Abstract：
:Glucocorticoids play a major role in attenuation of the inflammatory response. These steroid hormones are able to induce apoptosis in cells of the hematopoietic system such as monocytes, macrophages and T-lymphocytes that are involved in the inflammation reaction. In contrast, it was discovered recently that in glandular cells such as the mammary gland epithelia, hepatocytes, ovarian follicular cells and in fibroblasts glucocorticoids protect against apoptotic signals evoked by cytokines, cAMP, tumor suppressors and death genes. The anti-apoptotic effect of glucocorticoids is exerted by modulation of several survival genes such as Bcl-2, Bcl-x(L) and NFkappaB, in a cell type-specific manner. Moreover, up regulation or down regulation of the same gene product can occur in a cell type-dependent manner following stimulation by glucocorticoids. This phenomenon is probably due to composite regulatory cross-talk among multiple nuclear coactivators or corepressors, which mediate the transcriptional regulation of the genes, by their interaction with the glucocorticoid receptor (GR). These observations suggest that the anti-inflammatory action of glucocorticoids is exerted by two complementary mechanisms: on the one hand, they induce death of the cells that provoke the inflammation, and on the other hand, they protect the resident cells of the inflamed tissue by arresting apoptotic signals.
journal_name
Mol Cell Endocrinoljournal_title
Molecular and cellular endocrinologyauthors
Amsterdam A,Sasson Rdoi
10.1016/s0303-7207(01)00722-5keywords:
subject
Has Abstractpub_date
2002-03-28 00:00:00pages
1-9issue
1-2eissn
0303-7207issn
1872-8057pii
S0303720701007225journal_volume
189pub_type
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