TAILIEUCHUNG - Báo cáo y học: " Pro-inflammatory endothelial cell dysfunction is associated with intersectin-1s down-regulation"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài:" Pro-inflammatory endothelial cell dysfunction is associated with intersectin-1s down-regulation. | Singla et al. Respiratory Research 2011 12 46 http content 12 1 46 RESPIRATORY RESEARCH RESEARCH Open Access Pro-inflammatory endothelial cell dysfunction is associated with intersectin-1s down-regulation 1 2 2 2 1 Sunit Singla Dan Predescu 1 Cristina Bardita Minhua Wang Jian Zhang Robert A Balk and Sanda Predescu1 2 Abstract Background The response of lung microvascular endothelial cells ECs to lipopolysaccharide LPS is central to the pathogenesis of lung injury. It is dual in nature with one facet that is pro-inflammatory and another that is cyto-protective. In previous work overexpression of the anti-apoptotic Bcl-XL rescued ECs from apoptosis triggered by siRNA knockdown of intersectin-1s ITSN-1s a pro-survival protein crucial for ECs function. Here we further characterized the cyto-protective EC response to LPS and pro-inflammatory dysfunction. Methods and Results Electron microscopy EM analyses of LPS-exposed ECs revealed an activated dysfunctional phenotype while a biotin assay for caveolae internalization followed by biochemical quantification indicated that LPS causes a 40 inhibition in biotin uptake compared to controls. Quantitative PCR and Western blotting were used to evaluate the mRNA and protein expression respectively for several regulatory proteins of intrinsic apoptosis including ITSN-1s. The decrease in ITSN-1s mRNA and protein expression were countered by Bcl-XL and survivin upregulation as well as Bim downregulation events thought to protect ECs from impending apoptosis. Absence of apoptosis was confirmed by TUNEL and lack of cytochrome c cyt c efflux from mitochondria. Moreover LPS exposure caused induction and activation of inducible nitric oxide synthase iNOS and a mitochondrial variant mtNOS as well as augmented mitochondrial NO production as measured by an oxidation oxyhemoglobin oxyHb assay applied on mitochondrial-enriched fractions prepared from LPS-exposed ECs. Interestingly expression of myc-ITSN-1s .

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