Beta-adrenergic receptor regulation of growth factor protein levels in human choroidal endothelial cells

Steinle, Jena J.; Cappocia, Frank C.; Jiang, Youde

doi:10.1080/08977190802442070

Cited by 23 publications

(19 citation statements)

References 28 publications

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“…PEDF is becoming widely recognized as an important determinant of oxidative stress (Zhang et al 2008, Banumathi et al 2010, inflammation and angiogenesis (Jenkins et al 2007, Zhang et al 2008, is inversely associated with insulin sensitivity and metabolic flexibility (Richards et al 2010), is positively associated with characteristics of the metabolic syndrome (Yamagishi et al 2006), and is predictive of future clinical events in patients with heart failure (Rychli et al 2010). Contrary to animal and cell culture data (Lashbrook & Steinle 2005, Steinle et al 2008, we have demonstrated that short-term inhibition of the sympathetic nervous system does not affect circulating concentrations of PEDF. Differences between our data and previous studies (Lashbrook & Steinle 2005, Steinle et al 2008) may relate to species differences (adult humans versus female Sprague-Dawley rats), tissue differences (plasma versus cultured retinal pigment epithelial cells), method of sympathoadrenal inhibition (systemic pharmacology versus surgical sympathectomy), and/or duration of sympathoadrenal inhibition (6 days versus 6 weeks).…”

Section: Women Basalcontrasting

confidence: 46%

“…Contrary to animal and cell culture data (Lashbrook & Steinle 2005, Steinle et al 2008, we have demonstrated that short-term inhibition of the sympathetic nervous system does not affect circulating concentrations of PEDF. Differences between our data and previous studies (Lashbrook & Steinle 2005, Steinle et al 2008) may relate to species differences (adult humans versus female Sprague-Dawley rats), tissue differences (plasma versus cultured retinal pigment epithelial cells), method of sympathoadrenal inhibition (systemic pharmacology versus surgical sympathectomy), and/or duration of sympathoadrenal inhibition (6 days versus 6 weeks). Given the multiple positive associations in adult humans between fat mass and the metabolic syndrome (Klaus et al 2009), and fat mass, metabolic syndrome and PEDF (Yamagishi et al 2006, Crowe et al 2009), identification of the biological processes responsible for the regulation of PEDF should be a high priority.…”

Section: Women Basalcontrasting

confidence: 41%

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Short-term sympathoadrenal inhibition augments the thermogenic response to β-adrenergic receptor stimulation

Newsom

Richards²,

Johnson³

et al. 2010

Journal of Endocrinology

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Sedentary behavior is associated with an attenuated thermogenic response to b-adrenergic receptor (b-AR) stimulation, an important regulator of energy expenditure (EE) in humans. Chronic stimulation of b-ARs, via heightened activity of the sympathoadrenal system, leads to diminished b-AR function. We have investigated the hypothesis that the thermogenic response of sedentary adults to b-AR stimulation will be increased during short-term sympathoadrenal inhibition. Using a randomly ordered, repeated measures study design, resting EE (REE; indirect calorimetry, ventilated hood technique) and the % increase in EE above REE (%DEE) during acute i.v. isoproterenol administration (nonselective b-AR agonist; 6, 12, and 24 ng/kg fat-free mass per min) were determined in 16 sedentary adults (nine females and seven males, 25G1 years, body mass index: 26 . 1G0 . 9 kg/m 2 , maximal oxygen uptake: 40G2 ml/kg per min (meanGS.E.M.)) in the basal state and on the 6th day of transdermal clonidine administration (centrally acting a2-AR agonist; 0 . 2 mg/day).Relative to baseline, clonidine inhibited sympathoadrenal activity, as evidenced by decreased plasma norepinephrine concentration (1 . 04G0 . 13 vs 0 . 34G0 . 03 nmol/l; P!0 . 001), skeletal muscle sympathetic nerve activity (22 . 5G3 . 8 vs 8 . 5 G1 . 9 bursts/min; PZ0 . 003), and resting heart rate (63G2 vs 49G1 beats/min; P!0 . 001). Sympathoadrenal inhibition decreased REE (6510G243 vs 5857G218 kJ/day; P!0 . 001), increased respiratory exchange ratio (0 . 84G0 . 01 vs 0 . 86 G0 . 01; PZ0 . 03), and augmented the thermogenic response to b-AR stimulation (%DEE: 11G2, 16G2, and 24G2 vs 14G1, 20G2, and 31G2; PZ0 . 04). These data demonstrate that in sedentary humans, short-term inhibition of sympathoadrenal activity increases the thermogenic response to b-AR stimulation, an important determinant of EE and hence energy balance.

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Section: Women Basalcontrasting

confidence: 46%

Section: Women Basalcontrasting

confidence: 41%

Short-term sympathoadrenal inhibition augments the thermogenic response to β-adrenergic receptor stimulation

Newsom

Richards²,

Johnson³

et al. 2010

Journal of Endocrinology

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“…Vascular endothelial growth factor (VEGF) is a potent pro-angiogenic factor in acute wounds (Barrientos et al , 2008), and βAR activation can increase VEGF expression in human choroid ECs (Steinle et al , 2008). To determine whether β2AR antagonism increased VEGF secretion from HDMECs, HKs, human dermal fibroblasts (HDFs), neutrophils, and macrophages, ELISAs were performed on control and β2AR antagonist–treated supernatants.…”

Section: Resultsmentioning

confidence: 99%

β2AR Antagonists and β2AR Gene Deletion Both Promote Skin Wound Repair Processes

Pullar

Provost

O'Leary

et al. 2012

Journal of Investigative Dermatology

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Skin wound healing is a complex process requiring the coordinated, temporal orchestration of numerous cell types and biological processes to regenerate damaged tissue. Previous work has demonstrated that a functional beta-adrenergic receptor (βAR) autocrine/paracrine network exists in skin, however the role of the β2AR in wound healing is unknown. A range of in vitro (single cell migration (SCM), collagen gel contraction, cord formation, ELISA, EIA), ex vivo (rat aortic ring assay) and in vivo (chick chorioallantoic membrane assay (CAM), zebrafish, murine wild-type and β2AR knock-out excisional skin wound models) models were used to demonstrate the finding that blockade or loss of the β2AR promotes wound repair. To our knowledge, this is previously unreported. Compared to vehicle-only controls, β2AR antagonism increased angiogenesis, dermal fibroblast (DF) function and re-epithelialization, while having no effect on wound inflammation in vivo. Skin wounds in β2AR knockout mice contracted and re-epithelialized faster in the first few days of wound repair in vivo. β2AR antagonism increased: cell motility through distinct intracellular signalling mechanisms; alpha smooth muscle actin (SMA) expression, increasing DF-mediated contractile ability and function and VEGF secretion from keratinocytes, presumably contributing to the promotion of angiogenesis observed ex vivo and in vivo, revealing a possible new avenue for therapeutic intervention.

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“…This stimulation of VEGF expression by β-adrenergic signaling is proportional to β-AR expression, dose-dependent and inhibited by β-AR antagonists [37,52]. There is evidence that expression of VEGF in endothelial cells may also be controlled by adrenergic stimulation; as demonstrated in different in vitro and in vivo models, β-AR agonists, including epinephrine, norepinephrine and ISO, can induce the expression of VEGF [53-55]. Conversely, β-AR antagonists (e.g., propranolol) lead to a reduced expression of VEGF and inhibit cell proliferation and angiogenesis [29,56].…”

Section: Discussionmentioning

confidence: 99%

The role of β-adrenergic receptor signaling in the proliferation of hemangioma-derived endothelial cells

Chen

et al. 2013

Cell Div

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BackgroundInfantile hemangioma (IH) is a benign vascular neoplasm that arises from the abnormal proliferation of endothelial cells and enhanced angiogenesis. Recently, propranolol has been found to be effective in the management of IH, suggesting that β-adrenergic receptors (β-ARs) may play an important role in the pathogenesis of IH.ResultsIn the present study, we investigated the β-adrenergic signaling that is associated with hemangioma-derived endothelial cell (HemEC) proliferation. The results showed that both β1- and β2-ARs were expressed in HemECs. Stimulation of the β-ARs by isoprenaline induced cell proliferation and elevation of second messenger cAMP levels. The proliferation-promoting action of isoprenaline was abolished by a β1-selective antagonist and was more effectively abolished by a β2-selective antagonist; the mechanism for the action of the antagonists was a G0/G1 phase cell cycle arrest which was associated with decreased cyclin D1, CDK-4, CDK-6 and phospho-Rb expression. Pre-treatment of the cells with VEGFR-2 or ERK inhibitors also prevented the isoprenaline-mediated proliferation of cells. In agreement with the involvement of β-ARs and VEGFR-2 in the HemEC response, β-AR antagonists and the VEGFR-2 inhibitor significantly attenuated isoprenaline-induced ERK phosphorylation. Moreover, treating the cells with isoprenaline markedly increased VEGF-A expression and VEGFR-2 activity in a β2-AR-dependent manner.ConclusionsWe have demonstrated that the activation of the β-ARs in the ERK pathway may be important mechanisms in promoting HemEC growth. Furthermore, stimulation of the β-AR may transactivate VEGFR-2 signaling and further increase HemEC proliferation.

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Beta-adrenergic receptor regulation of growth factor protein levels in human choroidal endothelial cells

Cited by 23 publications

References 28 publications

Short-term sympathoadrenal inhibition augments the thermogenic response to β-adrenergic receptor stimulation

Short-term sympathoadrenal inhibition augments the thermogenic response to β-adrenergic receptor stimulation

β2AR Antagonists and β2AR Gene Deletion Both Promote Skin Wound Repair Processes

The role of β-adrenergic receptor signaling in the proliferation of hemangioma-derived endothelial cells

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