Searchable abstracts of presentations at key conferences in endocrinology

ea0021p121 | Cytokines and growth factors | SFEBES2009

Peripheral blood mononuclear cells from active rheumatoid arthritis patients show a defective induction of adrenomedullin

Green Laura , Berry Andrew , Donn Rachelle , Ray David

Rheumatoid arthritis (RA) is a common chronic systemic inflammatory disease. Several new therapies exist for RA but long-term patient management remains problematic.We have discovered that hypoxia, a characteristic of inflamed tissues, potently inhibits glucocorticoid (Gc) sensitivity. This effect is mediated, in part by HIF1α, whose activity is induced in hypoxia. HIF1α gene expression is also induced in primary peripheral blood mononuclear ce...

ea0013oc4 | Steroid synthesis and action | SFEBES2007

Modulation of membrane initiated glucocorticoid signalling by caveolin-1

Matthews Laura , Berry Andrew , Ohanian Jaqui , Ohanian Vasken , Ray David

Many glucocorticoid (Gc) actions are of rapid onset, and therefore require acute regulation of intracellular signalling cascades. We have previously identified rapid Gc-dependent activation of the caveolae specific integral membrane protein caveolin, and the cytosolic kinase PKB in the lung epithelial cells, A549.Immunofluorescence studies demonstrate the appearance of activated glucocorticoid receptor (P-ser211-GR) localised to focal points around the c...

ea0013p127 | Growth and development | SFEBES2007

Neural stem cell differentiation in the injured adult mouse brain

Leadbeater Wendy , Summerfield Michael , Berry Martin , Logan Ann

Constitutive neurogenesis in the adult mammalian brain (sub-ventricular zone, SVZ and dentate gyrus) implies the capacity for self-repair following brain injury. However, brain injury is usually permanently debilitating as neuronal self-repair responses are not sustained and resident neural stem cells (NSC) do not repopulate damaged tissue. Identification of NSC differentiating factors transiently activated post-injury will be key to enhancing NSC mobilisation and differentiat...

ea0011p333 | Diabetes, metabolism and cardiovascular | ECE2006

Adult pancreatic islet progenitor cells exhibit plasticity in vitro

Leadbeater WE , Summerfield MR , Hill DJ , Berry M , Logan A

Adult progenitor cells exist in most adult tissues, their differentiation being primed by insult, repopulating damaged or dysfunctional tissue. Utilisation of resident progenitor cells has the potential to cure many diseases, including neurodegenerative disorders or diabetes which presently can only be managed. This potential is limited in the brain by constraints on endogenous progenitor cell mobilisation and by difficulties in progenitor cell harvesting for ex vivo ex...

ea0010p26 | Cytokines, growth factors, growth and development | SFE2005

Ahmed Z , Mazibrada G , Dent R , Berry M , Logan A

Upon binding of myelin-derived axon growth inhibitory ligands to the Nogo receptor (NgR), a complex is formed with LINGO-1 and the low affinity neurotrophin receptor p75NTR, which initiates axon growth cone collapse via a Rho-A-mediated pathway. We reasoned that, after tumor necrosis factor-α converting enzyme (TACE) cleavage of p75NTR, which triggers the initiation of regulated intramembrane proteolysis (RIP), signalling of growth cone collap...

ea0008go2 | (1) | SFE2004

siRNA-Mediated Knock Down of NgR, p75NTR and Rho-A Disinhibits Neurotrophin-Induced Dorsal Root Ganglia Neurite Outgrowth on CNS Myelin

Ahmed Z , Dent RG , Suggate EL , Berry M , Logan A

Central nervous system neurones are generally incapable of regenerating their axons after injury due to the limited availability of neurotrophins, the development of a glial scar, and the presence of multiple axon growth inhibitors. We therefore designed short interfering RNA (siRNA) sequences to knock down components of the inhibitory signalling cascade and tested their ability to disinhibit the growth of FGF2-stimulated dorsal root ganglia neurone (DRGN) neurites in the pres...

ea0094op5.1 | Adrenal and Cardiovascular | SFEBES2023

Nocturnal metyrapone administration for cortisol suppression in macs: tolerability and impact on metabolic outcomes

Berry Simon , Iqbal Ahmed , Newell-Price John , Debono Miguel

Background: Mild autonomous cortisol secretion (MACS) in patients with adrenal incidentalomas has been associated with elevated cortisol levels during the nocturnal period resulting in a disturbed cortisol rhythm. We hypothesised that administration of nocturnal metyrapone, an 11-beta-hydroxylase inhibitor, previously shown to restore cortisol rhythm in MACS patients, could reduce metabolic complications in this patient group.Met...

ea0094p8 | Adrenal and Cardiovascular | SFEBES2023

A conundrum of steroid absorption and metabolism in the treatment of diamond blackfan anaemia

Berry Simon , Bates Suzanne , Wright Josh , Samuelson Clare , Debono Miguel

Background: Diamond Blackfan anaemia (DBA) is a condition caused by mutations in ribosomal protein genes. After the first year of life, the mainstay of treatment is corticosteroids whilst red blood cell transfusions are used for patients who do not respond.Case: We present a case of a 20-year-old woman with a history of DBA (RPS19 mutation), initially treated with courses of prednisolone, who aged 3 developed steroid-ind...

ea0029s66.3 | HPA axis, stress metabolism and adaptation | ICEECE2012

Modulation of cortisol action

Jangani M. , Berry A. , Matthews L. , Farrow S. , Donn R. , Ray D.

Variation in glucocorticoid (Gc) sensitivity underlies metabolic disease, and affects therapeutic response in inflammation. Using an in-vitro screening approach we identify two new mechanisms capable of regulating Gc sensitivity.The first involves interferon induced factor 16 (IFI16). IFI16 potentiated both transactivation, and Gc repression of NFκB. IFI16 did not affect glucocorticoid receptor (GR) expression, ligand dependent repression of GR expr...

ea0019p210 | Neuroendocrinology and behaviour | SFEBES2009

EGFR antagonists promote disinhibited retinal ganglion cell axon regeneration by a glial-dependent mechanism

Morrison K , Ahmed Z , Leadbeater W , Gonzalez AM , Berry M , Logan A

It was reported that the inhibition of central nervous system (CNS) axon growth is mediated by Ca2+-dependent phosphorylation of epidermal growth factor receptor (pEGFR) and that local administration of small molecule EGFR antagonists to optic nerve lesions promoted retinal ganglion cell (RGC) axon regeneration (Koprivica et al. 2005). This result was attributed to suppression of EGFR kinase, which neutralised the axonal growth inhibitory potency of CNS myeli...