scholarly journals Investigation of galectin-3, lipocalin 2, retinol binding protein (RBP), small dense low-density lipoprotein (sdLDL) in patients with hirsutism

2019 ◽  
Vol 36 (2) ◽  
pp. 177-183
Author(s):  
Ibrahim Halil Yavuz ◽  
Goknur Ozaydin-Yavuz ◽  
Erdem Çokluk ◽  
Zehra Kurtoğlu ◽  
Serap Gunes Bilgili
Keyword(s):  
Binding Protein ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Retinol Binding Protein ◽  
Low Density ◽  
Lipocalin 2 ◽  
Galectin 3

The Changes in Plasma Retinol-Binding Protein 4 Levels are Associated With Those of the Apolipoprotein B-Containing Lipoproteins During Dietary and Drug Treatment

Angiology ◽  
2011 ◽  
Vol 63 (1) ◽  
pp. 67-75 ◽  
Author(s):  
Georgios A. Christou ◽  
Constantinos C. Tellis ◽  
Moses S. Elisaf ◽  
Alexandros D. Tselepis ◽  
Dimitrios N. Kiortsis
Keyword(s):  
Apolipoprotein B ◽  
Binding Protein ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Retinol Binding Protein ◽  
Percentage Change ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Retinol Binding Protein 4

We investigated the association between retinol-binding protein 4 (RBP4) and apolipoprotein B (ApoB)-containing lipoproteins. Obese or overweight, hypertriglyceridemic patients underwent the following interventions for 3 months: (1) Diet (n = 20), (2) Diet + fenofibrate (n = 18), (3) Diet + rimonabant (n = 8). Circulating RBP4 decreased during dietary treatment. The percentage change in RBP4 was positively correlated with the percentage changes in very-low density lipoprotein cholesterol ( r = .570, P = .02), low-density lipoprotein cholesterol ([LDL-C]; r = .605, P = .01), ApoB ( r = .705, P = .007), and small dense LDL-C ([sdLDL-C]; r = .872, P < .001). The percentage change in RBP4 was the best predictor of the percentage changes in sdLDL-C and ApoB. Rimonabant treatment reduced RBP4, whereas fenofibrate increased RBP4 during the first month of therapy followed by a subsequent decrease. In conclusion, RBP4 may significantly influence the metabolic pathways responsible for changes in ApoB lipoprotein subspecies, thus RBP4 may be associated with cardiovascular disease risk.

scholarly journals Lipocalin 2 Deficiency Alters Estradiol Production and Estrogen Receptor Signaling in Female Mice

Endocrinology ◽  
2012 ◽  
Vol 153 (3) ◽  
pp. 1183-1193 ◽  
Author(s):  
Hong Guo ◽  
Yuanyuan Zhang ◽  
David A. Brockman ◽  
Wendy Hahn ◽  
David A. Bernlohr ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Adipose Tissue ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Lipocalin 2 ◽  
Wild Type ◽  
Female Mice ◽  
Estrogen Receptor Signaling ◽  
Age Related

We have previously characterized lipocalin 2 (Lcn2) as a new adipokine having a critical role in energy and lipid metabolism in male mice. Previous studies by others have suggested that Lcn2 is a putative target gene of estrogens. In this study, we reported the effect of Lcn2 deficiency on estradiol biosynthesis and estrogen receptor signaling in female Lcn2-deficient (Lcn2−/−) mice. We found that Lcn2 expression in white adipose tissue is gender, depot, and age dependent. In female mice, Lcn2 is predominantly expressed in inguinal adipose tissue but at relatively very low levels in perigonadal depot and ovary. After 22 wk of high-fat diet (HFD) feeding or at old age, Lcn2−/− female mice had significantly reduced levels of serum 17β-estradiol and down-regulated expression of estrogen receptor α in multiple metabolic tissues. Consistently, the expression of estrogen-regulated genes involved in cholesterol homeostasis, such as liver X receptor β and low-density lipoprotein receptor was also down-regulated in the adipose tissue of Lcn2−/− mice. These changes were in line with the development of atherogenic dyslipidemia in response to HFD feeding; female Lcn2−/− mice had significantly elevated levels of total cholesterol and low-density lipoprotein cholesterol, whereas reduced high-density lipoprotein cholesterol levels compared with wild-type female mice. Interestingly, when compared with wild-type controls, HFD-fed female Lcn2−/− mice had significantly reduced expression levels of aromatase, a key enzyme regulating estradiol biosynthesis, in adipose tissue. Moreover, Lcn2 deficiency markedly blunted age-related increase in adipose aromatase expression but had no significant impact on age-related reduction in ovarian aromatase expression. Our findings suggest that Lcn2 has a tissue-specific role in adipose estradiol biosynthesis, which may link Lcn2 to obesity- and age-related estradiol production and metabolic complications in females.

scholarly journals A Novel Oxidized Low-Density Lipoprotein-Binding Protein, Asp-Hemolysin, Recognizes Lysophosphatidylcholine

2002 ◽  
Vol 25 (6) ◽  
pp. 787-790 ◽  
Author(s):  
Yoichi Kudo ◽  
Toshihiro Ootani ◽  
Takeshi Kumagai ◽  
Yuji Fukuchi ◽  
Keiichi Ebina ◽  
...  
Keyword(s):  
Binding Protein ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Lipoprotein Binding

A novel oxidized low-density lipoprotein-binding protein from Pseudomonas aeruginosa

Microbiology ◽  
2008 ◽  
Vol 154 (2) ◽  
pp. 654-665 ◽  
Author(s):  
Jayasimha Rao ◽  
Antonio DiGiandomenico ◽  
Jason Unger ◽  
Yongde Bao ◽  
Renata K. Polanowska-Grabowska ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Binding Protein ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Lipoprotein Binding

scholarly journals Intracellular AIBP (Apolipoprotein A-I Binding Protein) Regulates Oxidized LDL (Low-Density Lipoprotein)-Induced Mitophagy in Macrophages

2020 ◽  
Author(s):  
Soo-Ho Choi ◽  
Colin Agatisa-Boyle ◽  
Ayelet Gonen ◽  
Alisa Kim ◽  
Jungsu Kim ◽  
...  
Keyword(s):  
Quality Control ◽  
Cell Death ◽  
Binding Protein ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Wild Type ◽  
Atherosclerotic Lesions ◽  
Apolipoprotein A ◽  
Human And Mouse

Objective: Atherosclerotic lesions are often characterized by accumulation of OxLDL (oxidized low-density lipoprotein), which is associated with vascular inflammation and lesion vulnerability to rupture. Extracellular AIBP (apolipoprotein A-I binding protein; encoded by APOA1BP gene), when secreted, promotes cholesterol efflux and regulates lipid rafts dynamics, but its role as an intracellular protein in mammalian cells remains unknown. The aim of this work was to determine the function of intracellular AIBP in macrophages exposed to OxLDL and in atherosclerotic lesions. Approach and Results: Using a novel monoclonal antibody against human and mouse AIBP, which are highly homologous, we demonstrated robust AIBP expression in human and mouse atherosclerotic lesions. We observed significantly reduced autophagy in bone marrow-derived macrophages, isolated from Apoa1bp −/− compared with wild-type mice, which were exposed to OxLDL. In atherosclerotic lesions from Apoa1bp −/− mice subjected to Ldlr knockdown and fed a Western diet, autophagy was reduced, whereas apoptosis was increased, when compared with that in wild-type mice. AIBP expression was necessary for efficient control of reactive oxygen species and cell death and for mitochondria quality control in macrophages exposed to OxLDL. Mitochondria-localized AIBP, via its N-terminal domain, associated with E3 ubiquitin-protein ligase PARK2 (Parkin), MFN (mitofusin)1, and MFN2, but not BNIP3 (Bcl2/adenovirus E1B 19-kDa-interacting protein-3), and regulated ubiquitination of MFN1 and MFN2, key components of mitophagy. Conclusions: These data suggest that intracellular AIBP is a new regulator of autophagy in macrophages. Mitochondria-localized AIBP augments mitophagy and participates in mitochondria quality control, protecting macrophages against cell death in the context of atherosclerosis.

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