E-viri
Recenzirano
Odprti dostop
-
Leng, Yi‐Ping; Ma, Ye‐Shuo; Li, Xiao‐Gang; Chen, Rui‐Fang; Zeng, Ping‐Yu; Li, Xiao‐Hui; Qiu, Cheng‐feng; Li, Ya‐Pei; Zhang, Zhen; Chen, Alex F
British journal of pharmacology, April 2018, Letnik: 175, Številka: 8Journal Article
Background and Purpose Vascular inflammation, including the expression of inflammatory cytokines in endothelial cells, plays a critical role in hyperhomocysteinaemia‐associated vascular diseases. Cathepsin V, specifically expressed in humans, is involved in vascular diseases through its elastolytic and collagenolytic activities. The aim of this study was to determine the effects of cathepsin V on l‐homocysteine‐induced vascular inflammation. Experimental Approach A high methionine diet‐induced hyperhomocysteinaemic mouse model was used to assess cathepsin V expression and vascular inflammation. Cultures of HUVECs were challenged with l‐homocysteine and the cathepsin L/V inhibitor SID to assess the pro‐inflammatory effects of cathepsin V. Transfection and antisense techniques were utilized to investigate the effects of cathepsin V on the dual‐specificity protein phosphatases (DUSPs) and MAPK pathways. Key Results Cathepsin L (human cathepsin V homologous) was increased in the thoracic aorta endothelial cells of hyperhomocysteinaemic mice; l‐homocysteine promoted cathepsin V expression in HUVECs. SID suppressed the activity of cathepsin V and reversed the up‐regulation of inflammatory cytokines (IL‐6, IL‐8 and TNF‐α), adhesion and chemotaxis of leukocytes and vascular inflammation induced by l‐homocysteine in vivo and in vitro. Increased cathepsin V promoted the degradation of DUSP6 and DUSP7, phosphorylation and subsequent nuclear translocation of ERK1/2, phosphorylation of STAT1 and expression of IL‐6, IL‐8 and TNF‐α. Conclusions and Implications This study has identified a novel mechanism, which shows that l‐homocysteine‐induced upregulation of cathepsin V mediates vascular endothelial inflammation under high homocysteine condition partly via ERK1/2/STAT1 pathway. This mechanism could represent a potential therapeutic target in hyperaemia‐associated vascular diseases. Linked Articles This article is part of a themed section on Spotlight on Small Molecules in Cardiovascular Diseases. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.8/issuetoc
Avtor
![loading ... loading ...](themes/default/img/ajax-loading.gif)
Vnos na polico
Trajna povezava
- URL:
Faktor vpliva
Dostop do baze podatkov JCR je dovoljen samo uporabnikom iz Slovenije. Vaš trenutni IP-naslov ni na seznamu dovoljenih za dostop, zato je potrebna avtentikacija z ustreznim računom AAI.
Leto | Faktor vpliva | Izdaja | Kategorija | Razvrstitev | ||||
---|---|---|---|---|---|---|---|---|
JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
Baze podatkov, v katerih je revija indeksirana
Ime baze podatkov | Področje | Leto |
---|
Povezave do osebnih bibliografij avtorjev | Povezave do podatkov o raziskovalcih v sistemu SICRIS |
---|
Vir: Osebne bibliografije
in: SICRIS
To gradivo vam je dostopno v celotnem besedilu. Če kljub temu želite naročiti gradivo, kliknite gumb Nadaljuj.