FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2789633344> ?p ?o ?g. }

• W2789633344 endingPage "275" @default.
• W2789633344 startingPage "263" @default.
• W2789633344 abstract "The deposition of advanced glycation end products (AGEs) is accelerated in photoaged skin, but the underlying mechanisms remain elusive. Intracellular degradation has been recently considered to play an important role in AGEs removal. Although lysosomal cathepsin D (CatD), B (CatB), L(CatL) and proteasomes are found to degrade internalized AGEs, it remains unknown which protease degrades internalized AGEs in human dermal fibroblasts (HDFs), and whether a decrease in intracellular degradation contributes to enhanced AGEs deposition in photoaged skin.This study aims to investigate the specific proteases that contribute to intracellular AGEs degradation in HDFs and regulate AGEs accumulation in photoaged skin.Repetitive UVA irradiation was used to induce primary HDF photoaging in vitro. Uptake and degradation of AGE-BSA were verified and compared between photoaged and non-photoaged fibroblasts with flow cytometry, ELISA and confocal microscopy. Proteasomal and lysosomal activity, expression of CatD, CatB and CatL were also investigated between photoaged and non-photoaged fibroblasts. Further, the effect of protease inhibitors and CatD overexpression via lentiviral transduction on AGE-BSA degradation was analyzed. Finally, the correlation between CatD expression and AGEs accumulation in sun-exposed and sun-protected skin of people from different age was studied with immunohistochemistry.Fibroblasts underwent photoaging in vitro after repetitive UVA irradiation. AGE-BSA was taken up by both photoaged and non-photoaged fibroblasts, but its degradation was significantly decreased in photoaged cells than that of non-photoaged cells. Although the activity of proteasome, CatB, Cat L and Cat D was significantly reduced in photoaged fibroblasts compared to that of non-photoaged cells, and the expression of CatB, CatL and CatD was profoundly attenuated in photoaged fibroblasts, inhibiting proteasome, CatB and CatL did not affect AGE-BSA degradation in HDFs. In contrast, inhibiting CatD activity dose-dependently decreased AGE-BSA degradation; whereas CatD overexpression significantly increased AGE-BSA degradation. Importantly, AGEs accumulation in photo-damaged skin in vivo was inversely correlated with CatD expression.CatD plays a major role in intracellular AGEs degradation. Decreased CatD expression and activity impairs intracellular AGEs degradation in photoaged fibroblasts, which may contribute to accelerated AGEs deposition in photoaged skin. The present study provides a potentially novel molecular basis for antiphotoaging therapy." @default.
• W2789633344 created "2018-03-29" @default.
• W2789633344 creator A5015196405 @default.
• W2789633344 creator A5025275209 @default.
• W2789633344 creator A5042951793 @default.
• W2789633344 creator A5057793246 @default.
• W2789633344 creator A5067988089 @default.
• W2789633344 creator A5071054983 @default.
• W2789633344 creator A5073341733 @default.
• W2789633344 creator A5090780152 @default.
• W2789633344 creator A5090915785 @default.
• W2789633344 date "2018-06-01" @default.
• W2789633344 modified "2023-10-16" @default.
• W2789633344 title "Cathepsin D contributes to the accumulation of advanced glycation end products during photoaging" @default.
• W2789633344 cites W1501698769 @default.
• W2789633344 cites W1559274360 @default.
• W2789633344 cites W1965706192 @default.
• W2789633344 cites W1968386889 @default.
• W2789633344 cites W1968862009 @default.
• W2789633344 cites W1972024904 @default.
• W2789633344 cites W1972771840 @default.
• W2789633344 cites W1972971462 @default.
• W2789633344 cites W1973492134 @default.
• W2789633344 cites W1983668743 @default.
• W2789633344 cites W1987716012 @default.
• W2789633344 cites W1987876460 @default.
• W2789633344 cites W1990380577 @default.
• W2789633344 cites W1992706642 @default.
• W2789633344 cites W1994972521 @default.
• W2789633344 cites W1996895672 @default.
• W2789633344 cites W2006193286 @default.
• W2789633344 cites W2008128102 @default.
• W2789633344 cites W2022776385 @default.
• W2789633344 cites W2027008375 @default.
• W2789633344 cites W2029032182 @default.
• W2789633344 cites W2029388843 @default.
• W2789633344 cites W2048842224 @default.
• W2789633344 cites W2049320510 @default.
• W2789633344 cites W2050518120 @default.
• W2789633344 cites W2051612655 @default.
• W2789633344 cites W2055385755 @default.
• W2789633344 cites W2061662212 @default.
• W2789633344 cites W2118925247 @default.
• W2789633344 cites W2119627924 @default.
• W2789633344 cites W2125550664 @default.
• W2789633344 cites W2130266843 @default.
• W2789633344 cites W2155845629 @default.
• W2789633344 cites W2318905955 @default.
• W2789633344 cites W2404082493 @default.
• W2789633344 cites W2551119957 @default.
• W2789633344 cites W2581475444 @default.
• W2789633344 cites W4256045236 @default.
• W2789633344 doi "https://doi.org/10.1016/j.jdermsci.2018.02.009" @default.
• W2789633344 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29501392" @default.
• W2789633344 hasPublicationYear "2018" @default.
• W2789633344 type Work @default.
• W2789633344 sameAs 2789633344 @default.
• W2789633344 citedByCount "13" @default.
• W2789633344 countsByYear W27896333442019 @default.
• W2789633344 countsByYear W27896333442020 @default.
• W2789633344 countsByYear W27896333442021 @default.
• W2789633344 countsByYear W27896333442022 @default.
• W2789633344 countsByYear W27896333442023 @default.
• W2789633344 crossrefType "journal-article" @default.
• W2789633344 hasAuthorship W2789633344A5015196405 @default.
• W2789633344 hasAuthorship W2789633344A5025275209 @default.
• W2789633344 hasAuthorship W2789633344A5042951793 @default.
• W2789633344 hasAuthorship W2789633344A5057793246 @default.
• W2789633344 hasAuthorship W2789633344A5067988089 @default.
• W2789633344 hasAuthorship W2789633344A5071054983 @default.
• W2789633344 hasAuthorship W2789633344A5073341733 @default.
• W2789633344 hasAuthorship W2789633344A5090780152 @default.
• W2789633344 hasAuthorship W2789633344A5090915785 @default.
• W2789633344 hasBestOaLocation W27896333441 @default.
• W2789633344 hasConcept C147990577 @default.
• W2789633344 hasConcept C153911025 @default.
• W2789633344 hasConcept C16005928 @default.
• W2789633344 hasConcept C167844969 @default.
• W2789633344 hasConcept C170493617 @default.
• W2789633344 hasConcept C181199279 @default.
• W2789633344 hasConcept C185592680 @default.
• W2789633344 hasConcept C202751555 @default.
• W2789633344 hasConcept C2776960578 @default.
• W2789633344 hasConcept C2778005187 @default.
• W2789633344 hasConcept C2780381497 @default.
• W2789633344 hasConcept C2909910311 @default.
• W2789633344 hasConcept C553184892 @default.
• W2789633344 hasConcept C55493867 @default.
• W2789633344 hasConcept C71924100 @default.
• W2789633344 hasConcept C79879829 @default.
• W2789633344 hasConcept C86803240 @default.
• W2789633344 hasConcept C95444343 @default.
• W2789633344 hasConceptScore W2789633344C147990577 @default.
• W2789633344 hasConceptScore W2789633344C153911025 @default.
• W2789633344 hasConceptScore W2789633344C16005928 @default.
• W2789633344 hasConceptScore W2789633344C167844969 @default.
• W2789633344 hasConceptScore W2789633344C170493617 @default.
• W2789633344 hasConceptScore W2789633344C181199279 @default.

• next