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  • 1
    Online Resource
    Online Resource
    IL-10 Suppresses Calcium-Mediated Costimulation of Receptor Activator NF-κB Signaling during Human Osteoclast Differentiation by Inhibiting TREM-2 Expression
    The American Association of Immunologists ; 2009
    In:  The Journal of Immunology Vol. 183, No. 4 ( 2009-08-15), p. 2444-2455
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 183, No. 4 ( 2009-08-15), p. 2444-2455
    Abstract: Induction of effective osteoclastogenesis by RANK (receptor activator of NF-κB) requires costimulation by ITAM-coupled receptors. In humans, the TREM-2 (triggering receptor expressed on myeloid cells 2) ITAM-coupled receptor plays a key role in bone remodeling, as patients with TREM-2 mutations exhibit defective osteoclastogenesis and bone lesions. We have identified a new rapidly induced costimulatory pathway for RANK signaling that is dependent on TREM-2 and mediated by calcium signaling. TREM-2-dependent calcium signals are required for RANK-mediated activation of calcium/calmodulin-dependent protein kinase (CaMK)II and downstream MEK and ERK MAPKs that are important for osteoclastogenesis. IL-10 inhibited RANK-induced osteoclastogenesis and selectively inhibited calcium signaling downstream of RANK by inhibiting transcription of TREM-2. Down-regulation of TREM-2 expression resulted in diminished RANKL-induced activation of the CaMK-MEK-ERK pathway and decreased expression of the master regulator of osteoclastogenesis NFATc1. These findings provide a new mechanism of inhibition of human osteoclast differentiation. The results also yield insights into crosstalk between ITAM-coupled receptors and heterologous receptors such as RANK, and they identify a mechanism by which IL-10 can suppress cellular responses to TNFR family members.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.0804165
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2009
    detail.hit.zdb_id: 1475085-5
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  • 2
    Online Resource
    Online Resource
    Ectonucleoside Triphosphate Diphosphohydrolase1/CD39, Localized in Neurons of Human and Porcine Heart, Modulates ATP-Induced Norepinephrine Exocytosis
    American Society for Pharmacology & Experimental Therapeutics (ASPET) ; 2005
    In:  Journal of Pharmacology and Experimental Therapeutics Vol. 313, No. 2 ( 2005-05), p. 570-577
    Details
    In: Journal of Pharmacology and Experimental Therapeutics, American Society for Pharmacology & Experimental Therapeutics (ASPET), Vol. 313, No. 2 ( 2005-05), p. 570-577
    Type of Medium: Online Resource
    ISSN: 0022-3565 , 1521-0103
    URL: Article
    DOI: 10.1124/jpet.104.081240
    Language: English
    Publisher: American Society for Pharmacology & Experimental Therapeutics (ASPET)
    Publication Date: 2005
    detail.hit.zdb_id: 1475023-5
    SSG: 15,3
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  • 3
    Online Resource
    Online Resource
    Ventilatory and Acid-Base Responses to Long-Term Hypercapnia in the Freshwater Turtle, Chrysemys Picta Bellii
    The Company of Biologists ; 1985
    In:  Journal of Experimental Biology Vol. 114, No. 1 ( 1985-01-01), p. 661-672
    Details
    In: Journal of Experimental Biology, The Company of Biologists, Vol. 114, No. 1 ( 1985-01-01), p. 661-672
    Abstract: The response to hypercapnia was studied in western painted turtles, Chrysemys picta bellii at 20°C. Ventilation, metabolic rate, arterial blood gases, blood pH and blood plasma ions were monitored periodically on individual turtles exposed to 5·7% CO2 for 72 h and then allowed to recover in air. In response to hypercapnia, there is an immediate 10-to 15-fold increase in ventilation from control levels, which was maintained throughout the entire 5·7% CO2 breathing period. The first hour of CO2 breathing caused an increase in from 24–39 mmHg with a concomitant decrease in pH and rise in [HCO3−]. [HCO3−] rose from 42 to 50 mmol l−1 in the next 24 h of CO2 breathing and remained at this level for the rest of the hypercapnic period. Small, significant increases in total [Ca2+] and total [Mg2+] were found; however, no changes were observed in the plasma Na+, K+ or Cl− concentrations and the overall change in measured ions could not account for the increased [HCO3−]. The maximum change in [HCO3−] attained in Chrysemys exposed to a more severe acidosis (14·3% CO2) for up to 18 h was the same as that seen in the animals breathing 5·7% CO2 (10 mmol l−1) implying that there is an upper limit for the accumulation of [HCO3−] in Chrysemys at 20 °C. The blood pH of turtles recovering in air returned to the control value (7−56–7’74) within the first hour although did not return to the control value. The HCO3− ion concentration also remained elevated throughout the 48-h recovery period, which suggests that ionic compensation is a slower process. The freshwater turtle employs two mechanisms to reduce the severity of an imposed respiratory acidosis: increased ventilation and changes in the strong ion difference. In spite of these responses, blood pH is not restored to the control value.
    Type of Medium: Online Resource
    ISSN: 0022-0949 , 1477-9145
    URL: Article
    DOI: 10.1242/jeb.114.1.661
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 1985
    detail.hit.zdb_id: 1482461-9
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Histamine H 3 -Receptor-Induced Attenuation of Norepinephrine Exocytosis: A Decreased Protein Kinase A Activity Mediates a Reduction in Intracellular Calcium
    American Society for Pharmacology & Experimental Therapeutics (ASPET) ; 2005
    In:  Journal of Pharmacology and Experimental Therapeutics Vol. 312, No. 1 ( 2005-01), p. 272-280
    Details
    In: Journal of Pharmacology and Experimental Therapeutics, American Society for Pharmacology & Experimental Therapeutics (ASPET), Vol. 312, No. 1 ( 2005-01), p. 272-280
    Type of Medium: Online Resource
    ISSN: 0022-3565 , 1521-0103
    URL: Article
    DOI: 10.1124/jpet.104.072504
    Language: English
    Publisher: American Society for Pharmacology & Experimental Therapeutics (ASPET)
    Publication Date: 2005
    detail.hit.zdb_id: 1475023-5
    SSG: 15,3
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  • 5
    Online Resource
    Online Resource
    Renin: at the heart of the mast cell
    Wiley ; 2007
    In:  Immunological Reviews Vol. 217, No. 1 ( 2007-06), p. 123-140
    Details
    In: Immunological Reviews, Wiley, Vol. 217, No. 1 ( 2007-06), p. 123-140
    Type of Medium: Online Resource
    ISSN: 0105-2896 , 1600-065X
    URL: Issue
    URL: Article
    DOI: 10.1111/imr.2007.217.issue-1
    DOI: 10.1111/j.1600-065X.2007.00514.x
    Language: English
    Publisher: Wiley
    Publication Date: 2007
    detail.hit.zdb_id: 2038276-5
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    The mast cell exosome-fibroblast connection: A novel pro-fibrotic pathway
    Frontiers Media SA ; 2023
    In:  Frontiers in Medicine Vol. 10 ( 2023-2-23)
    Details
    In: Frontiers in Medicine, Frontiers Media SA, Vol. 10 ( 2023-2-23)
    Abstract: In addition to the traditional activation of resident receptors by release of local mediators, new evidence favors the existence of exosomes in cell-to-cell communication that mediates delivery of specific cargo to modulate recipient cell function. We report that mast cell exosomes are an additional source of pro-fibrotic substances and constitute a unique pathway for the generation of excess collagen. Methods We use primary human lung fibroblasts (HLFs) to demonstrate the uptake of labeled exosomes isolated from the human mast cell line HMC-1 (MC-EXOs), previously shown to contain protein cargo in common with human mast cell exosomes. Results The MC-EXO uptake by HLF is to the cytosol and increases both proline hydroxylation in HLF lysate and secreted collagen, within 24 h, which is sustained over 72 h, the same time required for transforming growth factor-β (TGF-β) to activate collagen synthesis in the HLFs. Unlike TGF-β, MC-EXO uptake does not induce fibrillar gene activation or invoke the Smad-nuclear transcription pathway. We show that MC-EXO uptake and TGF-β have an additive effect on collagen synthesis in HLF and postulate that MC-EXO uptake by HLFs is a contributing factor to excess collagen synthesis and represents a unique paradigm for understanding fibrosis. Discussion It is known that, in the lungs, mast cells are more activated and increase in number with inflammation, injury and viral infection associated with fibrosis. With the reported increased incidence of post-COVID-pulmonary fibrosis (PCPF), data from patients with severe COVID-19 are presented that show an increase in the mast cell number in lung parenchyma, the site of PCPF. Our findings provide a rationale for targeting multiple fibrogenic pathways in the management of lung fibrosis and the use of mast cell exosomes as a biomarker for the prognostic and diagnostic management of evolving fibrotic lung disease.
    Type of Medium: Online Resource
    ISSN: 2296-858X
    URL: Article
    DOI: 10.3389/fmed.2023.1139397
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2775999-4
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  • 7
    Online Resource
    Online Resource
    Mast Cells: A Pivotal Role in Pulmonary Fibrosis
    Mary Ann Liebert Inc ; 2013
    In:  DNA and Cell Biology Vol. 32, No. 4 ( 2013-04), p. 206-218
    Details
    In: DNA and Cell Biology, Mary Ann Liebert Inc, Vol. 32, No. 4 ( 2013-04), p. 206-218
    Type of Medium: Online Resource
    ISSN: 1044-5498 , 1557-7430
    URL: Article
    DOI: 10.1089/dna.2013.2005
    RVK:
    WA 15000
    Language: English
    Publisher: Mary Ann Liebert Inc
    Publication Date: 2013
    detail.hit.zdb_id: 2026832-4
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Low-NaCl diet increases H-K-ATPase in intercalated cells from rat cortical collecting duct
    American Physiological Society ; 1998
    In:  American Journal of Physiology-Renal Physiology Vol. 275, No. 1 ( 1998-07-01), p. F94-F102
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 275, No. 1 ( 1998-07-01), p. F94-F102
    Abstract: Extracellular K + -dependent H + extrusion after an acute acid load, an index of H/K exchange, was monitored in intercalated cells (ICs) from rat cortical collecting tubule (CCT) using ratiometric fluorescence imaging of the intracellular pH (pH i ) indicator, 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF). The hypothesis tested was that 12- to 14-day NaCl deprivation increases H-K-ATPase in rat ICs. The rate of H/K exchange in the low-NaCl ICs was double that of controls. In control ICs, H/K exchange was inhibited by Sch-28080 (10 μM). In the low-NaCl ICs, it was partially blocked by Sch-28080 or ouabain (1 mM). Simultaneous addition of both inhibitors abolished K-dependent pH i recovery. The induced H/K exchange observed with NaCl restriction was not due to elevated plasma aldosterone as evidenced by experiments on ICs from rats implanted with osmotic minipumps administering aldosterone such that plasma levels were comparable to those of NaCl-deficient rats. The results suggest that NaCl deficiency induces two isoforms of H-K-ATPase in ICs and that this effect is not mediated by elevated plasma aldosterone.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.1998.275.1.F94
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1998
    detail.hit.zdb_id: 1477287-5
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  • 9
    Online Resource
    Online Resource
    Potassium depletion increases proton pump (H + -ATPase) activity in intercalated cells of cortical collecting duct
    American Physiological Society ; 2000
    In:  American Journal of Physiology-Renal Physiology Vol. 279, No. 1 ( 2000-07-01), p. F195-F202
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 279, No. 1 ( 2000-07-01), p. F195-F202
    Abstract: Intercalated cells (ICs) from kidney collecting ducts contain proton-transporting ATPases (H + -ATPases) whose plasma membrane expression is regulated under a variety of conditions. It has been shown that net proton secretion occurs in the distal nephron from chronically K + -depleted rats and that upregulation of tubular H + - ATPase is involved in this process. However, regulation of this protein at the level of individual cells has not so far been examined. In the present study, H + -ATPase activity was determined in individually identified ICs from control and chronically K + -depleted rats (9–14 days on a low-K + diet) by monitoring K + - and Na + -independent H + extrusion rates after an acute acid load. Split-open rat cortical collecting tubules were loaded with the intracellular pH (pH i ) indicator 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein, and pH i was determined by using ratiometric fluorescence imaging. The rate of pH i recovery in ICs in response to an acute acid load, a measure of plasma membrane H + -ATPase activity, was increased after K + depletion to almost three times that of controls. Furthermore, the lag time before the start of pH i recovery after the cells were maximally acidified fell from 93.5 ± 13.7 s in controls to 24.5 ± 2.1 s in K + -depleted rats. In all ICs tested, Na + - and K + -independent pH i recovery was abolished in the presence of bafilomycin (100 nM), an inhibitor of the H + -ATPase. Analysis of the cell-to-cell variability in the rate of pH i recovery reveals a change in the distribution of membrane-bound proton pumps in the IC population of cortical collecting duct from K + -depleted rats. Immunocytochemical analysis of collecting ducts from control and K + -depleted rats showed that K + -depletion increased the number of ICs with tight apical H + ATPase staining and decreased the number of cells with diffuse or basolateral H + -ATPase staining. Taken together, these data indicate that chronic K + depletion induces a marked increase in plasma membrane H + ATPase activity in individual ICs.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.2000.279.1.F195
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
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  • 10
    Online Resource
    Online Resource
    H + -K + -ATPases: regulation and role in pathophysiological states
    American Physiological Society ; 1999
    In:  American Journal of Physiology-Renal Physiology Vol. 276, No. 6 ( 1999-06-01), p. F799-F811
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 276, No. 6 ( 1999-06-01), p. F799-F811
    Abstract: Molecular cloning experiments have identified the existence of two H + -K + -ATPases (HKAs), colonic and gastric. Recent functional and molecular studies indicate the presence of both transporters in the kidney, which are presumed to mediate the exchange of intracellular H + for extracellular K + . On the basis of these studies, a picture is evolving that indicates differential regulation of HKAs at the molecular level in acid-base and electrolyte disorders. Of the two transporters, gastric HKA is expressed constitutively along the length of the collecting duct and is responsible for H + secretion and K + reabsorption under normal conditions and may be stimulated with acid-base perturbations and/or K + depletion. This regulation may be species specific. To date there are no data to indicate that the colonic HKA (HKAc) plays a role in H + secretion or K + reabsorption under normal conditions. However, HKAc shows adaptive regulation in pathophysiological conditions such as K + depletion, NaCl deficiency, and proximal renal tubular acidosis, suggesting an important role for this exchanger in potassium, [Formula: see text], and sodium (or chloride) reabsorption in disease states. The purpose of this review is to summarize recent functional and molecular studies on the regulation of HKAs in physiological and pathophysiological states. Possible signals responsible for regulation of HKAs in these conditions will be discussed. Furthermore, the role of these transporters in acid-base and electrolyte homeostasis will be evaluated in the context of genetically altered animals deficient in HKAc.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.1999.276.6.F799
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1477287-5
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