FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2018514893> ?p ?o ?g. }

• W2018514893 endingPage "90" @default.
• W2018514893 startingPage "79" @default.
• W2018514893 abstract "Summary Background Degranulation of mast cells is stimulated by store‐operated C a 2+ ‐entry ( SOCE ). In other cell types, C a 2+ ‐entry is modified by ceramide. Exogenously added ceramide has been shown to trigger mast cell apoptosis. Effects of endogenously produced ceramide in mast cells remained, however, elusive. Ceramide may be produced from sphingomyelin by acid sphingomyelinase ( A sm). Objective This study explored the impact of A sm on mast cell functions. Methods Mast cells were isolated from bone marrow ( BMMC s) or peritoneal lavage of gene‐targeted mice lacking A sm ( asm −/− ) and their wild‐type littermates ( asm +/+ ). BMMC maturation and apoptosis‐associated annexin V binding were determined by flow cytometry. Asm activity was assessed enzymatically, cytosolic C a 2+ activity ([ C a 2+ ] i ) utilizing F ura‐2 fluorescence, current across the cell membrane by whole‐cell patch clamp, degranulation from hexosaminidase‐release and migration utilizing a transwell chamber. In vivo anaphylaxis was derived from decrease in body temperature. Results Peritoneal mast cell number, BMMC phenotype, spontaneous BMMC apoptosis as well as BMMC CD 117, CD 34 and F cε RI expression were similar in both genotypes. In asm +/+ BMMC s, stimulation with antigen resulted in a fast ~2.5‐fold increase in A sm activity. Release of C a 2+ from internal stores and hence several C a 2+ ‐dependent functions were strongly impaired in asm −/− BMMCs. Thus, antigen‐induced increase in [ C a 2+ ] i in IgE‐sensitized cells, antigen‐ but not ionomycin‐induced currents through C a 2+ ‐activated K + ‐channels ( K Ca 3.1), I g E /antigen‐triggered β‐hexosaminidase release, and antigen‐induced migration were all lower in asm −/− BMMC s than in asm +/+ BMMC s. Pharmacological inhibition of A sm by amitriptyline (500 n m , 3 h) in asm +/+ BMMC s similarly decreased antigen‐induced increase in [ C a 2+ ] i , K Ca 3.1 currents, ß‐hexosaminidase release and migration. The decrease in body temperature upon the induction of systemic anaphylaxis was significantly less pronounced in asm −/− mice than in asm +/+ mice, an observation pointing to in vivo significance of A sm. Conclusions and Clinical Relevance Asm is a novel, powerful regulator of mast cell function and thus a potential target in the treatment of allergic reactions." @default.
• W2018514893 created "2016-06-24" @default.
• W2018514893 creator A5001414010 @default.
• W2018514893 creator A5002321842 @default.
• W2018514893 creator A5004630250 @default.
• W2018514893 creator A5021214926 @default.
• W2018514893 creator A5041073789 @default.
• W2018514893 creator A5047283512 @default.
• W2018514893 creator A5050589869 @default.
• W2018514893 creator A5067772985 @default.
• W2018514893 creator A5079550119 @default.
• W2018514893 creator A5084208566 @default.
• W2018514893 date "2013-12-20" @default.
• W2018514893 modified "2023-10-04" @default.
• W2018514893 title "Role of acid sphingomyelinase in the regulation of mast cell function" @default.
• W2018514893 cites W1498297691 @default.
• W2018514893 cites W1514093028 @default.
• W2018514893 cites W1527592659 @default.
• W2018514893 cites W1538518979 @default.
• W2018514893 cites W1575766207 @default.
• W2018514893 cites W1772083081 @default.
• W2018514893 cites W1949045883 @default.
• W2018514893 cites W1963640549 @default.
• W2018514893 cites W1971543548 @default.
• W2018514893 cites W1972660643 @default.
• W2018514893 cites W1974228674 @default.
• W2018514893 cites W1977433548 @default.
• W2018514893 cites W1980871101 @default.
• W2018514893 cites W1984439034 @default.
• W2018514893 cites W1985859938 @default.
• W2018514893 cites W1986542865 @default.
• W2018514893 cites W1993620399 @default.
• W2018514893 cites W1995126002 @default.
• W2018514893 cites W1998080282 @default.
• W2018514893 cites W2005985025 @default.
• W2018514893 cites W2007280129 @default.
• W2018514893 cites W2008330541 @default.
• W2018514893 cites W2008603261 @default.
• W2018514893 cites W2009667219 @default.
• W2018514893 cites W2016934076 @default.
• W2018514893 cites W2017197907 @default.
• W2018514893 cites W2019005050 @default.
• W2018514893 cites W2022497999 @default.
• W2018514893 cites W2023708059 @default.
• W2018514893 cites W2023965621 @default.
• W2018514893 cites W2024900877 @default.
• W2018514893 cites W2025479275 @default.
• W2018514893 cites W2033184054 @default.
• W2018514893 cites W2034867646 @default.
• W2018514893 cites W2041690080 @default.
• W2018514893 cites W2044562348 @default.
• W2018514893 cites W2045282556 @default.
• W2018514893 cites W2050571341 @default.
• W2018514893 cites W2053147858 @default.
• W2018514893 cites W2053871805 @default.
• W2018514893 cites W2061769702 @default.
• W2018514893 cites W2069412624 @default.
• W2018514893 cites W2071076441 @default.
• W2018514893 cites W2074461942 @default.
• W2018514893 cites W2076022685 @default.
• W2018514893 cites W2078318929 @default.
• W2018514893 cites W2087016252 @default.
• W2018514893 cites W2092446496 @default.
• W2018514893 cites W2093535428 @default.
• W2018514893 cites W2094288810 @default.
• W2018514893 cites W2094494114 @default.
• W2018514893 cites W2097506986 @default.
• W2018514893 cites W2100723329 @default.
• W2018514893 cites W2102291237 @default.
• W2018514893 cites W2103893977 @default.
• W2018514893 cites W2104740033 @default.
• W2018514893 cites W2111474925 @default.
• W2018514893 cites W2115278949 @default.
• W2018514893 cites W2117328672 @default.
• W2018514893 cites W2117568560 @default.
• W2018514893 cites W2120959166 @default.
• W2018514893 cites W2125355937 @default.
• W2018514893 cites W2127855108 @default.
• W2018514893 cites W2131929080 @default.
• W2018514893 cites W2133980433 @default.
• W2018514893 cites W2135525156 @default.
• W2018514893 cites W2135687585 @default.
• W2018514893 cites W2142885312 @default.
• W2018514893 cites W2147601976 @default.
• W2018514893 cites W2148163755 @default.
• W2018514893 cites W2155183573 @default.
• W2018514893 cites W2156015098 @default.
• W2018514893 cites W2159361967 @default.
• W2018514893 cites W2164509237 @default.
• W2018514893 doi "https://doi.org/10.1111/cea.12229" @default.
• W2018514893 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24164338" @default.
• W2018514893 hasPublicationYear "2013" @default.
• W2018514893 type Work @default.
• W2018514893 sameAs 2018514893 @default.
• W2018514893 citedByCount "10" @default.
• W2018514893 countsByYear W20185148932014 @default.
• W2018514893 countsByYear W20185148932015 @default.
• W2018514893 countsByYear W20185148932016 @default.

• next