FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W300068448> ?p ?o ?g. }

• W300068448 endingPage "77" @default.
• W300068448 startingPage "73" @default.
• W300068448 abstract "Although it is recognized that bronchial smooth muscle cells (BSMCs) play a key role in airway remodeling during chronic asthma, it is not well understood how BSMCs exert their inflammatory functions. The extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway is an important signaling pathway in chronic asthma, but its influence on secretion by BSMCs has not been well-studied. We investigated the impact of ERK1/2 signaling pathway on secretion by BSMCs in a rat model of chronic asthma in this study.To create a rat model of chronic asthma, Wistar rats underwent ovalbumim (OVA) injection and eight weeks of inhalation. BSMCs were isolated and cultured in vitro. Epidermal growth factor, PD98059 and ERK1/2 antisense oligonucleotide were used to explore the role of ERK1/2 signaling pathway. The expression of P-ERK1/2 (phospho-ERK1/2) in BSMCs was analyzed by Western blot and reverse transcriptase-polymerase chain reaction (RT-PCR). Secretion of BSMCs was detected by enzyme-linked immunosorbent assay (ELISA).Phospho-ERK1/2 expression was increased in BSMCs of chronic asthmatic rats compared with the controls. PD98059 inhibited expression of phospho-ERK1/2 protein, while treatment with an antisense oligonucleotide inhibited the expression of P-ERK1/2 mRNA and protein. BSMCs obtained from the chronic asthma group secreted significantly greater quantities of growth factors (transforming growth factor (TGF)-beta(1), vascular endothelial growth factor (VEGF) and connective tissue growth factor (CTGF)), cytokines (regulated upon activation, normal T cell-expressed and secreted (RANTES) and eotaxin), and extracellular matrix (fibronectin and collagen I) compared with normal controls. Epidermal growth factor stimulated secretion in both groups, but the response of the chronic asthma group was more intense. Both PD98059 and antisense oligonucleotide suppressed secretion by BSMCs in chronic ashmatic rats. Antisense oligonucleotide reduced the level of RANTES nearly to that of normal controls, while PD98059 could not.These results suggest that ERK1/2 signaling pathway may play an important role in the augmented secretion of BSMCs in chronic asthmatic rats, and ERK1/2 antisense oligonucleotide effectively inhibits the process." @default.
• W300068448 created "2016-06-24" @default.
• W300068448 creator A5003377806 @default.
• W300068448 creator A5020139919 @default.
• W300068448 creator A5031091839 @default.
• W300068448 creator A5046045131 @default.
• W300068448 creator A5056416945 @default.
• W300068448 creator A5058805192 @default.
• W300068448 creator A5088352466 @default.
• W300068448 date "2008-01-01" @default.
• W300068448 modified "2023-10-02" @default.
• W300068448 title "Role of the extracellular signal-regulated kinase 1/2 signaling pathway in regulating the secretion of bronchial smooth muscle cells in a rat model of chronic asthma" @default.
• W300068448 cites W1970354248 @default.
• W300068448 cites W1982140654 @default.
• W300068448 cites W2006705655 @default.
• W300068448 cites W2011991411 @default.
• W300068448 cites W2013740811 @default.
• W300068448 cites W2051808553 @default.
• W300068448 cites W2072440487 @default.
• W300068448 cites W2094233080 @default.
• W300068448 cites W2099196939 @default.
• W300068448 cites W2104675269 @default.
• W300068448 cites W2117081272 @default.
• W300068448 cites W2121582695 @default.
• W300068448 cites W2135555439 @default.
• W300068448 cites W2188764126 @default.
• W300068448 cites W2325769889 @default.
• W300068448 doi "https://doi.org/10.1097/00029330-200801010-00014" @default.
• W300068448 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18208670" @default.
• W300068448 hasPublicationYear "2008" @default.
• W300068448 type Work @default.
• W300068448 sameAs 300068448 @default.
• W300068448 citedByCount "8" @default.
• W300068448 countsByYear W3000684482012 @default.
• W300068448 countsByYear W3000684482013 @default.
• W300068448 countsByYear W3000684482014 @default.
• W300068448 countsByYear W3000684482017 @default.
• W300068448 crossrefType "journal-article" @default.
• W300068448 hasAuthorship W300068448A5003377806 @default.
• W300068448 hasAuthorship W300068448A5020139919 @default.
• W300068448 hasAuthorship W300068448A5031091839 @default.
• W300068448 hasAuthorship W300068448A5046045131 @default.
• W300068448 hasAuthorship W300068448A5056416945 @default.
• W300068448 hasAuthorship W300068448A5058805192 @default.
• W300068448 hasAuthorship W300068448A5088352466 @default.
• W300068448 hasBestOaLocation W3000684481 @default.
• W300068448 hasConcept C118131993 @default.
• W300068448 hasConcept C126322002 @default.
• W300068448 hasConcept C134018914 @default.
• W300068448 hasConcept C170493617 @default.
• W300068448 hasConcept C184235292 @default.
• W300068448 hasConcept C203014093 @default.
• W300068448 hasConcept C2775960820 @default.
• W300068448 hasConcept C2776042228 @default.
• W300068448 hasConcept C2777037409 @default.
• W300068448 hasConcept C2777716647 @default.
• W300068448 hasConcept C2780631158 @default.
• W300068448 hasConcept C28406088 @default.
• W300068448 hasConcept C49039625 @default.
• W300068448 hasConcept C62478195 @default.
• W300068448 hasConcept C71924100 @default.
• W300068448 hasConcept C86803240 @default.
• W300068448 hasConcept C95444343 @default.
• W300068448 hasConceptScore W300068448C118131993 @default.
• W300068448 hasConceptScore W300068448C126322002 @default.
• W300068448 hasConceptScore W300068448C134018914 @default.
• W300068448 hasConceptScore W300068448C170493617 @default.
• W300068448 hasConceptScore W300068448C184235292 @default.
• W300068448 hasConceptScore W300068448C203014093 @default.
• W300068448 hasConceptScore W300068448C2775960820 @default.
• W300068448 hasConceptScore W300068448C2776042228 @default.
• W300068448 hasConceptScore W300068448C2777037409 @default.
• W300068448 hasConceptScore W300068448C2777716647 @default.
• W300068448 hasConceptScore W300068448C2780631158 @default.
• W300068448 hasConceptScore W300068448C28406088 @default.
• W300068448 hasConceptScore W300068448C49039625 @default.
• W300068448 hasConceptScore W300068448C62478195 @default.
• W300068448 hasConceptScore W300068448C71924100 @default.
• W300068448 hasConceptScore W300068448C86803240 @default.
• W300068448 hasConceptScore W300068448C95444343 @default.
• W300068448 hasIssue "1" @default.
• W300068448 hasLocation W3000684481 @default.
• W300068448 hasLocation W3000684482 @default.
• W300068448 hasOpenAccess W300068448 @default.
• W300068448 hasPrimaryLocation W3000684481 @default.
• W300068448 hasRelatedWork W1987783367 @default.
• W300068448 hasRelatedWork W2009389088 @default.
• W300068448 hasRelatedWork W2020884724 @default.
• W300068448 hasRelatedWork W2085048026 @default.
• W300068448 hasRelatedWork W2090408064 @default.
• W300068448 hasRelatedWork W2114259434 @default.
• W300068448 hasRelatedWork W2159390875 @default.
• W300068448 hasRelatedWork W2161296685 @default.
• W300068448 hasRelatedWork W2169525455 @default.
• W300068448 hasRelatedWork W4255681344 @default.
• W300068448 hasVolume "121" @default.
• W300068448 isParatext "false" @default.
• W300068448 isRetracted "false" @default.

• next