Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: KEGG:D03301 (PDL)
658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma aldosterone level (PAL) and deoxycorticosterone level (PDL) were determined in 5 subjects of normal sodium intake and 5 subjects of low sodium intake after the intramuscular administrations of ACTH (Upjohn, Cortrosyn) 40 IU, using radioligand methods. PAL and PDL reached their peaks at one hour after the administrations of ACTH, and then decreased in their normal ranges. Pretreated with the oral administrations of Dexamethasone 2 mg/day for 2 days, these subjects had, when ACTH were injected, such a similiar pattern in PAL and PDL as the peak of one hour and the consecutive falling without the pretreating of Dexamethasone. PAL and PDL of these subjects were not different between normal sodium intake and low sodium intake during the course of the experiment.
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PMID:[Effect of ACTH on plasma renin activity, aldosterone level and deoxycorticosterone level in humans (author's transl)]. 19 74

Orthodontic tooth movement is recognized as a pro-inflammatory stressor of human periodontal ligament (hPDL) cells. However, the cell-signaling pathways linking interleukin-8 (IL-8), intercellular adhesion molecule-1 (ICAM-1), pro-inflammatory cytokines, and dexamethasone in hPDL cells have not been well elucidated. In this study, we investigated the role of mitogen-activated protein (MAP) kinases in dexamethasone- and TNF-alpha-induced IL-8 and ICAM-1 expression in hPDL cells. IL-8 production was measured by enzyme-linked immunosorbent assay (ELISA) and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. MAP kinase activation and IkappaB degradation were determined by Western blot analysis, and ICAM-1 expression was determined by RT-PCR and FACS analysis. TNF-alpha increased IL-8 mRNA expression and protein secretion in a dose- and time-dependent manner. Dexamethasone suppressed TNF-alpha-induced IL-8 production in a dose-dependent manner. In addition, dexamethasone inhibited TNF-alpha-induced phosphorylation of p38 MAP kinase and extracellular-regulated kinases (ERKs), IkappaB degradation, and NF-kappaB activation. Selective inhibitors for ERKs and p38 attenuated TNF-alpha-induced IL-8 and ICAM-1 expression in the presence and absence of dexamethasone, indicating that MAP kinases play a role in the response of hDPL cells to TNF-alpha. Furthermore, these results suggest that inflammatory cytokine- and dexamethasone-induced IL-8 and ICAM-1, produced via a MAP kinase pathway, may serve as an important mediator of PDL immunoregulation involved in bone remodeling during orthodontic tooth movement.
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PMID:Roles of p38 and ERK MAP kinases in IL-8 expression in TNF-alpha- and dexamethasone-stimulated human periodontal ligament cells. 1694 35