Chronic treatment with PDGF-BB and endothelin-1 synergistically induces vascular hyperplasia and loss of contractility in organ-cultured rat tail artery

Kida, Taiki; Chuma, Hiroko; Murata, Takahisa; Yamawaki, Hideyuki; Matsumoto, Shigeko; Hori, Masaru; Ozaki, Hiroshi

doi:10.1016/j.atherosclerosis.2010.11.001

Cited by 14 publications

(8 citation statements)

References 29 publications

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“…The PDGF family consists of 5 members: PDGF-AA, PDGF-BB, PDGF-CC, PDGF-DD, and PDGF-AB. Genetic manipulations combined with various inhibitory strategies have provided strong evidence for the prominent role of PDGF-BB in the development of neointimal hyperplasia after injury and in atherosclerosis (52)(53)(54)(55)(56). Although PDGF and its receptors are detected in many cultured vascular cells and in arteries after injury, PDGF-BB is expressed at very low or undetectable levels in normal vessels (52).…”

Section: Resultsmentioning

confidence: 99%

Skeleton-secreted PDGF-BB mediates arterial stiffening

Santhanam¹,

Liu²,

Jandu³

et al. 2021

Journal of Clinical Investigation

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Section: Resultsmentioning

confidence: 99%

Skeleton-secreted PDGF-BB mediates arterial stiffening

Santhanam¹,

Liu²,

Jandu³

et al. 2021

Journal of Clinical Investigation

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“…IVF derived blastocysts were also incubated in OPN containing medium for 90 min and then examined for VCL expression and AKT phosphorylation. During the 90 min incubation with OPN, PF-573228 (30 µM; Sigma-Aldrich), LY294002 (30 µM; Sigma-Aldrich) or PD98059 (30 µM; Cell Signaling, Danvers, MA) were added into the medium to inhibit focal adhesion kinase (FAK), phosphatidylinositol 3-kinase (PI3K) or mitogen-activated protein kinase kinase 1/2 (MEK1/2) activities, respectively, as previously described [42], [43].…”

Section: Methodsmentioning

confidence: 99%

Estrogen-Dependent Uterine Secretion of Osteopontin Activates Blastocyst Adhesion Competence

Chaen

Konno²,

Egashira³

et al. 2012

PLoS ONE

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Embryo implantation is a highly orchestrated process that involves blastocyst-uterine interactions. This process is confined to a defined interval during gestation referred to as the “window of embryo implantation receptivity”. In mice this receptive period is controlled by ovarian estrogen and involves a coordination of blastocyst adhesion competence and uterine receptivity. Mechanisms coordinating the acquisition of blastocyst adhesion competence and uterine receptivity are largely unknown. Here, we show that ovarian estrogen indirectly regulates blastocyst adhesion competence. Acquisition of blastocyst adhesion competence was attributed to integrin activation (e.g. formation of adhesion complexes) rather than de novo integrin synthesis. Osteopontin (OPN) was identified as an estrogen-dependent uterine endometrial gland secretory factor responsible for activating blastocyst adhesion competence. Increased adhesion complex assembly in OPN-treated blastocysts was mediated through focal adhesion kinase (FAK)- and phosphatidylinositol 3-kinase (PI3K)-dependent signaling pathways. These findings define for the first time specific regulatory components of an estrogen-dependent pathway coordinating blastocyst adhesion competence and uterine receptivity.

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“…mTORC1 signaling is activated in VSMCs upon arterial injury or in response to PDGF [13, 14, 17–21]. The downstream targets of mTORCl include p70S6K/S6 and eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) [13–18, 22].…”

Section: Introductionmentioning

confidence: 99%

Sulforaphane inhibits platelet-derived growth factor-induced vascular smooth muscle cell proliferation by targeting mTOR/p70S6kinase signaling independent of Nrf2 activation

Shawky

Segar

2017

Pharmacological Research

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Activation of nuclear factor erythroid 2-related factor 2 (Nrf2, a transcription factor) and/or inhibition of mammalian target of rapamycin (mTOR) are implicated in the suppression of vascular smooth muscle cell (VSMC) proliferation. The present study has examined the likely regulatory effects of sulforaphane (SFN, an antioxidant) on Nrf2 activation and platelet-derived growth factor (PDGF)-induced mTOR signaling in VSMCs. Using human aortic VSMCs, nuclear extraction and siRNA-mediated downregulation studies were performed to determine the role of Nrf2 on SFN regulation of PDGF-induced proliferative signaling. Immunoprecipitation and/or immunoblot studies were carried out to determine how SFN regulates PDGF-induced mTOR/p70S6K/S6 versus ERK and Akt signaling. Immunohistochemical analysis was performed to determine SFN regulation of S6 phosphorylation in the injured mouse femoral artery. SFN (5 μM) inhibits PDGF-induced activation of mTOR without affecting mTOR association with raptor in VSMCs. While SFN inhibits PDGF-induced phosphorylation of p70S6K and 4E-BP1 (downstream targets of mTOR), it does not affect ERK or Akt phosphorylation. In addition, SFN diminishes exaggerated phosphorylation of S6 ribosomal protein (a downstream target of p70S6K) in VSMCs in vitro and in the neointimal layer of injured artery in vivo. Although SFN promotes Nrf2 accumulation to upregulate cytoprotective genes (e.g., heme oxygenase-1 and thioredoxin-1), downregulation of endogenous Nrf2 by target-specific siRNA reveals an Nrf2-independent effect for SFN-mediated inhibition of mTOR/p70S6K/S6 signaling and suppression of VSMC proliferation. Strategies that utilize local delivery of SFN at the lesion site may limit restenosis after angioplasty by targeting mTOR/p70S6K/S6 axis in VSMCs independent of Nrf2 activation.

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Chronic treatment with PDGF-BB and endothelin-1 synergistically induces vascular hyperplasia and loss of contractility in organ-cultured rat tail artery

Cited by 14 publications

References 29 publications

Skeleton-secreted PDGF-BB mediates arterial stiffening

Skeleton-secreted PDGF-BB mediates arterial stiffening

Estrogen-Dependent Uterine Secretion of Osteopontin Activates Blastocyst Adhesion Competence

Sulforaphane inhibits platelet-derived growth factor-induced vascular smooth muscle cell proliferation by targeting mTOR/p70S6kinase signaling independent of Nrf2 activation

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