scholarly journals Platelet and Erythrocyte Extravasation across Inflamed Corneal Venules Depend on CD18, Neutrophils and Mast Cell Degranulation

2021 ◽  
Vol 22 (14) ◽  
pp. 7360
Author(s):  
Angie De La Cruz ◽  
Aubrey Hargrave ◽  
Sri Magadi ◽  
Justin A. Courson ◽  
Paul T. Landry ◽  
...  
Keyword(s):  
Mast Cell ◽  
Cell Types ◽  
Mast Cell Degranulation ◽  
Wild Type ◽  
Delayed Wound Healing ◽  
Corneal Epithelial ◽  
Corneal Abrasion ◽  
Low Levels ◽  
Endothelial Pores

Platelet extravasation during inflammation is under-appreciated. In wild-type (WT) mice, a central corneal epithelial abrasion initiates neutrophil (PMN) and platelet extravasation from peripheral limbal venules. The same injury in mice expressing low levels of the β2-integrin, CD18 (CD18hypo mice) shows reduced platelet extravasation with PMN extravasation apparently unaffected. To better define the role of CD18 on platelet extravasation, we focused on two relevant cell types expressing CD18: PMNs and mast cells. Following corneal abrasion in WT mice, we observed not only extravasated PMNs and platelets but also extravasated erythrocytes (RBCs). Ultrastructural observations of engorged limbal venules showed platelets and RBCs passing through endothelial pores. In contrast, injured CD18hypo mice showed significantly less venule engorgement and markedly reduced platelet and RBC extravasation; mast cell degranulation was also reduced compared to WT mice. Corneal abrasion in mast cell-deficient (KitW-sh/W-sh) mice showed less venule engorgement, delayed PMN extravasation, reduced platelet and RBC extravasation and delayed wound healing compared to WT mice. Finally, antibody-induced depletion of circulating PMNs prior to corneal abrasion reduced mast cell degranulation, venule engorgement, and extravasation of PMNs, platelets, and RBCs. In summary, in the injured cornea, platelet and RBC extravasation depends on CD18, PMNs, and mast cell degranulation.

Phospholipase D1 regulates high-affinity IgE receptor-induced mast cell degranulation

Blood ◽  
2004 ◽  
Vol 104 (13) ◽  
pp. 4122-4128 ◽  
Author(s):  
Tomohiro Hitomi ◽  
Juan Zhang ◽  
Liliana M. Nicoletti ◽  
Ana Cristina G. Grodzki ◽  
Maria C. Jamur ◽  
...  
Keyword(s):  
Mast Cell ◽  
Phosphatidic Acid ◽  
Mast Cell Degranulation ◽  
Dominant Negative ◽  
Acid Formation ◽  
Wild Type ◽  
High Affinity ◽  
Phospholipase D1 ◽  
High Affinity Ige Receptor

Abstract To investigate the role of phospholipase D (PLD) in FcϵRI signaling, the wild-type or the catalytically inactive forms of PLD1 or PLD2 were stably overexpressed in RBL-2H3 mast cells. FcϵRI stimulation resulted in the activation of both PLD1 and PLD2. However, PLD1 was the source of most of the receptor-induced PLD activity. There was enhanced FcϵRI-induced degranulation only in cells that overexpressed the catalytically inactive PLD1. This dominant-negative PLD1 enhanced FcϵRI-induced tyrosine phosphorylations of early signaling molecules such as the receptor subunits, Syk and phospholipase C-γ which resulted in faster release of Ca2+ from intracellular sources. Therefore, PLD1 negatively regulates signals upstream of the Ca2+ response. However, FcϵRI-induced PLD activation required Syk and was downstream of the Ca2+response, suggesting that basal PLD1 activity rather than that activated by cell stimulation controlled these early signaling events. Dominant-negative PLD1 reduced the basal phosphatidic acid formation in unstimulated cells, which was accompanied by an increase in FcϵRI within the lipid rafts. These results indicate that constitutive basal PLD1 activity by regulating phosphatidic acid formation controls the early signals initiated by FcϵRI aggregation that lead to mast cell degranulation. (Blood. 2004;104:4122-4128)

scholarly journals Microtubule–microtubule sliding by kinesin-1 is essential for normal cytoplasmic streaming in Drosophila oocytes

2016 ◽  
Vol 113 (34) ◽  
pp. E4995-E5004 ◽  
Author(s):  
Wen Lu ◽  
Michael Winding ◽  
Margot Lakonishok ◽  
Jill Wildonger ◽  
Vladimir I. Gelfand
Keyword(s):  
Cytoplasmic Streaming ◽  
Cell Types ◽  
Nurse Cells ◽  
Wild Type ◽  
Actin Cortex ◽  
Microtubule Motor ◽  
Multiple Cell ◽  
Cytoplasmic Microtubules ◽  
Two Populations

Cytoplasmic streaming in Drosophila oocytes is a microtubule-based bulk cytoplasmic movement. Streaming efficiently circulates and localizes mRNAs and proteins deposited by the nurse cells across the oocyte. This movement is driven by kinesin-1, a major microtubule motor. Recently, we have shown that kinesin-1 heavy chain (KHC) can transport one microtubule on another microtubule, thus driving microtubule–microtubule sliding in multiple cell types. To study the role of microtubule sliding in oocyte cytoplasmic streaming, we used a Khc mutant that is deficient in microtubule sliding but able to transport a majority of cargoes. We demonstrated that streaming is reduced by genomic replacement of wild-type Khc with this sliding-deficient mutant. Streaming can be fully rescued by wild-type KHC and partially rescued by a chimeric motor that cannot move organelles but is active in microtubule sliding. Consistent with these data, we identified two populations of microtubules in fast-streaming oocytes: a network of stable microtubules anchored to the actin cortex and free cytoplasmic microtubules that moved in the ooplasm. We further demonstrated that the reduced streaming in sliding-deficient oocytes resulted in posterior determination defects. Together, we propose that kinesin-1 slides free cytoplasmic microtubules against cortically immobilized microtubules, generating forces that contribute to cytoplasmic streaming and are essential for the refinement of posterior determinants.

Role of 5-HT3 receptors and afferent fibers in the effects of mast cell degranulation on colonic motility in rats

1994 ◽  
Vol 107 (4) ◽  
pp. 976-984 ◽  
Author(s):  
Nathalie Castex ◽  
Jean Fioramonti ◽  
Marie JoséFargeas ◽  
Jean More ◽  
Lionel Bueno
Keyword(s):  
Mast Cell ◽  
Colonic Motility ◽  
Mast Cell Degranulation ◽  
Afferent Fibers

Arteriolar constriction in skeletal muscle during vascular stunning: role of mast cells

1997 ◽  
Vol 272 (5) ◽  
pp. H2154-H2163 ◽  
Author(s):  
M. W. Keller
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Vascular Reactivity ◽  
Striated Muscle ◽  
Mast Cell Degranulation ◽  
Response Curves ◽  
Maximal Diameter ◽  
Muscle Tissues ◽  
Stimulation Of

Striated muscle becomes stunned during reperfusion after sublethal ischemia. Resistance vessel tone and reactivity are altered in stunned muscle tissues. The hypothesis that adenosine-regulated mast cell degranulation occurs during reperfusion and leads to constriction of resistance arterioles was tested. The hamster cremaster muscle was subjected to 1 h of ischemia followed by reperfusion. Resistance arterioles constricted during reperfusion (74% of maximal diameter at baseline vs. 42% of maximal diameter after 30 min of reperfusion; P < 0.01). Mast cells degranulated in reperfusion concomitant with arteriolar constriction. Stimulation of mast cell degranulation in control animals with compound 48/80 or cold superfusate (21 degrees C) caused vasoconstriction that mimicked that seen in reperfusion. The mast cell stabilizer cromolyn blocked degranulation and constriction. If mast cell granules were depleted by applying compound 48/80 before inducing ischemia, then arterioles failed to constrict during reperfusion. Adenosine A3-antagonist BW-A1433 abolished constriction. These findings suggest that arterioles constrict in reperfusion due to adenosine-regulated mast cell degranulation. Vasodilation in response to sodium nitroprusside and acetylcholine was normal in stunned, constricted arterioles. However, the dose-response curves to adenosine were shifted to the left in arterioles constricted by either stunning, compound 48/80, exposure to cold superfusate, or cromolyn compared with control vessels. Depletion of granular components via stunning, compound 48/80, cold superfusate, or inhibition of secretion with cromolyn results in unopposed A1- or A2-mediated vasodilation in response to adenosine, whereas the dilatory effects of adenosine are blunted by simultaneous release of vasoconstrictors from mast cells in control animals. In summary, it was found that mast cell degranulation occurs during reperfusion and leads to constriction of resistance arterioles and altered vascular reactivity to adenosine. Adenosine is released in ischemia and stimulates mast cell degranulation via the A3 receptor located on mast cells during reperfusion.

Role of eNOS-derived NO in the postischemic anti-inflammatory effects of antecedent ethanol ingestion in murine small intestine

2007 ◽  
Vol 292 (3) ◽  
pp. H1435-H1442 ◽  
Author(s):  
Taiji Yamaguchi ◽  
Kazuhiro Kamada ◽  
Catherine Dayton ◽  
F. Spencer Gaskin ◽  
Mozow Yusof ◽  
...  
Keyword(s):  
Ethanol Exposure ◽  
Ethanol Ingestion ◽  
Leukocyte Rolling ◽  
Wild Type ◽  
No Donor ◽  
Nos Inhibitors ◽  
Low Levels ◽  
Ethanol Preconditioning ◽  
Dependent Mechanism

Ingestion of low levels of ethanol 24 h before [ethanol preconditioning (EPC)] ischemia and reperfusion (I/R) prevents postischemic leukocyte rolling (LR) and adhesion (LA), effects that were abolished by adenosine A2 receptor (ADO-A2R) antagonists or nitric oxide (NO) synthase (NOS) inhibitors. The aims of this study were to determine whether NO derived from endothelial NOS (eNOS) during the period of ethanol exposure triggered entrance into this preconditioned state and whether these events were initiated by an ADO-A2R-dependent mechanism. Ethanol or distilled water vehicle was administered to C57BL/6J [wild type (WT)] or eNOS-deficient (eNOS−/−) mice by gavage. Twenty-four hours later, the superior mesenteric artery was occluded for 45 min. LR and LA were quantified by intravital microscopy after 30 and 60 min of reperfusion. I/R increased LR and LA in WT mice, effects that were abolished by EPC or NO donor preconditioning (NO-PC). NO-PC was not attenuated by coincident administration of an ADO-A2R antagonist. I/R increased LR and LA in eNOS−/− mice to levels comparable with those noted in WT animals. However, EPC only slightly attenuated postischemic LR and LA, whereas NO-PC remained effective as a preconditioning stimulus in eNOS−/− mice. Preconditioning with an ADO-A2R agonist (which we previously demonstrated prevents I/R-induced LR and LA in WT animals) failed to attenuate these postischemic adhesive responses in eNOS−/− mice. Our results indicate that EPC is triggered by NO formed secondary to ADO-A2R-dependent eNOS activation during the period of ethanol exposure 24 h before I/R.

Lack of histamine alters gastric mucosal morphology: comparison of histidine decarboxylase-deficient and mast cell-deficient mice

2004 ◽  
Vol 287 (5) ◽  
pp. G1053-G1061 ◽  
Author(s):  
Eiji Nakamura ◽  
Takashi Kataoka ◽  
Kazuharu Furutani ◽  
Keisuke Jimbo ◽  
Takeshi Aihara ◽  
...  
Keyword(s):  
Mast Cell ◽  
Histidine Decarboxylase ◽  
Serum Gastrin ◽  
Cell Types ◽  
Intragastric Ph ◽  
Wild Type ◽  
Mucosal Morphology ◽  
Immunohistochemical Techniques ◽  
Stomach Weight ◽  
Deficient Mice

Histamine plays an important role in the regulation of gastric acid secretion; however, its role in maintenance of gastric morphology remains unclear. To clarify the necessity of histamine for gastric mucosal development and maintenance, we evaluated two different kinds of mice that lacked either mast cells (one of the gastric histamine-producing cell types) or histidine decarboxylase (HDC; a histamine-synthesizing enzyme). Measurements of stomach weight, intragastric pH, mucosal histamine levels, as well as serum gastrin and albumin levels were performed in mice. Gastric mucosal appearance was examined by immunohistochemical techniques. Although gastric mucosal histamine levels in mast cell-deficient mice were half of those observed in the wild-type mice, intragastric pH, serum gastrin levels, and gastric morphology at 12 mo were unchanged compared with the wild-type mice. In contrast, HDC-deficient mice possessed no detectable gastric histamine, but did exhibit hypergastrinemia, as well as marked increases in intragastric pH and stomach weight compared with the wild-type mice. Histological analysis revealed that 9-mo-old HDC-deficient mice demonstrated hyperplasia in the oxyntic glandular base region, as well as increased numbers of parietal and enterochromaffin-like cells. These results indicate that enterochromaffin-like cell-derived histamine is potentially involved in gastric mucosal morphology regulation.

scholarly journals Atypical Cristae Morphology of Human Syncytiotrophoblast Mitochondria

2011 ◽  
Vol 286 (27) ◽  
pp. 23911-23919 ◽  
Author(s):  
Daniela De Los Rios Castillo ◽  
Mariel Zarco-Zavala ◽  
Sofia Olvera-Sanchez ◽  
Juan Pablo Pardo ◽  
Oscar Juarez ◽  
...  
Keyword(s):  
Atp Synthase ◽  
Physiological Function ◽  
Cell Types ◽  
Dimeric Complex ◽  
Inhibitory Protein ◽  
Low Levels ◽  
Mitochondrial Complexes

Mitochondrial complexes I, III2, and IV from human cytotrophoblast and syncytiotrophoblast associate to form supercomplexes or respirasomes, with the following stoichiometries: I1:(III2)1 and I1:(III2)1–2:IV1–4. The content of respirasomes was similar in both cell types after isolating mitochondria. However, syncytiotrophoblast mitochondria possess low levels of dimeric complex V and do not have orthodox cristae morphology. In contrast, cytotrophoblast mitochondria show normal cristae morphology and a higher content of ATP synthase dimer. Consistent with the dimerizing role of the ATPase inhibitory protein (IF1) (García, J. J., Morales-Ríos, E., Cortés-Hernandez, P., and Rodríguez-Zavala, J. S. (2006) Biochemistry 45, 12695–12703), higher relative amounts of IF1 were observed in cytotrophoblast when compared with syncytiotrophoblast mitochondria. Therefore, there is a correlation between dimerization of complex V, IF1 expression, and the morphology of mitochondrial cristae in human placental mitochondria. The possible relationship between cristae architecture and the physiological function of the syncytiotrophoblast mitochondria is discussed.

Role of reactive oxygen species in mast cell degranulation

2016 ◽  
Vol 81 (12) ◽  
pp. 1564-1577 ◽  
Author(s):  
M. A. Chelombitko ◽  
A. V. Fedorov ◽  
O. P. Ilyinskaya ◽  
R. A. Zinovkin ◽  
B. V. Chernyak
Keyword(s):  
Reactive Oxygen Species ◽  
Mast Cell ◽  
Reactive Oxygen ◽  
Mast Cell Degranulation ◽  
Oxygen Species

Mast cell degranulation and the role of T cell RANTES in oral lichen planus

Oral Diseases ◽  
2001 ◽  
Vol 7 (4) ◽  
pp. 246-251 ◽  
Author(s):  
ZZ Zhao ◽  
PB Sugerman ◽  
XJ Zhou ◽  
LJ Walsh ◽  
NW Savage
Keyword(s):  
Mast Cell ◽  
T Cell ◽  
Lichen Planus ◽  
Oral Lichen Planus ◽  
Mast Cell Degranulation ◽  
Oral Lichen

scholarly journals Effects of Altered Fructose 2,6-Bisphosphate Levels on Carbohydrate Metabolism in Carnation

HortScience ◽  
2007 ◽  
Vol 42 (2) ◽  
pp. 403-406 ◽  
Author(s):  
Antal Szőke ◽  
Erzsébet Kiss ◽  
László Heszky ◽  
Ildikó Kerepesi ◽  
Ottó Toldi
Keyword(s):  
Carbohydrate Metabolism ◽  
Dianthus Caryophyllus ◽  
Bifunctional Enzyme ◽  
Starch Metabolism ◽  
Wild Type ◽  
Type Transformation ◽  
Key Enzyme ◽  
Low Levels ◽  
Hexose Phosphates

The aim of this work was to examine the role of fructose 2,6-bisphosphate (fru 2,6P2) in the carbohydrate metabolism in carnation (Dianthus caryophyllus L.). For this purpose, transgenic plants harboring two modified bifunctional enzyme complementary DNAs of rat liver origin (6-phosphofructo-2-kinase/fructose 2,6-biphosphatase) were generated. Transformation with the kinase construct resulted in a 45% to 85% increase in fru 2,6P2 concentrations compared with the wild type. Transformation with the phosphatase construct reduced the fru 2,6P2 contents by 45% and 70%. These alterations in fru 2,6P2 amounts affected the key enzyme activities of sucrose and starch metabolism. Accordingly, plants with elevated fru 2,6P2 concentrations had high levels of starch, fructose, and triose phosphates, and low levels of sucrose, glucose, and hexose phosphates. In plants with reduced amounts of fru 2,6P2 different results could be observed in major carbohydrate compounds.

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