Matches in SemOpenAlex for { <https://semopenalex.org/work/W2156065370> ?p ?o ?g. }
- W2156065370 endingPage "40" @default.
- W2156065370 startingPage "30" @default.
- W2156065370 abstract "Bacterially induced osteoblast apoptosis may be a major contributor to bone loss during osteomyelitis. We provide evidence for the functional expression in osteoblasts of NLRP3, a member of the NLR family of cytosolic receptors that has been implicated in the initiation of programmed cell death.Osteoblasts undergo apoptosis after exposure to intracellular bacterial pathogens commonly associated with osteomyelitis. Death of this bone-forming cell type, in conjunction with increased numbers and activity of osteoclasts, may underlie the destruction of bone tissue at sites of bacterial infection. To date, the mechanisms responsible for bacterially induced apoptotic osteoblast cell death have not been resolved.We used flow cytometric techniques to determine whether intracellular invasion is needed for maximal apoptotic cell death in primary osteoblasts after challenge with Salmonella enterica. In addition, we used real-time PCR and immunoblot analyses to assess osteoblast expression of members of the nucleotide-binding domain leucine-rich repeat region-containing family of intracellular receptors (NLRs) that have been predicted to be involved in the induction of programmed cell death. Furthermore, we have used co-immunoprecipitation and siRNA techniques to confirm the functionality of such sensors in this cell type.In this study, we showed that invasion of osteoblasts by Salmonella is necessary for maximal induction of apoptosis. We showed that murine and human osteoblasts express NLRP3 (previously known as CIAS1, cryopyrin, PYPAF1, or NALP3) but not NLRC4 (IPAF) and showed that the level of expression of this cytosolic receptor is modulated after bacterial challenge. We showed that osteoblasts express ASC, an adaptor molecule for NLRP3, and that these molecules associate after Salmonella infection. In addition, we showed that a reduction in the expression of NLRP3 attenuates Salmonella-induced reductions in the activity of an anti-apoptotic transcription factor in osteoblasts. Furthermore, we showed that NLRP3 expression is needed for caspase-1 activation and maximal induction of apoptosis in osteoblasts after infection with Salmonella.The functional expression of NLRP3 in osteoblasts provides a potential mechanism underlying apoptotic cell death of this cell type after challenge with intracellular bacterial pathogens and may be a significant contributory factor to bone loss at sites of infection." @default.
- W2156065370 created "2016-06-24" @default.
- W2156065370 creator A5006019460 @default.
- W2156065370 creator A5010663597 @default.
- W2156065370 creator A5019419731 @default.
- W2156065370 creator A5028921086 @default.
- W2156065370 creator A5034508784 @default.
- W2156065370 creator A5046608295 @default.
- W2156065370 creator A5083698757 @default.
- W2156065370 date "2008-01-01" @default.
- W2156065370 modified "2023-10-18" @default.
- W2156065370 title "Osteoblasts Express NLRP3, a Nucleotide-Binding Domain and Leucine-Rich Repeat Region Containing Receptor Implicated in Bacterially Induced Cell Death" @default.
- W2156065370 cites W1514224413 @default.
- W2156065370 cites W1675877390 @default.
- W2156065370 cites W1923022727 @default.
- W2156065370 cites W1966405258 @default.
- W2156065370 cites W1971707389 @default.
- W2156065370 cites W1973603028 @default.
- W2156065370 cites W1975032025 @default.
- W2156065370 cites W1977415935 @default.
- W2156065370 cites W1999235853 @default.
- W2156065370 cites W2004578137 @default.
- W2156065370 cites W2010743469 @default.
- W2156065370 cites W2029218036 @default.
- W2156065370 cites W2037576028 @default.
- W2156065370 cites W2038648913 @default.
- W2156065370 cites W2044210137 @default.
- W2156065370 cites W2044736154 @default.
- W2156065370 cites W2076454811 @default.
- W2156065370 cites W2077127766 @default.
- W2156065370 cites W2079936328 @default.
- W2156065370 cites W2080210471 @default.
- W2156065370 cites W2082508773 @default.
- W2156065370 cites W2085006185 @default.
- W2156065370 cites W2090859543 @default.
- W2156065370 cites W2099537310 @default.
- W2156065370 cites W2102948981 @default.
- W2156065370 cites W2103234321 @default.
- W2156065370 cites W2110590976 @default.
- W2156065370 cites W2114315853 @default.
- W2156065370 cites W2114421459 @default.
- W2156065370 cites W2115082169 @default.
- W2156065370 cites W2118749559 @default.
- W2156065370 cites W2119968907 @default.
- W2156065370 cites W2120815988 @default.
- W2156065370 cites W2127406402 @default.
- W2156065370 cites W2133982468 @default.
- W2156065370 cites W2139004889 @default.
- W2156065370 cites W2142865674 @default.
- W2156065370 cites W2156384755 @default.
- W2156065370 cites W2157783137 @default.
- W2156065370 cites W2157985992 @default.
- W2156065370 cites W2158804540 @default.
- W2156065370 cites W2161175463 @default.
- W2156065370 cites W2315210740 @default.
- W2156065370 cites W4292199267 @default.
- W2156065370 doi "https://doi.org/10.1359/jbmr.071002" @default.
- W2156065370 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2663588" @default.
- W2156065370 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17907925" @default.
- W2156065370 hasPublicationYear "2008" @default.
- W2156065370 type Work @default.
- W2156065370 sameAs 2156065370 @default.
- W2156065370 citedByCount "71" @default.
- W2156065370 countsByYear W21560653702012 @default.
- W2156065370 countsByYear W21560653702013 @default.
- W2156065370 countsByYear W21560653702014 @default.
- W2156065370 countsByYear W21560653702015 @default.
- W2156065370 countsByYear W21560653702016 @default.
- W2156065370 countsByYear W21560653702017 @default.
- W2156065370 countsByYear W21560653702018 @default.
- W2156065370 countsByYear W21560653702019 @default.
- W2156065370 countsByYear W21560653702020 @default.
- W2156065370 countsByYear W21560653702021 @default.
- W2156065370 countsByYear W21560653702022 @default.
- W2156065370 countsByYear W21560653702023 @default.
- W2156065370 crossrefType "journal-article" @default.
- W2156065370 hasAuthorship W2156065370A5006019460 @default.
- W2156065370 hasAuthorship W2156065370A5010663597 @default.
- W2156065370 hasAuthorship W2156065370A5019419731 @default.
- W2156065370 hasAuthorship W2156065370A5028921086 @default.
- W2156065370 hasAuthorship W2156065370A5034508784 @default.
- W2156065370 hasAuthorship W2156065370A5046608295 @default.
- W2156065370 hasAuthorship W2156065370A5083698757 @default.
- W2156065370 hasBestOaLocation W21560653701 @default.
- W2156065370 hasConcept C170493617 @default.
- W2156065370 hasConcept C190283241 @default.
- W2156065370 hasConcept C202751555 @default.
- W2156065370 hasConcept C2778260815 @default.
- W2156065370 hasConcept C31573885 @default.
- W2156065370 hasConcept C55493867 @default.
- W2156065370 hasConcept C79879829 @default.
- W2156065370 hasConcept C86803240 @default.
- W2156065370 hasConcept C95444343 @default.
- W2156065370 hasConceptScore W2156065370C170493617 @default.
- W2156065370 hasConceptScore W2156065370C190283241 @default.
- W2156065370 hasConceptScore W2156065370C202751555 @default.
- W2156065370 hasConceptScore W2156065370C2778260815 @default.
- W2156065370 hasConceptScore W2156065370C31573885 @default.