FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4307707389> ?p ?o ?g. }

• W4307707389 abstract "Aim: Bladder outlet obstruction (BOO) leads to bladder wall remodeling accompanying the progression from inflammation to fibrosis where pathological hydrostatic pressure (HP)-induced alteration of bladder smooth muscle cells (BSMCs) hypertrophic and excessive extracellular matrix (ECM) deposition play a pivotal role. Recently, we have predicted survivin (BIRC5) as a potential hub gene that might be critical during bladder fibrosis by bioinformatics analyses from rat BOO bladder, but its function during BOO progression remains unknown. Here, we investigated the role of survivin protein on bladder dysfunction of BOO both in vitro and in vivo. Methods: Sprague-Dawley female rats were divided into three groups: control group, BOO group, and BOO followed by the treatment with YM155 group. Bladder morphology and function were evaluated by Masson staining and urodynamic testing. To elucidate the underlying mechanism, hBSMCs were subjected to pathological HP of 200 cm H2O and co-cultured with the presence or absence of survivin siRNA and/or autophagy inhibitor 3-MA. Autophagy was evaluated by the detection of Beclin1 and LC3B-II expression, proliferation was conducted by the EdU analysis and PCNA expression, and fibrosis was assessed by the examination of Col 1 and Fn expression. Results: BOO led to a gradual alteration of hypertrophy and fibrosis of the bladder, and subsequently induced bladder dysfunction accompanied by increased survivin expression, while these histological and function changes were attenuated by the treatment with YM155. HP significantly increased survivin expression, upregulated Col1 and Fn expression, enhanced proliferation, and downregulated autophagy markers, but these changes were partially abolished by survivin siRNA treatment, which was consistent with the results of the BOO rat experiment. In addition, the anti-fibrotic and anti-proliferative effects of the survivin siRNA treatment on hBSMCs were diminished after the inhibition of autophagy by the treatment with 3-MA. Conclusion: In summary, the upregulation of survivin increased cell proliferation and fibrotic protein expression of hBSMC and drove the onset of bladder remodeling through autophagy during BOO. Targeting survivin in pathological hBSMCs could be a promising way to anti-fibrotic therapeutic approach in bladder remodeling secondary to BOO." @default.
• W4307707389 created "2022-11-05" @default.
• W4307707389 creator A5013171074 @default.
• W4307707389 creator A5017793449 @default.
• W4307707389 creator A5022368878 @default.
• W4307707389 creator A5052374848 @default.
• W4307707389 creator A5052434596 @default.
• W4307707389 creator A5078024000 @default.
• W4307707389 creator A5079868220 @default.
• W4307707389 creator A5082583096 @default.
• W4307707389 creator A5084810789 @default.
• W4307707389 date "2022-10-28" @default.
• W4307707389 modified "2023-10-14" @default.
• W4307707389 title "Survivin knockdown alleviates pathological hydrostatic pressure-induced bladder smooth muscle cell dysfunction and BOO-induced bladder remodeling via autophagy" @default.
• W4307707389 cites W1592112433 @default.
• W4307707389 cites W1601034261 @default.
• W4307707389 cites W1982061390 @default.
• W4307707389 cites W2001960543 @default.
• W4307707389 cites W2036151512 @default.
• W4307707389 cites W2083623063 @default.
• W4307707389 cites W2102046771 @default.
• W4307707389 cites W2102087112 @default.
• W4307707389 cites W2107358956 @default.
• W4307707389 cites W2146124002 @default.
• W4307707389 cites W2191913967 @default.
• W4307707389 cites W2337061518 @default.
• W4307707389 cites W2409715454 @default.
• W4307707389 cites W2415386252 @default.
• W4307707389 cites W2511134629 @default.
• W4307707389 cites W2540191325 @default.
• W4307707389 cites W2768681503 @default.
• W4307707389 cites W2792845439 @default.
• W4307707389 cites W2801558063 @default.
• W4307707389 cites W2804614928 @default.
• W4307707389 cites W2809139475 @default.
• W4307707389 cites W2884914303 @default.
• W4307707389 cites W2886881211 @default.
• W4307707389 cites W2903915221 @default.
• W4307707389 cites W2905320117 @default.
• W4307707389 cites W3008129342 @default.
• W4307707389 cites W3087737804 @default.
• W4307707389 cites W3095723266 @default.
• W4307707389 cites W3135533724 @default.
• W4307707389 cites W3141519003 @default.
• W4307707389 cites W3155339975 @default.
• W4307707389 cites W3176819705 @default.
• W4307707389 cites W3209132289 @default.
• W4307707389 cites W4213429478 @default.
• W4307707389 cites W4225406980 @default.
• W4307707389 cites W4256388608 @default.
• W4307707389 doi "https://doi.org/10.3389/fcell.2022.999547" @default.
• W4307707389 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36393846" @default.
• W4307707389 hasPublicationYear "2022" @default.
• W4307707389 type Work @default.
• W4307707389 citedByCount "0" @default.
• W4307707389 crossrefType "journal-article" @default.
• W4307707389 hasAuthorship W4307707389A5013171074 @default.
• W4307707389 hasAuthorship W4307707389A5017793449 @default.
• W4307707389 hasAuthorship W4307707389A5022368878 @default.
• W4307707389 hasAuthorship W4307707389A5052374848 @default.
• W4307707389 hasAuthorship W4307707389A5052434596 @default.
• W4307707389 hasAuthorship W4307707389A5078024000 @default.
• W4307707389 hasAuthorship W4307707389A5079868220 @default.
• W4307707389 hasAuthorship W4307707389A5082583096 @default.
• W4307707389 hasAuthorship W4307707389A5084810789 @default.
• W4307707389 hasBestOaLocation W43077073891 @default.
• W4307707389 hasConcept C104317684 @default.
• W4307707389 hasConcept C121332964 @default.
• W4307707389 hasConcept C121608353 @default.
• W4307707389 hasConcept C126322002 @default.
• W4307707389 hasConcept C126894567 @default.
• W4307707389 hasConcept C127561419 @default.
• W4307707389 hasConcept C142724271 @default.
• W4307707389 hasConcept C173396325 @default.
• W4307707389 hasConcept C190283241 @default.
• W4307707389 hasConcept C203522944 @default.
• W4307707389 hasConcept C2775975398 @default.
• W4307707389 hasConcept C2779762690 @default.
• W4307707389 hasConcept C2780559512 @default.
• W4307707389 hasConcept C2780616540 @default.
• W4307707389 hasConcept C2910081258 @default.
• W4307707389 hasConcept C502942594 @default.
• W4307707389 hasConcept C55493867 @default.
• W4307707389 hasConcept C71924100 @default.
• W4307707389 hasConcept C86803240 @default.
• W4307707389 hasConcept C97355855 @default.
• W4307707389 hasConceptScore W4307707389C104317684 @default.
• W4307707389 hasConceptScore W4307707389C121332964 @default.
• W4307707389 hasConceptScore W4307707389C121608353 @default.
• W4307707389 hasConceptScore W4307707389C126322002 @default.
• W4307707389 hasConceptScore W4307707389C126894567 @default.
• W4307707389 hasConceptScore W4307707389C127561419 @default.
• W4307707389 hasConceptScore W4307707389C142724271 @default.
• W4307707389 hasConceptScore W4307707389C173396325 @default.
• W4307707389 hasConceptScore W4307707389C190283241 @default.
• W4307707389 hasConceptScore W4307707389C203522944 @default.
• W4307707389 hasConceptScore W4307707389C2775975398 @default.
• W4307707389 hasConceptScore W4307707389C2779762690 @default.
• W4307707389 hasConceptScore W4307707389C2780559512 @default.
• W4307707389 hasConceptScore W4307707389C2780616540 @default.

• next