Abstract 505: Targeting FOXM1 in Vascular Smooth Muscle Cells Induces Apoptotic Cell Death

2018 ◽  
Vol 38 (Suppl_1) ◽  
Author(s):  
Sarah R Franco ◽  
Amelia Stranz ◽  
Fiona Ljumani ◽  
Go Urabe ◽  
Danielle Stewart ◽  
...  
Keyword(s):  
Cell Death ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Apoptotic Cell ◽  
Muscle Cells ◽  
Apoptotic Cell Death

scholarly journals Cigarette Smoke Extract Causes Non-Apoptotic Cell Death in Neonatal Vascular Smooth Muscle Cells

1999 ◽  
Vol 45 (4, Part 2 of 2) ◽  
pp. 294A-294A
Author(s):  
Namasivayam Ambalavanan ◽  
Waldemar F Carlo ◽  
Arlene Bulger ◽  
Jian Shi ◽  
Joseph B Philips
Keyword(s):  
Cell Death ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Cigarette Smoke ◽  
Vascular Smooth Muscle Cells ◽  
Apoptotic Cell ◽  
Muscle Cells ◽  
Cigarette Smoke Extract ◽  
Apoptotic Cell Death

scholarly journals Antioxidant Properties of Olive Mill Wastewater Polyphenolic Extracts on Human Endothelial and Vascular Smooth Muscle Cells

Foods ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 800
Author(s):  
Anna Maria Posadino ◽  
Annalisa Cossu ◽  
Roberta Giordo ◽  
Amalia Piscopo ◽  
Wael M Abdel-Rahman ◽  
...  
Keyword(s):  
Antioxidant Activity ◽  
Cell Death ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Olive Oil ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Olive Mill Wastewater ◽  
Olive Mill

This work aims to analyze the chemical and biological evaluation of two extracts obtained by olive mill wastewater (OMW), an olive oil processing byproduct. The exploitation of OMW is becoming an important aspect of development of the sustainable olive oil industry. Here we chemically and biologically evaluated one liquid (L) and one solid (S) extract obtained by liquid–liquid extraction followed by acidic hydrolysis (LLAC). Chemical characterization of the two extracts indicated that S has higher phenol content than L. Hydroxytyrosol and tyrosol were the more abundant phenols in both OMW extracts, with hydroxytyrosol significantly higher in S as compared to L. Both extracts failed to induce cell death when challenged with endothelial cells and vascular smooth muscle cells in cell viability experiments. On the contrary, the higher extract dosages employed significantly affected cell metabolic activity, as indicated by the MTT tests. Their ability to counteract H2O2-induced oxidative stress and cell death was assessed to investigate potential antioxidant activities of the extracts. Fluorescence measurements obtained with the reactive oxygen species (ROS) probe H2DCF-DA indicated strong antioxidant activity of the two OMW extracts in both cell models, as indicated by the inhibition of H2O2-induced ROS generation and the counteraction of the oxidative-induced cell death. Our results indicate LLAC-obtained OMW extracts as a safe and useful source of valuable compounds harboring antioxidant activity.

scholarly journals Calcium Phosphate Crystals Induce Cell Death in Human Vascular Smooth Muscle Cells

2008 ◽  
Vol 103 (5) ◽  
Author(s):  
Alexandra E. Ewence ◽  
Martin Bootman ◽  
H. Llewelyn Roderick ◽  
Jeremy N. Skepper ◽  
Geraldine McCarthy ◽  
...  
Keyword(s):  
Cell Death ◽  
Smooth Muscle ◽  
Calcium Phosphate ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Induce Cell Death

Fas/Fas ligand-mediated death pathway is involved in oxLDL-induced apoptosis in vascular smooth muscle cells

2001 ◽  
Vol 280 (3) ◽  
pp. C709-C718 ◽  
Author(s):  
Tzong-Shyuan Lee ◽  
Lee-Young Chau
Keyword(s):  
Cell Death ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Fas Ligand ◽  
Density Lipoprotein ◽  
Muscle Cells ◽  
Potent Inducer ◽  
Apoptotic Death

Oxidized low-density lipoprotein (oxLDL) is a potent inducer of apoptosis for vascular cells. In the present study, we demonstrate that the expression of death mediators, including p53, Fas, and Fas ligand (FasL) was substantially upregulated by oxLDL in cultured vascular smooth muscle cells (SMCs). The induction of these death mediators was time dependent and was accompanied by an increase in apoptotic death of SMCs following oxLDL treatment. Two oxysterols, 7β-hydroxycholesterol and 25-hydroxycholesterol, were also effective to induce the expression of death mediators and apoptosis. α-Tocopherol and deferoxamine significantly attenuated the induction of death mediators and cell death induced by oxLDL and oxysterols, suggesting that reactive oxygen species are involved in triggering the apoptotic event. Incubation of cells with FasL-neutralizing antibody inhibited the oxLDL-induced cell death up to 50%. Furthermore, caspase 8 and caspase 3 activities were induced time dependently in SMCs following oxLDL treatment. Collectively, these data suggest that the Fas/FasL death pathway is activated and responsible for, at least in part, the apoptotic death in vascular SMCs upon exposure to oxLDL.

Endothelin-1 Enhances Nitric Oxide-Induced Cell Death in Cultured Vascular Smooth-Muscle Cells

1998 ◽  
Vol 31 ◽  
pp. S351-S353 ◽  
Author(s):  
Takeshi Nakahashi ◽  
Keisuke Fukuo ◽  
Hiroyuki Nishimaki ◽  
Shigeki Hata ◽  
Masumi Shimizu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Endothelin 1

scholarly journals Chemokines protect vascular smooth muscle cells from cell death induced by cyclic mechanical stretch

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Jing Zhao ◽  
Yuhei Nishimura ◽  
Akihiko Kimura ◽  
Kentaro Ozawa ◽  
Toshikazu Kondo ◽  
...  
Keyword(s):  
Cell Death ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Mechanical Stretch

Abstract 353: Elastase-Activated Stress Response of Vascular Cells

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Irina Grechowa ◽  
Bernhard Dorweiler ◽  
Anja Wallrath ◽  
Sven Horke
Keyword(s):  
Flow Cytometry ◽  
Endothelial Cells ◽  
Cell Death ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Apoptotic Cell ◽  
Muscle Cells ◽  
Apoptotic Cell Death ◽  
Atherosclerotic Plaques ◽  
Vascular Cells

Introduction: Rupture of atherosclerotic plaques is the most abundant cause for stroke. The serine protease elastase plays an important role as it induces death of endothelial cells (ECs) and smooth muscle cells (SMCs), and breaks down the fibrous cap of atherosclerotic plaques. Increased elastase concentrations were found in patients with symptomatic stenosis. We previously showed that elastase activates the endoplasmic reticulum (ER) stress signaling pathway unfolded protein response (UPR) in rupture-prone plaques of human carotid artery. However, signaling pathways elicited by elastase in vascular cells were largely unknown. We hypothesized that elastase induces cell-type dependent responses in ECs, SMCs and macrophages (M[[Unable to Display Character: &#1060;]]). Methods and Results: Different forms of cell death and UPR activation were analyzed in primary and immortalized endothelial cells, coronary artery smooth muscle cells (HCASMCs) and M[[Unable to Display Character: &#1060;]] after treatment with human neutrophil elastase. To discriminate between the involved cell death types, three independent assays were performed. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-assay by confocal microscopy (p < .01), caspase3/7 activity by chemiluminescence-assays (p < .01) and cell-cycle analysis by flow cytometry revealed that an autophagic/apoptotic cell death was induced upon elastase treatment. This appeared specific for ECs, as it was absent in M[[Unable to Display Character: &#1060;]]. Necrosis (as determined by chemiluminescent lactate dehydrogenase-release assay) and necroptosis (assessed by flow cytometry) played only minor roles. The involvement of the UPR was investigated on protein and / or gene expression level. The high levels of GRP78, phospho-PERK, phospho-eIF2α, spliced XBP1 and CHOP indicate a strongly activated UPR that may give rise to the subsequent induced autophagic/apoptotic cell death. Conclusion: Elastase plays a significant role in plaque stability and cell survival likely through activation of a UPR/autophagic type of endothelial cell death. This may explain underlying molecular links how elastase destabilizes atherosclerotic plaques.

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