Metabolic syndrome (MetS) is defined as a of cluster factors that increase the risk of cardiovascular diseases. The criteria for diagnosis for MetS include increased triglycerides, reduced HDL cholesterol levels, raised plasma glucose concentration, and body mass index > 30 kg/m2. In the Puerto Rican population the prevalence of MetS is estimated in approximately 43.3%. Some studies suggested that MetS is linked to higher levels of oxidative stress (OxS). However, there is no data available using OxS markers at Puerto Rican community. Our objective was to determine levels of oxidized lipids and the activity of antioxidant enzymes Glutathione Peroxidase (GPx) and lipid peroxidation. We further expect to evaluate if there is there exist an association between the obtained levels and the presence of MetS in a Puerto Rican population. We hypothesized GPx activity will be significantly lower in participants with MetS and that lipid peroxidation will be higher in these persons. Data was analyzed using Prism Graph Pad and SPSSv12.0 Softwares. Our preliminary results showed no significant differences in plasma lipid peroxidation (n=224; p=0.229) and GPx (n=70; p=0.163). This study is important because excessive accumulation of oxidative molecules may be prevented by ingesting antioxidant supplements and this may create awareness of the consequences of the MetS and the potential benefit of intaking antioxidants. Grant Funding Source: Support by R25GM096955 (NIH RISE Program)
Every year, approximately half a million people die due to breast cancer (BC), comprising 16% of the incidence of all cancer occurrences in females. It is the most prevalent invasive cancer among women around the world. In several studies, researchers have suggested the presence of certain chemokines associated with cancer. The chemokine receptor CXCR4, a G‐protein coupled receptor, has a role in trafficking, cell activation, and differentiation in non‐malignant. It has been shown that CXCR4 is overexpressed in cancerous tissues compared to non‐malignant cells. This overexpression has led to an increase in proliferation, migration, and angiogenesis of malignant cells. Tissues with higher expression of the CXCR4 specific ligand CXCL12, are more likely to metastasis to tissue expressing CXCR4. These target tissues include lungs, bone marrow, and lymph nodes. Due to the impact of this disease, there is a need of developing new therapies or adjuvants to target BC. For example, resveratrol is a natural product and a polyphenol derived from grapes, wine, and nuts, among others. Recent studies found that it plays a role in apoptosis, inflammation, and neovascularization. We hypothesized that resveratrol will decrease the expression of CXCR4 in a dose and time‐dependent manner, leading to a decrease in the migration and invasion cellular processes. Using western blot analysis of HS578T (Human Breast Carcinoma) compared with CCD1074Sk (Non‐malignant Human Breast Tissue) cell lines we studied the effects of resveratrol at the CXCR4 protein level and invasion markers involved in metastatic processes. Migration and invasion were assessed using a wound healing assay and matrigel invasion assay, respectively. The preliminary data shows that as the concentration (25, 50, 100, 200μM) increases the cell migration and invasion decreases compared to our control vehicle (EtOH). In addition, we observed a decrease in the expression of pro‐migration and invasion proteins such as N‐cadherin and Cathepsin‐b. This study suggests an effect of resveratrol in cell migration and invasion leading to a decrease of the in‐vitro cell metastatic potential. Currently we are evaluating CXCR4 at the protein expression level to complete our data.Support or Funding InformationThis work was supported by UPR PRISE Program NIH‐NIGMS #2R25GM096955This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Nanodisc soluble lipid bilayer systems are vital in rendering membrane proteins soluble in aqueous solutions where they remain monodisperse and active in a membrane‐like environment. Nanodiscs or nanolipidprotein particles (NLPs), are bordered by an amphipathic helical protein belt or membrane scaffolding protein (MSP) mimicking a cell membrane. Past works have shown that fragments of bacteriorhodopsin when placed in separate nanodisc do not interact to form the functional protein. The introduction of bicelles enabled the fragments to form oligomers inside the bicelles. An analysis of the kinetics of the aforementioned NLP‐bicelle interaction showed a sigmoid curve suggesting the possibility of an autocatalyzed reaction. We hypothesized that the kinetics where due to MSP1E3D1′s dissociation from the nanodisc which catalyzed the reaction. Using fluorescently labeled lipids 1,2‐dioleoyl‐sn‐glycero‐3‐phosphoethanolamine‐N‐(lissamine rhodamine B sulfonyl), 1,2‐diphytanoyl‐sn‐glycero‐3‐phosphoethanolamine‐N‐(7‐nitro‐2‐1,3‐benzoxadiazol‐4‐yl) LR‐PE and NBD‐PE, respectively with 1,2‐dimyristoyl‐sn‐glycero‐3‐phosphocholine (DMPC) and MSP1E3D1 we constructed NLPs. Bicelles were prepared using 1,2‐dihexanoyl‐sn‐glycero‐3‐phosphocholine (DHPC) and DMPC. Kinetics of NLP‐bicelle interactions and fluorescently labeled lipid dispersion were observed measuring fluorescence resonance energy transfer (FRET) using stopped‐flow spectroscopy. The NLP‐bicelle interaction followed previously observed kinetics and continued to do so after the addition of excess MSP1E3D1. Our results show that MSP1E3D1 is not responsible for the observed kinetics of the transfer of lipids between NLPs and bicelles.
The cellular and molecular environment of normal cells from breast cancer patients are particulary understood. Chemokines and their receptors have roles in cellular proliferation, metastasis, and angiogenesis. Specifically, CXCR4, a G‐protein coupled receptor is expressed in high levels in breast neoplastic tissues and in low levels in normal breast tissue. CXCR4 expression may induce proliferation, migration, invasion and angiogenesis. Recent studies have identify resveratrol (a natural polyphenol) to play a role on inflammation, apoptosis, and neovascularization. Due to limited scientific literature on the effects of resveratrol on CXCR4, the biological process in which both coincide, (inflammation, apoptosis, and neovascularization), and the potential use of resveratrol, as a therapeutic agent in cancer, we studied the effect of this polyphenol on CXCR4. In addition, we explored the effects on the apoptosis mediator Bax. We hypothesized that resveratrol increases the expression of CXCR4 in normal cells from a breast cancer patient. We determined the effects of resveratrol at concentrations of 25, 50, 100, 200 μM after 24 hours of treatment in the protein levels of CXCR4 and Bax‐2 by western blot using CCD1097 a fibroblastic cell line, derived from normal skin from the breast of a patient undergoing biopsy of a grade III infiltrating ductal carcinoma. Our preliminary results indicate that higher doses increased expression of CXCR4 in a dose‐dependent compared to control vehicle treated cells. Similarly, Bax expression increased in all treated cells but in a non‐dependent dose manner. These results may suggest that resveratrol have an effect on CXCR4 protein levels, leading to an increase in proliferation in normal cells from cancer patients. As reported, at lower doses resveratrol may have antiapoptotic effects and at higher doses may induce apoptosis. Resveratrol may prompt for clearance of cancer cells using different pathways but additional experiments will be necessary to identify the exact mechanism of action. Additional experiments are underway to identify the proliferative effects of resveratrol including apoptosis (caspases) and inflammation (TNF‐α and SOD‐2).Support or Funding InformationThis work was supported by UPR PRISE Program NIH Grant #R25GM096955.
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