FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1582463089> ?p ?o ?g. }

• W1582463089 endingPage "1206" @default.
• W1582463089 startingPage "1205" @default.
• W1582463089 abstract "Bax, a death promoting member of the Bcl-2-related family of proteins, is required for the induction of apoptosis in several cell lineages, including thymocytes, B cells, and certain neurons; by contrast, Bcl-2 promotes cell survival by suppressing apoptosis via an interaction with Bax (Knudson and Korsmeyer, 1997Knudson C.M. Korsmeyer S.J. Bcl-2 and Bax function independently to regulate cell death.Nature Genet. 1997; 16: 358-363Crossref PubMed Scopus (337) Google Scholar). To determine whether Bax or Bcl-2 might also be involved in the regulation of mast cell (MC) populations in vivo, the numbers of MC in the stomach and skin of Bax-deficient (Bax–/–) mice (Knudson et al., 1995Knudson C.M. Tung K.S. Tourtellotte W.G. Brown G.A. Korsmeyer S.J. Bax-deficient mice with lymphoid hyperplasia and male germ cell death.Science. 1995; 270: 96-99Crossref PubMed Scopus (1273) Google Scholar) and Bcl-2 deficient (Bcl-2–/–) mice (Veis et al., 1993Veis D.J. Sorenson C.M. Shutter J.R. Korsmeyer S.J. Bcl-2-deficient mice demonstrate fulminant lymphoid apoptosis, polycystic kidneys, and hypopigmented hair.Cell. 1993; 75: 229-240Abstract Full Text PDF PubMed Scopus (1403) Google Scholar), and the corresponding wild-type (+/+) and heterozygous (+/–) mice, were assessed by histologic analysis. The numbers of MC in the stomach mucosa of adult Bax–/– mice were more than 2-fold those of Bax+/– mice or wild-type (Bax+/+) mice (p < 0.005, Figure 1a). By contrast, MC numbers in the ear skin or back skin of Bax–/– mice were only slightly greater than in Bax+/+ mice (p = 0.06 or 0.02, respectively, Figure 1a). Bcl-2–/– or +/– mice had numbers of gastric mucosal MC that were reduced ∼ 65% versus those of wild-type mice, but there were no other statistically significant differences in MC numbers in any of the other anatomical sites analyzed in Bcl-2–/–, +/–, or +/+ mice (Figure 1b). The differences in the effects of a lack of Bax or Bcl-2 on numbers of MC in the stomach mucosa versus the skin may be related to a number of factors, including the relatively short lifespan of mucosal MC as opposed to cutaneous MC in the mouse (Walker, 1961Walker B.E. Mast cell turn-over in adult mice.Nature. 1961; 192: 980-981Crossref PubMed Scopus (18) Google Scholar). To assess more directly whether Bax might be involved in the regulation of MC-apoptosis, we examined the survival of IL-3-derived Bax–/– versus Bax+/+ MC after withdrawal of IL-3 in vitro (Mekori et al., 1993Mekori Y.A. Oh C.K. Metcalfe D.D. IL-3-dependent murine mast cell undergo apoptosis on removal of IL-3.J Immunol. 1993; 151: 3775-3784PubMed Google Scholar;Iemura et al., 1994Iemura A. Tsai M. Ando A. Wershil B.K. Galli S.J. The c-kit ligand, stem cell factor, promotes mast cell survival by suppressing apoptosis.Am J Pathol. 1994; 144: 321-328PubMed Google Scholar). MC were generated by maintaining femoral bone marrow cells of Bax–/– or Bax+/+ mice for 6 wk in media containing IL-3 (Iemura et al., 1994Iemura A. Tsai M. Ando A. Wershil B.K. Galli S.J. The c-kit ligand, stem cell factor, promotes mast cell survival by suppressing apoptosis.Am J Pathol. 1994; 144: 321-328PubMed Google Scholar). Apoptosis was then induced in these bone marrow-derived cultured MC (BMCMC) by removal of IL-3 from the culture medium (Mekori et al., 1993Mekori Y.A. Oh C.K. Metcalfe D.D. IL-3-dependent murine mast cell undergo apoptosis on removal of IL-3.J Immunol. 1993; 151: 3775-3784PubMed Google Scholar;Iemura et al., 1994Iemura A. Tsai M. Ando A. Wershil B.K. Galli S.J. The c-kit ligand, stem cell factor, promotes mast cell survival by suppressing apoptosis.Am J Pathol. 1994; 144: 321-328PubMed Google Scholar). We found that Bax–/– BMCMC exhibited enhanced survival upon withdrawal of IL-3 compared with BMCMC derived from wild-type mice (more than 50% of which died within the first 24 h after the removal of IL-3) (Figure 2a). Because of the difficulty in producing Bcl-2–/– mice, we were not able to generate sufficient Bcl-2–/– BMCMC to repeat these experiments with Bcl-2–/– versus Bcl-2+/+ BMCMC. To test whether Bax might be involved in the induction of MC-apoptosis in vivo, the glucocorticoid fluocinonide was applied topically twice daily for 14 d to the ear skin of Bax–/– mice and wild-type (Bax+/+) mice. It has been reported that such treatment reduces the number of dermal MC by inducing apoptosis, perhaps as a result of diminished local production of the c-kit ligand, stem cell factor (Finotto et al., 1997Finotto S. Mekori Y.A. Metcalfe D.D. Glucocorticoids decrease tissue mast cell number by reducing the production of the c-kit ligand, stem cell factor, by resident cells.J Clin Invest. 1997; 99: 1721-1728Crossref PubMed Scopus (114) Google Scholar). As seen in Figure 2(b), numbers of dermal MC were significantly lower (∼24% lower) in the fluocinonide-treated ears of wild-type (Bax+/+) mice than in the vehicle-treated contralateral control ears; however, fluocinonide treatment did not result in decreased numbers of dermal MC in Bax–/– mice (Figure 2b). Because Bcl-2–/– mice exhibit poor health within a few weeks of birth, we could not repeat these experiments in Bcl-2–/– versus+/+ mice. While much has been learned about the growth factors which regulate mouse MC development in vitro and in vivo (Galli et al., 1994Galli S.J. Zsebo K.M. Geissler E.N. The kit ligand, stem cell factor.Adv Immunol. 1994; 55: 1-96Crossref PubMed Scopus (542) Google Scholar), little is known about the molecular regulation of apoptosis by members of the Bcl-2-related family of proteins in this specialized population of hematopoietic cells. Our in vivo findings indicate that numbers of MC in the gastric mucosa are substantially increased, versus wild-type mice, in Bax–/– mice (and decreased in Bcl-2–/– mice). Cutaneous MC numbers were only slightly increased at baseline in Bax–/– versus Bax+/+ mice, but Bax–/– cutaneous MC appeared to be more resistant to fluocinonide-induced depletion than were the cutaneous MC of wild-type mice. These in vivo findings are consistent with the hypothesis that Bax is important for the promotion of apoptosis in the MC lineage in mice, at least under certain circumstances; however, such in vivo studies can not formally rule out indirect effects of Bax on MC survival or development that reflect actions of Bax in other cell types. By contrast, our in vitro studies of IL-3 depletion were performed using nearly pure populations of immature mouse MC. Accordingly, the results of these experiments directly support a role for Bax in the regulation of apoptosis in mouse MC." @default.
• W1582463089 created "2016-06-24" @default.
• W1582463089 creator A5004151297 @default.
• W1582463089 creator A5010135113 @default.
• W1582463089 creator A5046841847 @default.
• W1582463089 creator A5067167243 @default.
• W1582463089 creator A5089266223 @default.
• W1582463089 creator A5091156366 @default.
• W1582463089 date "2000-06-01" @default.
• W1582463089 modified "2023-10-12" @default.
• W1582463089 title "A Role for Bax in the Regulation of Apoptosis in Mouse Mast Cells" @default.
• W1582463089 cites W1950481374 @default.
• W1582463089 cites W2000415265 @default.
• W1582463089 cites W2008597649 @default.
• W1582463089 cites W2021115405 @default.
• W1582463089 cites W2036274324 @default.
• W1582463089 cites W2045204290 @default.
• W1582463089 cites W2049648341 @default.
• W1582463089 doi "https://doi.org/10.1046/j.1523-1747.2000.00005.x" @default.
• W1582463089 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10844568" @default.
• W1582463089 hasPublicationYear "2000" @default.
• W1582463089 type Work @default.
• W1582463089 sameAs 1582463089 @default.
• W1582463089 citedByCount "31" @default.
• W1582463089 countsByYear W15824630892012 @default.
• W1582463089 countsByYear W15824630892014 @default.
• W1582463089 countsByYear W15824630892015 @default.
• W1582463089 countsByYear W15824630892016 @default.
• W1582463089 countsByYear W15824630892022 @default.
• W1582463089 countsByYear W15824630892023 @default.
• W1582463089 crossrefType "journal-article" @default.
• W1582463089 hasAuthorship W1582463089A5004151297 @default.
• W1582463089 hasAuthorship W1582463089A5010135113 @default.
• W1582463089 hasAuthorship W1582463089A5046841847 @default.
• W1582463089 hasAuthorship W1582463089A5067167243 @default.
• W1582463089 hasAuthorship W1582463089A5089266223 @default.
• W1582463089 hasAuthorship W1582463089A5091156366 @default.
• W1582463089 hasBestOaLocation W15824630891 @default.
• W1582463089 hasConcept C185592680 @default.
• W1582463089 hasConcept C190283241 @default.
• W1582463089 hasConcept C203014093 @default.
• W1582463089 hasConcept C2779655021 @default.
• W1582463089 hasConcept C2779726688 @default.
• W1582463089 hasConcept C54355233 @default.
• W1582463089 hasConcept C86803240 @default.
• W1582463089 hasConcept C95444343 @default.
• W1582463089 hasConceptScore W1582463089C185592680 @default.
• W1582463089 hasConceptScore W1582463089C190283241 @default.
• W1582463089 hasConceptScore W1582463089C203014093 @default.
• W1582463089 hasConceptScore W1582463089C2779655021 @default.
• W1582463089 hasConceptScore W1582463089C2779726688 @default.
• W1582463089 hasConceptScore W1582463089C54355233 @default.
• W1582463089 hasConceptScore W1582463089C86803240 @default.
• W1582463089 hasConceptScore W1582463089C95444343 @default.
• W1582463089 hasIssue "6" @default.
• W1582463089 hasLocation W15824630891 @default.
• W1582463089 hasLocation W15824630892 @default.
• W1582463089 hasOpenAccess W1582463089 @default.
• W1582463089 hasPrimaryLocation W15824630891 @default.
• W1582463089 hasRelatedWork W2066593496 @default.
• W1582463089 hasRelatedWork W2349984481 @default.
• W1582463089 hasRelatedWork W2353734644 @default.
• W1582463089 hasRelatedWork W2365436766 @default.
• W1582463089 hasRelatedWork W2388471936 @default.
• W1582463089 hasRelatedWork W2746654039 @default.
• W1582463089 hasRelatedWork W3037594056 @default.
• W1582463089 hasRelatedWork W3167662755 @default.
• W1582463089 hasRelatedWork W3194739067 @default.
• W1582463089 hasRelatedWork W3113234623 @default.
• W1582463089 hasVolume "114" @default.
• W1582463089 isParatext "false" @default.
• W1582463089 isRetracted "false" @default.
• W1582463089 magId "1582463089" @default.
• W1582463089 workType "article" @default.