Hydrocortisone suppresses intranuclear activator-protein-1 (AP-1) binding activity in mononuclear cells and plasma matrix metalloproteinase 2 and 9 (MMP-2 and MMP-9)

A. Aljada, H. Ghanim, P. Mohanty, D. Hofmeyer, Devjit Tripathy, P. Dandona

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

Having demonstrated recently that hydrocortisone (HC) suppresses intranuclear and total cellular nuclear factor-κB (NF-κB) and increases inhibitor κB (IκB) in mononuclear cells (MNC), in vivo, we have now investigated the effect of hydrocortisone on the other major pro-inflammatory transcription factor, AP-1 and the two proteins, MMP-2 and MMP-9, whose transcription is modulated by it. MMP's hydrolyze extracellular matrix proteins and thus, allow the spread of inflammation. HC (100 mg) was given intravenously to eight normal subjects following an overnight fast. Blood samples were obtained at 0, 1, 2, 4, 8 and 24 h. MNC were separated and the nuclear fractions and cellular homogenates were prepared by standard techniques. AP-1 binding activity was measured by electrophoretic mobility shift assay (EMSA). Plasma MMP-2 and MMP-9 were measured by ELISA. AP-1 binding activity fell significantly at 1, 2, 4 and 8 h. Plasma MMP-2 concentration also decreased significantly at 1, 2, 4 and 8 h while MMP-9 decreased at 1 and 2 h. These data demonstrate that the acute anti-inflammatory effect of HC, in vivo, is, in part, due to AP-1 suppression and a reduction in MMP-2 and MMP-9. Thus, HC may reduce the extracellular spread of inflammation through the inhibition of matrix metalloproteinases.

Original languageEnglish (US)
Pages (from-to)5988-5991
Number of pages4
JournalJournal of Clinical Endocrinology and Metabolism
Volume86
Issue number12
DOIs
StatePublished - 2001
Externally publishedYes

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Matrix Metalloproteinase 2
Matrix Metalloproteinase 9
Transcription Factor AP-1
Plasma Cells
Matrix Metalloproteinases
Protein Binding
Hydrocortisone
Plasmas
Inflammation
Electrophoretic mobility
Extracellular Matrix Proteins
Electrophoretic Mobility Shift Assay
Transcription
Assays
Blood
Anti-Inflammatory Agents
Transcription Factors
Enzyme-Linked Immunosorbent Assay

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

Hydrocortisone suppresses intranuclear activator-protein-1 (AP-1) binding activity in mononuclear cells and plasma matrix metalloproteinase 2 and 9 (MMP-2 and MMP-9). / Aljada, A.; Ghanim, H.; Mohanty, P.; Hofmeyer, D.; Tripathy, Devjit; Dandona, P.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 86, No. 12, 2001, p. 5988-5991.

Research output: Contribution to journalArticle

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abstract = "Having demonstrated recently that hydrocortisone (HC) suppresses intranuclear and total cellular nuclear factor-κB (NF-κB) and increases inhibitor κB (IκB) in mononuclear cells (MNC), in vivo, we have now investigated the effect of hydrocortisone on the other major pro-inflammatory transcription factor, AP-1 and the two proteins, MMP-2 and MMP-9, whose transcription is modulated by it. MMP's hydrolyze extracellular matrix proteins and thus, allow the spread of inflammation. HC (100 mg) was given intravenously to eight normal subjects following an overnight fast. Blood samples were obtained at 0, 1, 2, 4, 8 and 24 h. MNC were separated and the nuclear fractions and cellular homogenates were prepared by standard techniques. AP-1 binding activity was measured by electrophoretic mobility shift assay (EMSA). Plasma MMP-2 and MMP-9 were measured by ELISA. AP-1 binding activity fell significantly at 1, 2, 4 and 8 h. Plasma MMP-2 concentration also decreased significantly at 1, 2, 4 and 8 h while MMP-9 decreased at 1 and 2 h. These data demonstrate that the acute anti-inflammatory effect of HC, in vivo, is, in part, due to AP-1 suppression and a reduction in MMP-2 and MMP-9. Thus, HC may reduce the extracellular spread of inflammation through the inhibition of matrix metalloproteinases.",
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AU - Tripathy, Devjit

AU - Dandona, P.

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