FIFTEENTH GADDUM MEMORIAL LECTURE DECEMBER 1994 Stress and the neuroendocrine‐immune axis: the pivotal role of glucocorticoids and lipocortin 1

Buckingham, Julia C.

doi:10.1111/j.1476-5381.1996.tb15360.x

Cited by 70 publications

(50 citation statements)

References 138 publications

(163 reference statements)

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“…For instance, NF-IL-6 also activates this gene (Solito et al, 1998a). Our latest observation with TNF-a (which is also corroborated by experiments in vivo; E. Solito and M. Perretti, unpublished data) seems to con®rm the hypothesis of ANX1 acting as an acute phase protein: its synthesis is partially under the control of several pivotal pro-in¯amma-tory agents, and increased levels are clearly associated to several anti-in¯ammatory eects both in the periphery and in the central nervous system (Perretti, 1997;Buckingham, 1996). U937 cells transfected with the ANX1 fragment (clone ANX1-S) survived in cultured conditions and represented a useful tool to investigate potential alterations in biochemical pathways activated during the process of apoptosis.…”

Section: Discussionsupporting

confidence: 52%

Transfection of annexin 1 in monocytic cells produces a high degree of spontaneous and stimulated apoptosis associated with caspase‐3 activation

Solito

Coupade

Canaider

et al. 2001

British J Pharmacology

106

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1 Transfection of the pre-monomyelocytic U937 cell line with a plasmid coding for full-length annexin 1 (ANX1, 347 amino acid) leads to cell death by promoting apoptosis. In addition, overexpression of the N-terminal and the ®rst domain of the protein (144 amino acids, clone ANX1-S), which does not contain the Ca 2+ binding sites, gives susceptibility to cell apoptosis following activation by either 5 ng ml 71 tumour necrosis factor (TNF)-a or 1 ± 40 mg ml 71 etoposide. This was demonstrated by using the¯uorescent labelled annexin V, cell cycle and nuclear staining analyses. 2 Transfection with an empty plasmid (clone CMV) or with a plasmid carrying the cDNA antisense for ANX1 (clone ANX1-AS) did not alter U937 cells to the degree of apoptosis promoted by either stimulant. 3 Treatment of CMV U937 cells with TNF-a increased ANX1 mRNA and protein expression in a time-dependent manner, with maximal increases at 3 and 6 h, respectively. 4 Clone ANX1-S showed higher constitutive (more than 2 fold) and activated caspase-3 activity, associated with higher phospholipase A 2 (PLA 2 ) activity (in the region of +50 ± 100%), whereas expression of cytosolic PLA 2 Bax and Bcl-2 were similar in all cell clones, as determined by Western blotting. 5 In conclusion, this study demonstrates a complex regulatory role of cell apoptosis for ANX1, at least with regards to cells of the myelo-monocytic lineage.

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Section: Discussionsupporting

confidence: 52%

Transfection of annexin 1 in monocytic cells produces a high degree of spontaneous and stimulated apoptosis associated with caspase‐3 activation

Solito

Coupade

Canaider

et al. 2001

British J Pharmacology

106

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“…Unlike the effects on hormone synthesis which involve gene repression, the acute effects of GCs on CRH/AVP and ACTH release are effected in the first instance by non-genomic mechanisms and subsequently (within 2 h) by genomic mechanisms involving de novo protein synthesis. 3 Work within our laboratory aims to elucidate the signalling mechanisms mediating the GC-induced suppression of peptide release and is presently centred on investigating the role of annexin 1 in this regard.…”

Section: The Hypothalamo-pituitary-adrenocortical (Hpa) Axismentioning

confidence: 99%

Annexin 1: a paracrine/juxtacrine mediator of glucorticoid action in the neuroendocrine system

Buckingham

Solito

John

et al. 2003

Cell Biochemistry & Function

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Glucocorticoids (GCs) play an essential role in the maintenance of homeostasis. In normal circumstances their secretion is tightly regulated by a complex servo mechanism through which the steroids suppress the synthesis and release of ACTH and its hypothalamic releasing factors (CRH and AVP) and thereby reduce the positive drive to the adrenal cortex. The feedback actions of GCs on hormone release develop rapidly (within minutes), well before any changes in hormone synthesis are apparent. By using immunoneutralization, gene targeting and pharmacological strategies in in vivo and in vitro models, we have identified annexin 1, a Ca 2þ -and phospholipid-binding protein, as a key mediator of the early inhibitory actions of GCs on peptide release. This brief review outlines this work and describes molecular and cellular studies which have provided insight into the mechanism of annexin 1-dependent GC signalling in the neuroendocrine system.

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“…Subsequent research has shown that ANX-1 plays a major regulatory role in systems as diverse as cellgrowth regulation and differentiation, neutrophil migration, CNS responses to cytokines, neuroendocrine secretion, and neurodegeneration (Ahluwalia et al, 1996;Buckingham, 1996). The role of ANX-1 in mediating glucocorticoid-induced effects in these systems has been demonstrated using immunoneutralization and antisense strategies, and by the ability of highly purified or recombinant ANX-1 and ANX-1-derived fragments to mimic steroid actions.…”

mentioning

confidence: 99%

An Immunocytochemical and In Situ Hybridization Analysis of Annexin 1 Expression in Rat Mast Cells: Modulation by Inflammation and Dexamethasone

Oliani

Christian

Manston

et al. 2000

Laboratory Investigation

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SUMMARY:The presence and localization of the anti-inflammatory protein annexin 1 (also known as lipocortin 1) in perivenular rat mast cells was investigated here. Using the rat mesenteric microvascular bed and a combination of morphologic techniques ranging from immunofluorescence to electron microscopy analyses, we detected the presence of annexin 1 in discrete intracellular sites, both in the nucleus and in the cytoplasm. In resting mast cells, most of the protein pool (approximately 80% of the cytosolic portion) was localized to cytoplasmic granules. In agreement with other cell types, treatment of rats with dexamethasone (0.2 mg/kg, ip) increased annexin 1 expression in mast cells, inducing a remarkable appearance of clusters of protein immunoreactivity. This effect was most likely the result of de novo protein synthesis as determined by an increase in mRNA seen by in situ hybridization. Triggering an ongoing experimental inflammatory response (0.3 mg of carrageenin, ip) increased annexin 1 mRNA and protein levels. In conclusion, we report for the first time the localization of annexin 1 in connective tissue mast cells, and its susceptibility not only to glucocorticoid hormone treatment, but also to an experimental acute inflammatory response.

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FIFTEENTH GADDUM MEMORIAL LECTURE DECEMBER 1994 Stress and the neuroendocrine‐immune axis: the pivotal role of glucocorticoids and lipocortin 1

Cited by 70 publications

References 138 publications

Transfection of annexin 1 in monocytic cells produces a high degree of spontaneous and stimulated apoptosis associated with caspase‐3 activation

Transfection of annexin 1 in monocytic cells produces a high degree of spontaneous and stimulated apoptosis associated with caspase‐3 activation

Annexin 1: a paracrine/juxtacrine mediator of glucorticoid action in the neuroendocrine system

An Immunocytochemical and In Situ Hybridization Analysis of Annexin 1 Expression in Rat Mast Cells: Modulation by Inflammation and Dexamethasone

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