽  
Nuclear Gene Expression ◽  
Cell Energy ◽  
Cellular Stresses ◽  
Retrograde Signal

AbstractMitochondria are indispensable organelles for maintaining cell energy metabolism, and also are necessary to retain cell biological function by transmitting information as signal organelles. Hypoxia, one of the important cellular stresses, can directly regulates mitochondrial metabolites and mitochondrial reactive oxygen species (mROS), which affects the nuclear gene expression through mitochondrial retrograde signal pathways, and also promotes the delivery of signal components into cytoplasm, causing cellular injury. In addition, mitochondria can also trigger adaptive mechanisms to maintain mitochondrial function in response to hypoxia. Extracellular vesicles (EVs), as a medium of information transmission between cells, can change the biological effects of receptor cells by the release of cargo, including nucleic acids, proteins, lipids, mitochondria, and their compositions. The secretion of EVs increases in cells under hypoxia, which indirectly changes the mitochondrial function through the uptake of contents by the receptor cells. In this review, we focus on the mitochondrial regulation indirectly through EVs under hypoxia, and the possible mechanisms that EVs cause the changes in mitochondrial function. Finally, we discuss the significance of this EV-mitochondria axis in hypoxic diseases.

Ultrastructural Changes in Three Different Mammalian Cells Following Ultraviolet Laser Irradiation

1972 ◽  
Vol 30 ◽  
pp. 350-351
Author(s):  
K. Shankar Narayan ◽  
Kailash C. Gupta ◽  
Tohru Okigaki
Keyword(s):  
Ultraviolet Light ◽  
Mammalian Cells ◽  
Biological Effects ◽  
Survival Rates ◽  
Chinese Hamster ◽  
Cell Types ◽  
Differential Sensitivity ◽  
Ultrastructural Changes ◽  
Ultraviolet Laser

The biological effects of short-wave ultraviolet light has generally been described in terms of changes in cell growth or survival rates and production of chromosomal aberrations. Ultrastructural changes following exposure of cells to ultraviolet light, particularly at 265 nm, have not been reported.We have developed a means of irradiating populations of cells grown in vitro to a monochromatic ultraviolet laser beam at a wavelength of 265 nm based on the method of Johnson. The cell types studies were: i) WI-38, a human diploid fibroblast; ii) CMP, a human adenocarcinoma cell line; and iii) Don C-II, a Chinese hamster fibroblast cell strain. The cells were exposed either in situ or in suspension to the ultraviolet laser (UVL) beam. Irradiated cell populations were studied either "immediately" or following growth for 1-8 days after irradiation.Differential sensitivity, as measured by survival rates were observed in the three cell types studied. Pattern of ultrastructural changes were also different in the three cell types.

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