scholarly journals Calcium Signaling in Pancreatic Immune Cells In situ

Function ◽  
2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Oleksiy Gryshchenko ◽  
Julia V Gerasimenko ◽  
Ole H Petersen ◽  
Oleg V Gerasimenko
Keyword(s):  
Immune Cells ◽  
Stellate Cells ◽  
Normal Pancreas ◽  
Ip3 Receptors ◽  
Pharmacological Studies ◽  
High Concentrations ◽  
Primary Injury ◽  
Ca2 Channels ◽  
Live Mouse

Abstract Immune cells were identified in intact live mouse pancreatic lobules and their Ca2+ signals, evoked by various agents, characterized and compared with the simultaneously recorded Ca2+ signals in neighboring acinar and stellate cells. Immunochemistry in the live lobules indicated that the pancreatic immune cells most likely are macrophages. In the normal pancreas the density of these cells is very low, but induction of acute pancreatitis (AP), by a combination of ethanol and fatty acids, markedly increased the number of the immune cells. The principal agent eliciting Ca2+ signals in the pancreatic immune cells was ATP, but these cells also frequently produced Ca2+ signals in response to acetylcholine and to high concentrations of bradykinin. Pharmacological studies, using specific purinergic agonists and antagonists, indicated that the ATP-elicited Ca2+ signals were mediated by both P2Y1 and P2Y13 receptors. The pancreatic immune cells were not electrically excitable and the Ca2+ signals generated by ATP were primarily due to release of Ca2+ from internal stores followed by store-operated Ca2+ entry through Ca2+ release-activated Ca2+ channels. The ATP-induced intracellular Ca2+ liberation was dependent on both IP3 generation and IP3 receptors. We propose that the ATP-elicited Ca2+ signal generation in the pancreatic immune cells is likely to play an important role in the severe inflammatory response to the primary injury of the acinar cells that occurs in AP.

New Technologies for Decontamination of Radioactive Substances Scattered by Nuclear Accident / Nowe Technologie Dekontaminacji Radioaktywnych Substancji Rozproszonych Przez Awarie Nuklearna

2013 ◽  
Vol 58 (1) ◽  
pp. 283-290 ◽  
Author(s):  
Y. Nishizaki ◽  
H. Miyamae ◽  
S. Ichikawa ◽  
K. Izumiya ◽  
T. Takano ◽  
...  
Keyword(s):  
Radioactive Waste ◽  
New Technologies ◽  
Ferric Hydroxide ◽  
Nuclear Accident ◽  
Radioactive Cesium ◽  
Cesium Ions ◽  
Naoh Solution ◽  
High Concentrations ◽  
Water Rinsing

Our effort for decontamination of radioactive cesium scattered widely by nuclear accident in March 2011 in Fukushima, Japan has been described. Radioactive cesium scattered widely in Japan has been accumulating in arc or plasma molten-solidified ash in waste incinerating facilities up to 90,000 Bq/kg of the radioactive waste. Water rinsing of the ash resulted in dissolution of cesium ions together with high concentrations of potassium and sodium ions. Although potassium inhibits the adsorption of cesium on zeolite, we succeeded to precipitate cesium by in-situ formation of ferric ferrocyanide and iron rust in the radioactive filtrate after rinsing of the radioactive ash with water. Because the regulation of no preservation of any kind of cyanide substances, cesium was separated from the precipitate consisting of cesium-captured ferric ferrocyanide and ferric hydroxide in diluted NaOH solution and subsequent filtration gave rise to the potassium-free radioactive filtrate. Cesium was captured by zeolite from the potassium-free radioactive filtrate. The amount of this final radioactive waste of zeolite was significantly lower than that of the arc-molten-solidified ash.

scholarly journals An Autonomous Platform for Near Real-Time Surveillance of Harmful Algae and Their Toxins in Dynamic Coastal Shelf Environments

2021 ◽  
Vol 9 (3) ◽  
pp. 336
Author(s):  
Stephanie K. Moore ◽  
John B. Mickett ◽  
Gregory J. Doucette ◽  
Nicolaus G. Adams ◽  
Christina M. Mikulski ◽  
...  
Keyword(s):  
Real Time ◽  
Domoic Acid ◽  
Harmful Algae ◽  
Coastal Trapped Waves ◽  
Resource Managers ◽  
Bloom Formation ◽  
High Concentrations ◽  
Data Gap ◽  
Autonomous Technology

Efforts to identify in situ the mechanisms underpinning the response of harmful algae to climate change demand frequent observations in dynamic and often difficult to access marine and freshwater environments. Increasingly, resource managers and researchers are looking to fill this data gap using unmanned systems. In this study we integrated the Environmental Sample Processor (ESP) into an autonomous platform to provide near real-time surveillance of harmful algae and the toxin domoic acid on the Washington State continental shelf over a three-year period (2016–2018). The ESP mooring design accommodated the necessary subsystems to sustain ESP operations, supporting deployment durations of up to 7.5 weeks. The combination of ESP observations and a suite of contextual measurements from the ESP mooring and a nearby surface buoy permitted an investigation into toxic Pseudo-nitzschia spp. bloom dynamics. Preliminary findings suggest a connection between bloom formation and nutrient availability that is modulated by wind-forced coastal-trapped waves. In addition, high concentrations of Pseudo-nitzschia spp. and elevated levels of domoic acid observed at the ESP mooring location were not necessarily associated with the advection of water from known bloom initiation sites. Such insights, made possible by this autonomous technology, enable the formulation of testable hypotheses on climate-driven changes in HAB dynamics that can be investigated during future deployments.

scholarly journals Immune Cell Modulation of the Extracellular Matrix Contributes to the Pathogenesis of Pancreatic Cancer

Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 901
Author(s):  
Ramiz S. Ahmad ◽  
Timothy D. Eubank ◽  
Slawomir Lukomski ◽  
Brian A. Boone
Keyword(s):  
Pancreatic Cancer ◽  
Extracellular Matrix ◽  
Immune Cells ◽  
Immune Cell ◽  
Treatment Strategies ◽  
Stellate Cells ◽  
Pancreatic Stellate Cells ◽  
Ductal Adenocarcinoma ◽  
Cellular Mechanisms ◽  
Novel Treatment Strategies

Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy with a five-year survival rate of only 9%. PDAC is characterized by a dense, fibrotic stroma composed of extracellular matrix (ECM) proteins. This desmoplastic stroma is a hallmark of PDAC, representing a significant physical barrier that is immunosuppressive and obstructs penetration of cytotoxic chemotherapy agents into the tumor microenvironment (TME). Additionally, dense ECM promotes hypoxia, making tumor cells refractive to radiation therapy and alters their metabolism, thereby supporting proliferation and survival. In this review, we outline the significant contribution of fibrosis to the pathogenesis of pancreatic cancer, with a focus on the cross talk between immune cells and pancreatic stellate cells that contribute to ECM deposition. We emphasize the cellular mechanisms by which neutrophils and macrophages, specifically, modulate the ECM in favor of PDAC-progression. Furthermore, we investigate how activated stellate cells and ECM influence immune cells and promote immunosuppression in PDAC. Finally, we summarize therapeutic strategies that target the stroma and hinder immune cell promotion of fibrogenesis, which have unfortunately led to mixed results. An enhanced understanding of the complex interactions between the pancreatic tumor ECM and immune cells may uncover novel treatment strategies that are desperately needed for this devastating disease.

scholarly journals Fe3O4@C Nanoparticles Synthesized by In Situ Solid-Phase Method for Removal of Methylene Blue

Nanomaterials ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 330
Author(s):  
Hengli Xiang ◽  
Genkuan Ren ◽  
Yanjun Zhong ◽  
Dehua Xu ◽  
Zhiye Zhang ◽  
...  
Keyword(s):  
Methylene Blue ◽  
Solid Phase ◽  
Raw Materials ◽  
Phase Method ◽  
Maximum Adsorption Capacity ◽  
High Catalytic Activity ◽  
Solid Phase Reaction ◽  
Phase Reaction ◽  
High Concentrations

Fe3O4@C nanoparticles were prepared by an in situ, solid-phase reaction, without any precursor, using FeSO4, FeS2, and PVP K30 as raw materials. The nanoparticles were utilized to decolorize high concentrations methylene blue (MB). The results indicated that the maximum adsorption capacity of the Fe3O4@C nanoparticles was 18.52 mg/g, and that the adsorption process was exothermic. Additionally, by employing H2O2 as the initiator of a Fenton-like reaction, the removal efficiency of 100 mg/L MB reached ~99% with Fe3O4@C nanoparticles, while that of MB was only ~34% using pure Fe3O4 nanoparticles. The mechanism of H2O2 activated on the Fe3O4@C nanoparticles and the possible degradation pathways of MB are discussed. The Fe3O4@C nanoparticles retained high catalytic activity after five usage cycles. This work describes a facile method for producing Fe3O4@C nanoparticles with excellent catalytic reactivity, and therefore, represents a promising approach for the industrial production of Fe3O4@C nanoparticles for the treatment of high concentrations of dyes in wastewater.

Effects of hydrogen peroxide and hypochlorite on membrane potential of mitochondria in situ in rat heart cells

1991 ◽  
Vol 69 (11) ◽  
pp. 1705-1712 ◽  
Author(s):  
Noburu Konno ◽  
K. J. Kako
Keyword(s):  
Hydrogen Peroxide ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Rat Heart ◽  
Mitochondrial Membrane ◽  
Isolated Rat Heart ◽  
Heart Mitochondria ◽  
High Concentrations ◽  
Isolated Rat

Hydrogen peroxide (H2O2) and hypochlorite (HOCl) cause a variety of cellular dysfunctions. In this study we examined the effects of these agents on the electrical potential gradient across the inner membrane of mitochondria in situ in isolated rat heart myocytes. Myocytes were prepared by collagenase digestion and incubated in the presence of H2O2 or HOCl. Transmembrane electrical gradients were measured by distribution of [3H]triphenylmethylphosphonium+, a lipophilic cation. The particulate fraction was separated from the cytosolic compartment first by permeabilization using digitonin, followed by rapid centrifugal sedimentation through a bromododecane layer. We found that the mitochondrial membrane potential (161 ± 7 mV, negative inside) was relatively well maintained under oxidant stress, i.e., the potential was decreased only at high concentrations of HOCl and H2O2 and gradually with time. The membrane potential of isolated rat heart mitochondria was affected similarly by H2O2 and HOCl in a concentration- and time-dependent manner. High concentrations of oxidants also reduced the cellular ATP level but did not significantly change the matrix volume. When the extra-mitochondrial free calcium concentration was increased in permeabilized myocytes, the transmembrane potential was decreased proportionally, and this decrease was potentiated further by H2O2. These results support the view that heart mitochondria are equipped with well-developed defense mechanisms against oxidants, but the action of H2O2 on the transmembrane electrical gradient is exacerbated by an increase in cytosolic calcium. Keywords: ATP, calcium, cardiomyocyte, cell defense, mitochondrial membrane potential, oxidant, triphenylmethylphosphonium.

scholarly journals Inflammasome-mediated regulation of hepatic stellate cells

2009 ◽  
Vol 296 (6) ◽  
pp. G1248-G1257 ◽  
Author(s):  
Azuma Watanabe ◽  
Muhammad Adnan Sohail ◽  
Dawidson Assis Gomes ◽  
Ardeshir Hashmi ◽  
Jun Nagata ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Immune Cells ◽  
Hepatic Stellate Cells ◽  
Smooth Muscle Actin ◽  
Stellate Cells ◽  
Inflammasome Activation ◽  
Cellular Injury ◽  
Wild Type ◽  
Primary Mouse ◽  
Msu Crystals

The inflammasome is a cytoplasmic multiprotein complex that has recently been identified in immune cells as an important sensor of signals released by cellular injury and death. Analogous to immune cells, hepatic stellate cells (HSC) also respond to cellular injury and death. Our aim was to establish whether inflammasome components were present in HSC and could regulate HSC functionality. Monosodium urate (MSU) crystals (100 μg/ml) were used to experimentally induce inflammasome activation in LX-2 and primary mouse HSC. Twenty-four hours later primary mouse HSC were stained with α-smooth muscle actin and visualized by confocal microscopy, and TGF-β and collagen1 mRNA expression was quantified. LX-2 cells were further cultured with or without MSU crystals for 24 h in a transwell chemotaxis assay with PDGF as the chemoattractant. We also examined inhibition of calcium (Ca2+) signaling in LX-2 cells treated with or without MSU crystals using caged inositol 1,4,5-triphosphate (IP3). Finally, we confirmed an important role of the inflammasome in experimental liver fibrosis by the injection of carbon tetrachloride (CCl4) or thioacetamide (TAA) in wild-type mice and mice lacking components of the inflammasome. Components of the inflammasome are expressed in LX-2 cells and primary HSC. MSU crystals induced upregulation of TGF-β and collagen1 mRNA and actin reorganization in HSCs from wild-type mice but not mice lacking inflammasome components. MSU crystals inhibited the release of Ca2+ via IP3 in LX-2 cells and also inhibited PDGF-induced chemotaxis. Mice lacking the inflammasome-sensing and adaptor molecules, NLRP3 and apoptosis-associated speck-like protein containing CARD, had reduced CCl4 and TAA-induced liver fibrosis. We concluded that inflammasome components are present in HSC, can regulate a variety of HSC functions, and are required for the development of liver fibrosis.

MAPK p38/Ulk1 pathway inhibits autophagy and induces IL-1β expression in hepatic stellate cells

2022 ◽  
Author(s):  
Li Jin ◽  
Juan Li ◽  
ShuJuan Yang ◽  
Rou Zhang ◽  
Chunhua Hu ◽  
...  
Keyword(s):  
Immune Cells ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Hepatic Inflammation ◽  
The Past ◽  
Cytokine Induction ◽  
Cytokines And Chemokines ◽  
The Relationship ◽  
Autophagy Inhibition ◽  
Lps Treatment

Background: In the past, hepatic stellate cells (HSCs) were considered to be noninflammatory cells and contribute to liver fibrosis by producing extracellular matrix. Recently, it was found that HSCs can also secrete cytokines and chemokines and therefore participate in hepatic inflammation. Autophagy participates in many immune response processes in immune cells. It is unclear whether autophagy is involved in inflammatory cytokine induction in HSCs. Methods: MAPK p38, Ulk1 phosphorylation and the Ulk1-Atg13 complex were analyzed in HSC-T6 cells after LPS treatment. The relationship between autophagy inhibition and inflammation was investigated in primary rat HSCs. Results: We discovered that LPS inhibited autophagy through MAPK p38. The activation of MAPK p38 induced Ulk1 phosphorylation, which disrupted the Ulk1-Atg13 complex and therefore inhibited autophagy. Furthermore, in primary rat HSCs, we demonstrated that autophagy inhibition regulated IL-1β induction, which depended on the MAPK p38/Ulk1 pathway. Conclusions: Our results reveal a continuous signaling pathway, MAPK p38-Ulk1 phosphorylation-Ulk1/Atg13 disruption, which inhibits autophagy and induces IL-1β expression in HSCs.

scholarly journals INTEGRINS MEDIATE PLACENTAL EXTRACELLULAR VESICLE TRAFFICKING TO LUNG AND LIVER IN VIVO

2020 ◽  
Author(s):  
Sean L. Nguyen ◽  
Soo Hyun Ahn ◽  
Jacob W. Greenberg ◽  
Benjamin W. Collaer ◽  
Dalen W. Agnew ◽  
...  
Keyword(s):  
Immune Cells ◽  
Extracellular Vesicle ◽  
Dependent Manner ◽  
Cellular Phenotype ◽  
Reporter Mouse ◽  
Membrane Bound ◽  
First Time

ABSTRACTMembrane-bound extracellular vesicles (EVs) mediate intercellular communication in all organisms, and those produced by placental mammals have become increasingly recognized as significant mediators of fetal-maternal communication. Here, we aimed to identify maternal cells targeted by placental EVs and elucidate the mechanisms by which they traffic to these cells. Exogenously administered pregnancy-associated EVs traffic specifically to the lung; further, placental EVs associate with lung interstitial macrophages and liver Kupffer cells in an integrin-dependent manner. Localization of EV to maternal lungs was confirmed in unmanipulated pregnancy using a transgenic reporter mouse model, which also provided in situ and in vitro evidence that fetally-derived EVs, rarely, may cause genetic alteration of maternal cells. These results provide for the first time direct in vivo evidence for targeting of placental EVs to maternal immune cells, and further, evidence that EVs can alter cellular phenotype.

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