Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study is one of the first to test the relationship of formulation and structure of reconstituted high density lipoproteins (rHDL), drug behavior involved in remolding process and their targeting mechanism in a foam cell model. Tanshinone IIA-loaded rHDL (TA-rHDL) with different formulations and techniques were prepared and characterized. The targeting mechanism and drug behavior involved in remolding process were undertaken using a foam cell model. TA-rHDL prepared with cholesteryl ester (CE) and glycerol trioleate (TG) were spheres, or else discs. Guanidine hydrochloride denaturation experiments showed increased stability with TA-rHDL, compared to free apos. Phagocytosis tests demonstrated that the spherical TA-rHDL had targeting effect for foam cells through the scavenger receptor-BI and CE-TG interchange with TG-rich lipoproteins pathway under cholesteryl ester transfer protein. Discoidal TA-rHDL could reconstruct to spheres and target via a similar route as TA-rHDL spheres, showing a higher targeting efficiency. Lipophilic Tanshinone IIA could be re-entrapped in rHDL after remolding from discs to spheres and uptaken more by foam cells. Discoidal rHDL may serve as potential nanocarriers for targeting lipophilic cardiovascular drugs to atherosclerosis plaque.
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PMID:Structure and remodeling behavior of drug-loaded high density lipoproteins and their atherosclerotic plaque targeting mechanism in foam cell model. 2183 36

Extracellular matrix (ECM) is a fundamental component of multicellular organisms. Alteration of its structure and/or molecular composition are associated with several pathologies, among the others with atherosclerosis. To determine how the overall ECM architecture of a tissue as complex as the atheroma may change under varying pathological conditions constitutes a great technical challenge. This entails removing cell components and solubilisation of fibrillar proteins in order to allow enzymatic digestion and mass spectrometry analyses. This work aimed at testing and assessing an easy to use, standardized and reproducible proteomics protocol to map ECM proteins in carotid plaque specimens. To this end, plaques from endarterectomies were incubated in different buffers and the resulting solutions and tissue homogenates after incubation were processed for mass spectrometry. Comparison of the different workflows showed that 4M Guanidine treatment (following 0.5M NaCl and 0.08% SDS incubations) is the most promising in terms of ECM enrichment. The protocol can also be used to identify different and complementary classes of proteins both in plaque extracts and homogenates.
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PMID:Extracellular matrix characterization in plaques from carotid endarterectomy by a proteomics approach. 2873 90