Sp1, acetylated histone‐3 and p300 regulate TRAIL transcription: Mechanisms of PDGF‐BB‐mediated VSMC proliferation and migration

Azahri, Nor Saadah Md.; Bartolo, Belinda A. Di; Khachigian, Levon M.; Kavurma, Mary M.

doi:10.1002/jcb.24135

Cited by 43 publications

(47 citation statements)

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“…Primary mouse TRAIL −/− and wild-type C57Bl6 (WT) VSMCs were isolated from whole aortas as previously described [33]. Six week old male TRAIL −/− ApoE −/− and ApoE −/− mice [29] weighing approximately 16–18 g were placed on a HFD (Semi-Pure Rodent Diet, SF00-219, Specialty Feeds) for 12 and 20 w in specific pathogen-free conditions.…”

Section: Methodsmentioning

confidence: 99%

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TRAIL-Deficiency Accelerates Vascular Calcification in Atherosclerosis via Modulation of RANKL

et al. 2013

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The osteoprotegerin (OPG) and receptor activator of nuclear factor-κB ligand (RANKL) cytokine system, not only controls bone homeostasis, but has been implicated in regulating vascular calcification. TNF–related apoptosis-inducing ligand (TRAIL) is a second ligand for OPG, and although its effect in vascular calcification in vitro is controversial, its role in vivo is not yet established. This study aimed to investigate the role of TRAIL in vascular calcification in vitro using vascular smooth muscle cells (VSMCs) isolated from TRAIL−/− and wild-type mice, as well as in vivo, in advanced atherosclerotic lesions of TRAIL−/−ApoE−/− mice. The involvement of OPG and RANKL in this process was also examined. TRAIL dose-dependently inhibited calcium-induced calcification of human VSMCs, while TRAIL−/− VSMCs demonstrated accelerated calcification induced by multiple concentrations of calcium compared to wild-type cells. Consistent with this, RANKL mRNA was significantly elevated with 24 h calcium treatment, while OPG and TRAIL expression in human VSMCs was inhibited. Brachiocephalic arteries from TRAIL−/−ApoE−/− and ApoE−/− mice fed a high fat diet for 12 w demonstrated increased chondrocyte-like cells in atherosclerotic plaque, as well as increased aortic collagen II mRNA expression in TRAIL−/−ApoE−/− mice, with significant increases in calcification observed at 20 w. TRAIL−/−ApoE−/− aortas also had significantly elevated RANKL, BMP-2, IL-1β, and PPAR-γ expression at 12 w. Our data provides the first evidence that TRAIL deficiency results in accelerated cartilaginous metaplasia and calcification in atherosclerosis, and that TRAIL plays an important role in the regulation of RANKL and inflammatory markers mediating bone turn over in the vasculature.

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Section: Methodsmentioning

confidence: 99%

“…WT VSMCs were seeded into 6 well titre plates. At 80% confluence, the cells were serum arrested in M199 for 24 h followed by extraction of RNA using TriReagent (Sigma) [33]. RNA was extracted using TriReagent as above.…”

Section: Methodsmentioning

confidence: 99%

TRAIL-Deficiency Accelerates Vascular Calcification in Atherosclerosis via Modulation of RANKL

et al. 2013

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“…Cells were serum-arrested at 80% confluency. After 24 h, a sterile P200 pipette tip was used to perform a scratch as previously described [29,30]. Briefly, cells were washed once with sterile 1× PBS followed by the addition of fresh serum-free media (2 mL/well), with or without TRAIL, FGF-2 and VEGF-A (10 ng/mL of growth factor individually or in combination).…”

Section: Methodsmentioning

confidence: 99%

Comparative Evaluation of TRAIL, FGF-2 and VEGF-A-Induced Angiogenesis In Vitro and In Vivo

Cartland

Genner

Zahoor

et al. 2016

IJMS

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Tumor necrosis-factor-related apoptosis-inducing ligand (TRAIL) has been implicated in angiogenesis; the growth of new blood vessels from an existing vessel bed. Our aim was to compare pro-angiogenic responses of TRAIL, vascular endothelial growth-factor-A (VEGF-A) and fibroblast growth-factor-2 (FGF-2) either separately (10 ng/mL) or in combination, followed by the assessment of proliferation, migration and tubule formation using human microvascular endothelial-1 (HMEC-1) cells in vitro. Angiogenesis was also measured in vivo using the Matrigel plug assay. TRAIL and FGF-2 significantly augmented HMEC-1 cell proliferation and migration, with combination treatment having an enhanced effect on cell migration only. In contrast, VEGF-A did not stimulate HMEC-1 migration at 10 ng/mL. Tubule formation was induced by all three factors, with TRAIL more effective compared to VEGF-A, but not FGF-2. TRAIL at 400 ng/mL, but not VEGF-A, promoted CD31-positive staining into the Matrigel plug. However, FGF-2 was superior, stimulating cell infiltration and angiogenesis better than TRAIL and VEGF-A in vivo. These findings demonstrate that each growth factor is more effective at different processes of angiogenesis in vitro and in vivo. Understanding how these molecules stimulate different processes relating to angiogenesis may help identify new strategies and treatments aimed at inhibiting or promoting dysregulated angiogenesis in people.

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“…TRAIL-mediated anti-apoptotic effects on endothelial cells have been seen (Secchiero et al, 2004; Kavurma & Bennett, 2008; Kavurma et al, 2008). In vitro stimulation of VSMCs with physiologically relevant concentrations of TRAIL stimulates their proliferation and migration (Kavurma et al, 2008; Azahri et al, 2012). A similar effect of TRAIL on VSMCs has been reported in vivo, where vascular injury in Trail − / − mice results in reduced proliferation of VSMCs and intimal thickening (Chan et al, 2010).…”

Section: Immunotherapy Involving Trail Receptor Agonists In Non-camentioning

confidence: 99%

Therapeutic applications of TRAIL receptor agonists in cancer and beyond

Amarante-Mendes

Griffith

2015

Pharmacology & Therapeutics

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TRAIL/Apo-2L is a member of the TNF superfamily first described as an apoptosis-inducing cytokine in 1995. Similar to TNF and Fas ligand, TRAIL induces apoptosis in caspase-dependent manner following TRAIL death receptor trimerization. Because tumor cells were shown to be particularly sensitive to this cytokine while normal cells/tissues proved to be resistant along with being able to synthesize and release TRAIL, it was rapidly appreciated that TRAIL likely served as one of our major physiologic weapons against cancer. In line with this, a number of research laboratories and pharmaceutical companies have attempted to exploit the ability of TRAIL to kill cancer cells by developing recombinant forms of TRAIL or TRAIL receptor agonists (e.g., receptor-specific mAb) for therapeutic purposes. In this review article we will describe the biochemical pathways used by TRAIL to induce different cell death programs. We will also summarize the clinical trials related to this pathway and discuss possible novel uses of TRAIL-related therapies. In recent years, the physiological importance of TRAIL has expanded beyond being a tumoricidal molecule to one critical for a number of clinical settings — ranging from infectious disease and autoimmunity to cardiovascular anomalies. We will also highlight some of these conditions where modulation of the TRAIL/TRAIL receptor system may be targeted in the future.

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Sp1, acetylated histone‐3 and p300 regulate TRAIL transcription: Mechanisms of PDGF‐BB‐mediated VSMC proliferation and migration

Cited by 43 publications

References 47 publications

TRAIL-Deficiency Accelerates Vascular Calcification in Atherosclerosis via Modulation of RANKL

TRAIL-Deficiency Accelerates Vascular Calcification in Atherosclerosis via Modulation of RANKL

Comparative Evaluation of TRAIL, FGF-2 and VEGF-A-Induced Angiogenesis In Vitro and In Vivo

Therapeutic applications of TRAIL receptor agonists in cancer and beyond

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