Rat and human aortic smooth muscle cells display differing migration and matrix metalloproteinase activities in response to dexamethasone

Pross, C.; Farooq, Michael M.; Lane, John S.; Angle, Niren; Tomono, C. K.; Xavier, A. E.; Freischlag, Julie A.; Collins, Amy E; Law, Ronald E.; Gelabert, Hugh A.

doi:10.1067/mva.2002.123332

Cited by 15 publications

(13 citation statements)

References 29 publications

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“…These results are different from those reported by Bohlen et al They demonstrated that leptin inhibited proliferation of cultured human aortic smooth muscle cell and downregulated the short isoforms significantly, whereas the long isoforms were not influenced [18]. Data from experiments with rodent cells may differ from those with human ones, which is a possible explanation for the differences between their work and our current study [19]. However, there exit other possibilities.…”

Section: Discussioncontrasting

confidence: 56%

Leptin-induced vascular smooth muscle cell proliferation via regulating cell cycle, activating ERK1/2 and NF-κB

Huang¹,

Xiong²,

Wang³

et al. 2010

ABBS

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Leptin is a peptide hormone primarily involved in the regulation of food intake and energy expenditure. Recent studies have suggested that leptin is one of the risk factors for cardiovascular diseases including atherosclerosis and hypertension. Vascular smooth muscle cells (VSMCs) play a vital role in arterial intimal thickening and vascular remodeling. In this study, we investigated the effect of leptin on VSMC cell-cycle regulation and the possible pathway. We found that leptin stimulated VSMC proliferation and increased cell progression to S and G2/M phases. The expression of cyclinD1, phosphorylated extracellular signal-regulated kinase 1/2 (ERK1/2), and nuclear factor (NF)-kBp65 was increased. Treatment of the cells with leptin antagonist triple mutant attenuated the leptininduced ERK1/2 and NF-kB activation. These results suggested that leptin stimulated VSMC proliferation by promoting transition from G1 to S phase and ERK1/2 and NF-kB pathway might contribute to this procession.

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Section: Discussioncontrasting

confidence: 56%

Leptin-induced vascular smooth muscle cell proliferation via regulating cell cycle, activating ERK1/2 and NF-κB

Huang¹,

Xiong²,

Wang³

et al. 2010

ABBS

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“…It is also important to recognize that ␤-adrenergic agonists have both PKAdependent and -independent effects on actin depolymerization in airway smooth muscle and, therefore, PKA may not mediate all the effects that ␤-adrenergic agonists have on actin remodeling (29). Finally, even less is known about the mechanisms, probably multiple, that underlie the inhibitory effects of glucocorticoids on migration (30). However, given the evidence that p38 MAPK has a major role in regulating migration in ASMCs, it is interesting that, in HeLa cells, glucocorticoids did inhibit p38 MAPK signaling by inducing a sustained expression of MAPK phosphatase 1 (MKP-1) (31).…”

Section: Inhibition Of Asmc Migrationmentioning

confidence: 97%

Migration of Airway Smooth Muscle Cells

Madison

2003

Am J Respir Cell Mol Biol

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“…In vitro, dexamethasone has been shown to downregulate DNA synthesis, proliferation and chemotactic activity of human fetal lung fibroblasts in a dose-dependent fashion [30] . Dexamethasone further directly inhibits thrombin-stimulated proliferation of human airway smooth muscle cells [31] as well as proliferation, DNA synthesis [32] and migration of rat and human aortic smooth muscle cells in culture conditions [14] .…”

Section: Discussionmentioning

confidence: 99%

“…Nitric oxide (NO) inhibits smooth muscle cell migration and activity of MMP-2, one of the zinc-dependent metalloproteases, which has been specifically implicated in smooth muscle cell migration. Dexamethasone was recently shown to inhibit in vitro production and activity of MMP-2 both directly as well as through enhancing NO production [13,14] .…”

Section: Introductionmentioning

confidence: 99%

Effect of Maternal Administration of Betamethasone on Peripheral Arterial Development in Fetal Rabbit Lungs

et al. 2007

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Objectives: Glucocorticoids promote lung maturation and reduce the incidence of respiratory distress syndrome in premature newborns. We hypothesized that betamethasone (BM), which is known to induce thinning of the alveolar walls, would also thin the arterial media and adventitia of intra-parenchymatic vessels in developing rabbit lungs. Study Design: 112 fetuses from 21 time-mated, pregnant, giant white rabbits received maternal injections of BM at either 0.05 or 0.1 mg/kg/day on days 25–26 of gestational age. Controls received either saline (10 does, 56 fetuses) or no injection (10 does, 59 fetuses). Fetuses were harvested from day 27 onwards until term (day 31). 44 additional fetuses (8 does) were harvested between days 23 and 26. Endpoints were wet lung-to-body weight ratio, vascular morphometric indices and immunohistochemistry staining for α-smooth muscle actin, Flk-1, vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS). ANOVA (Tukey’s test) and independent t test (p < 0.05) were used for comparison between BM and saline groups. Results: Maternal BM injected on days 25–26 to pregnant rabbits induced a significant decrease in fetal body and lung weight and the lung-to-body weight ratio in the preterm pups shortly after injection. BM led to a dose-dependent thinning of the arterial media and adventitia (pulmonary arteries with an external diameter (ED) of <100 µm), to an increase in the percentage of non-muscularized peripheral vessels (ED <60 µm), in eNOS and VEGF immunoreactivity of the endothelial and smooth muscle cells in the pulmonary vessels and to an increase in Flk-1-positive pulmonary epithelial cell density. Conclusions: Maternal administration of BM caused thinning of the arterial wall of pulmonary vessels (ED <100 µm) and a decrease in muscularization in peripheral vessels (ED <60 µm). This coincided with increased expression of Flk-1 in the endothelium and smooth muscle cells of the pulmonary arteries. All the effects studied were dose-dependent.

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Rat and human aortic smooth muscle cells display differing migration and matrix metalloproteinase activities in response to dexamethasone

Cited by 15 publications

References 29 publications

Leptin-induced vascular smooth muscle cell proliferation via regulating cell cycle, activating ERK1/2 and NF-κB

Leptin-induced vascular smooth muscle cell proliferation via regulating cell cycle, activating ERK1/2 and NF-κB

Migration of Airway Smooth Muscle Cells

Effect of Maternal Administration of Betamethasone on Peripheral Arterial Development in Fetal Rabbit Lungs

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Rat and human aortic smooth muscle cells display differing migration and matrix metalloproteinase activities in response to dexamethasone

Cited by 15 publications

References 29 publications

Leptin-induced vascular smooth muscle cell proliferation via regulating cell cycle, activating ERK1/2 and NF-&kappa;B

Leptin-induced vascular smooth muscle cell proliferation via regulating cell cycle, activating ERK1/2 and NF-&kappa;B

Migration of Airway Smooth Muscle Cells

Effect of Maternal Administration of Betamethasone on Peripheral Arterial Development in Fetal Rabbit Lungs

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Product

Resources

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Leptin-induced vascular smooth muscle cell proliferation via regulating cell cycle, activating ERK1/2 and NF-κB

Leptin-induced vascular smooth muscle cell proliferation via regulating cell cycle, activating ERK1/2 and NF-κB