Cathepsins F and S block HDL3-induced cholesterol efflux from macrophage foam cells

Lindstedt, Leena; Lee, Miriam; Öörni, Katariina; Brὂmme, Dieter; Kovanen, Petri T.

doi:10.1016/j.bbrc.2003.11.020

Cited by 68 publications

(48 citation statements)

References 35 publications

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“…Likewise, the presence of a large HDL 2b subclass was found to be highly inversely correlated with the risk of coronary disease in the prospective Malmo Diet and Cancer Study 39) . Regardless, the changes in the HDL subclass profiles observed in our study were not associated with statin-induced CTSS-lowering, as we had hypothesized based on previously published in vitro evidence 14) .…”

Section: Discussionsupporting

confidence: 70%

“…The incubation of HDL3 (high-density lipoprotein isolated via sequential ultracentrifugation from the plasma within a density range of 1.125 to 1.210 g/mL) with cathepsin S leads to the rapid loss of preβ-HDL and reduced cholesterol efflux from macrophages 14) , and cathepsins in general (e.g. D, F, S and K) modify apolipoprotein B in LDL and subsequently induce foam cell formation 15) .…”

Section: Ctss Mrna Quantification In the Plasmamentioning

confidence: 99%

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Interrelated Cathepsin S-Lowering and LDL Subclass Profile Improvements Induced by Atorvastatin in the Plasma of Stable Angina Patients

Mirjanic-Azaric

Vekić

Zeljković

et al. 2014

JAT

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Aim:We hypothesized that, in stable angina patients, atorvastatin therapy lowers the cathepsin S (CTSS) concentrations, as assessed non-invasively according to a plasma analysis. In addition, the low-density lipoprotein (LDL) and high-density lipoprotein (HDL) size and subclasses in the plasma were analysed to establish the association between CTSS and lipoprotein metabolism and determine whether this association is atorvastatin-sensitive. Methods: A total of 43 patients with stable angina received atorvastatin therapy (20 mg/day, 10 weeks). The plasma CTSS mRNA levels, CTSS protein concentrations and CTSS activity, as well as LDL and HDL size and subclasses, were analysed before and after treatment. Results: Atorvastatin treatment did not change the plasma CTSS mRNA levels, although it lowered the plasma CTSS concentrations and activity. An increased plasma CTSS concentration and activity were found to be associated with a more atherogenic LDL subclass profile (a decreased dominant LDL size and increased percentage of small, dense LDL particles). The atorvastatin-induced CTSSlowering effect was concomitant with an improvement in the LDL subclass profile, and the changes were found to be interrelated. Concomitant, interrelated changes in the CTSS levels and LDL subclass profiles were found in the LDL phenotype B patients only (a dominant LDL diameter of ≤ 25.5 nm at the start of the study). In this subgroup, lowering of the plasma CTSS mRNA level also correlated with lowering of the proportion of small, dense LDL particles. Conclusions: Atorvastatin-induced CTSS-lowering and LDL subclass profile improvements in the plasma of LDL phenotype B patients with stable angina are concomitant and interrelated. J Atheroscler Thromb, 2014; 21:868-877.

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Section: Discussionsupporting

confidence: 70%

Section: Ctss Mrna Quantification In the Plasmamentioning

confidence: 99%

Interrelated Cathepsin S-Lowering and LDL Subclass Profile Improvements Induced by Atorvastatin in the Plasma of Stable Angina Patients

Mirjanic-Azaric

Vekić

Zeljković

et al. 2014

JAT

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“…However, cat F is unique in that it has a long pro-region whose function is unknown. In this regard, the previously reported potent activity of cat F in lipoprotein degradation is remarkable (17,26). Although the exact substrate of cat F in neurons is not known, we favor the view that a lipoprotein component of the lipofuscin complex is a preferential substrate of cat F. The unique, long amino-terminal pro-region of cat F may be a substrate recognition site for this putative lipoprotein.…”

Section: Discussionmentioning

confidence: 87%

“…Recombinant active cat F degrades the major histocompatibility complex (MHC) class II chaperone, invariant chain (Ii), as well or better than cathepsin S (cat S) (33). More recently, cat F has been implicated in lipoprotein biology by virtue of its ability to inhibit cholesterol efflux from peritoneal macrophages in vitro (17) and to degrade apolipoprotein B100 in vitro (26). However, a physiological role for cat F has not been established.…”

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confidence: 99%

Murine Cathepsin F Deficiency Causes Neuronal Lipofuscinosis and Late-Onset Neurological Disease

Tang

Lee

Galvez

et al. 2006

Molecular and Cellular Biology

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Cathepsin F (cat F) is a widely expressed lysosomal cysteine protease whose in vivo role is unknown. To address this issue, mice deficient in cat F were generated via homologous recombination. Although cat F−/− mice appeared healthy and reproduced normally, they developed progressive hind leg weakness and decline in motor coordination at 12 to 16 months of age, followed by significant weight loss and death within 6 months. cat F was found to be expressed throughout the central nervous system (CNS). cat F−/− neurons accumulated eosinophilic granules that had features typical of lysosomal lipofuscin by electron microscopy. Large amounts of autofluorescent lipofuscin, characteristic of the neurodegenerative disease neuronal ceroid lipofuscinosis (NCL), accumulated throughout the CNS but not in visceral organs, beginning as early as 6 weeks of age. Pronounced gliosis, an indicator of neuronal stress and neurodegeneration, was also apparent in older cat F−/− mice. cat F is the only cysteine cathepsin whose inactivation alone causes a lysosomal storage defect and progressive neurological features in mice. The late onset suggests that this gene may be a candidate for adult-onset NCL.

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“…The glycoprotein osteoprotegerin (OPG), which is positively related to coronary calcification, vascular stiffness, and the presence of unstable atherosclerotic plaques [34], is included among the candidate predictors because we found it to be an independent predictor of mortality in CAD patients [25]. The cathepsins are a group of proteinases that have been suggested to be causally involved in the different stages of the atherosclerotic process, from the early stages such as foam cell formation [35] to the later stages, such as destabilisation of the fibrous cap [36]. Endostatin is an endogenous angiogenesis inhibitor where circulating levels have been suggested to mirror an increased neovascularisation induced by vascular or myocardial ischaemia [37], but endostatin has also been suggested to be a marker for an increased extracellular matrix remodelling [38].…”

Section: Background Information On the Advanced Biochemical Predictorsmentioning

confidence: 99%

Predictors for major cardiovascular outcomes in stable ischaemic heart disease (PREMAC): statistical analysis plan for data originating from the CLARICOR (clarithromycin for patients with stable coronary heart disease) trial

et al. 2017

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Background: The purpose of the predictors for major cardiovascular outcomes in stable ischaemic heart disease (PREMAC) study is exploratory and hypothesis generating. We want to identify biochemical quantities which-conditionally on the values of available standard demographic, anamnestic, and biochemical data-may improve the prediction of cardiovascular outcomes and/or death in patients suffering from stable ischaemic heart disease. The candidate biochemical quantities include N-terminal pro-B-type natriuretic peptide, YKL-40, osteoprotegerin, high-sensitive assay cardiac troponin T (hs-cTnT), pregnancy-associated plasma protein-A (PAPP-A), cathepsin B, cathepsin S, soluble TNF receptor 1 and 2, neutrophil gelatinase-associated lipocalin, endostatin, and calprotectin. As an extra objective, we also want to assess if skewness in these predictors may explain why the clarithromycin for patients with stable coronary heart disease (CLARICOR) trial found increased all-cause and cardiovascular (CV) mortality on a brief clarithromycin regimen compared with placebo.

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Cathepsins F and S block HDL3-induced cholesterol efflux from macrophage foam cells

Cited by 68 publications

References 35 publications

Interrelated Cathepsin S-Lowering and LDL Subclass Profile Improvements Induced by Atorvastatin in the Plasma of Stable Angina Patients

Interrelated Cathepsin S-Lowering and LDL Subclass Profile Improvements Induced by Atorvastatin in the Plasma of Stable Angina Patients

Murine Cathepsin F Deficiency Causes Neuronal Lipofuscinosis and Late-Onset Neurological Disease

Predictors for major cardiovascular outcomes in stable ischaemic heart disease (PREMAC): statistical analysis plan for data originating from the CLARICOR (clarithromycin for patients with stable coronary heart disease) trial

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