The Glucocorticoid-Induced Leucine Zipper Gene (GILZ) Expression Decreases after Successful Treatment of Patients with Endogenous Cushing’s Syndrome and May Play a Role in Glucocorticoid-Induced Osteoporosis

Lekva, Tove; Bollerslev, Jens; Kristo, Cybéle; Olstad, Ole Krisoffer; Ueland, Thor; Jemtland, Rune

doi:10.1210/edrv.30.7.9985

Cited by 11 publications

(15 citation statements)

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“…biopsies before and after treatment for Cushing's syndrome. 21 The CDH1 gene expression was not changed by the treatment. Moreover, CDH1 expression was not regulated by glucocorticoids in the murine corticotroph cell line AtT-20, in the murine mammary adenocarcinoma cell line 3134, nor in murine pluripotent stem cells C3H10T1/2 cells.…”

Section: Discussionmentioning

confidence: 92%

Reduced levels of E-cadherin correlate with progression of corticotroph pituitary tumours

Evang

Berg

Casar‐Borota

et al. 2011

Clinical Endocrinology

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Section: Discussionmentioning

confidence: 92%

Reduced levels of E-cadherin correlate with progression of corticotroph pituitary tumours

Evang

Berg

Casar‐Borota

et al. 2011

Clinical Endocrinology

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“…The observed phenotype was suggested to be due to physical interaction of GILZ with C/EBPs resulting in an abrogated C/EBP-mediated PPAR␥ expression. Moreover, it has been shown in human fetal osteoblasts that dexamethasone-induced GILZ expression results in enhanced osteoblast maturation, whereas silencing of GILZ in these cells decreases the expression of typical osteoblast genes (192).…”

Section: The Glucocorticoid Receptor As a Modifier Of Mesenchymal Stementioning

confidence: 99%

Molecular Actions of Glucocorticoids in Cartilage and Bone During Health, Disease, and Steroid Therapy

Hartmann

Koenen

Schauer

et al. 2016

Physiological Reviews

184

174

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Cartilage and bone are severely affected by glucocorticoids (GCs), steroid hormones that are frequently used to treat inflammatory diseases. Major complications associated with long-term steroid therapy include impairment of cartilaginous bone growth and GC-induced osteoporosis. Particularly in arthritis, GC application can increase joint and bone damage. Contrarily, endogenous GC release supports cartilage and bone integrity. In the last decade, substantial progress in the understanding of the molecular mechanisms of GC action has been gained through genome-wide binding studies of the GC receptor. These genomic approaches have revolutionized our understanding of gene regulation by ligand-induced transcription factors in general. Furthermore, specific inactivation of GC signaling and the GC receptor in bone and cartilage cells of rodent models has enabled the cell-specific effects of GCs in normal tissue homeostasis, inflammatory bone diseases, and GC-induced osteoporosis to be dissected. In this review, we summarize the current view of GC action in cartilage and bone. We further discuss future research directions in the context of new concepts for optimized steroid therapies with less detrimental effects on bone.

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“…13 Global gene expression and proteomic profiling have provided useful additional information: bone biopsies of patients with CS obtained before and after surgical treatment revealed 975 significantly regulated mRNAs; 27 two of the most upregulated genes were further characterized: glucocorticoid-induced leucine zipper -GILZ and thioredoxin interacting protein-1 -TXNIP. 27,28 Heat-shock proteins (HSPs) in the chaperone family are further important players within the process of cellular action of glucocorticoids. 29 Wang et al reported the first proteomic study on GIO and revealed that HSP-60 protects bone cells against the bone damaging effect of excess glucocorticoids, at least in dexamethasone-treated rats.…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoid‐induced osteoporosis: lessons from Cushing's syndrome

Tóth

Grossman

2013

Clinical Endocrinology

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SummaryGlucocorticoid-induced osteoporosis (GIO) is the most frequent form of secondary bone disorders. Most of our knowledge on its pathogenesis and treatment has been obtained by investigating patients treated with exogenous glucocorticoids. This review will focus on the bone disorder in endogenous Cushing's syndrome, updating recent advances in its pathophysiology, diagnostic aspects and the various predictors which are important in determining bone mineral density (BMD) and fracture risk. We now know strong evidence that beside BMD, bone microarchitecture, one of the most important elements of bone quality, is a key factor in determining fracture risk. Recently, two new methods (spinal deformity index and trabecular bone score) have been shown to be useful markers of bone microarchitecture in GIO. Investigations of GIO in endogenous Cushing's syndrome have also contributed to our understanding on its natural history and reversibility. Relying on recently published guidelines for management of exogenous GIO, a short list of suggestions is provided regarding the optimal diagnostic and therapeutic approach to patients with endogenous GIO.

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The Glucocorticoid-Induced Leucine Zipper Gene (GILZ) Expression Decreases after Successful Treatment of Patients with Endogenous Cushing’s Syndrome and May Play a Role in Glucocorticoid-Induced Osteoporosis

Cited by 11 publications

References 0 publications

Reduced levels of E-cadherin correlate with progression of corticotroph pituitary tumours

Reduced levels of E-cadherin correlate with progression of corticotroph pituitary tumours

Molecular Actions of Glucocorticoids in Cartilage and Bone During Health, Disease, and Steroid Therapy

Glucocorticoid‐induced osteoporosis: lessons from Cushing's syndrome

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