PMID- 11152574
OWN - NLM
STAT- MEDLINE
DCOM- 20010125
LR  - 20061115
IS  - 1079-9907 (Print)
IS  - 1079-9907 (Linking)
VI  - 20
IP  - 12
DP  - 2000 Dec
TI  - Tumor necrosis factor-alpha (TNF-alpha)-induced and interleukin-1 beta (IL-1 
      beta)-induced shedding of TNF receptors from gingival fibroblasts.
PG  - 1077-82
AB  - Tumor necrosis factor-alpha (TNF-alpha) exerts its functions by binding two 
      different receptors (TNFR55 and TNFR75). Both TNFR55 and TNFR75 exist in 
      cell-associated and soluble forms. Soluble TNF receptors (sTNFR), sTNFR55 and 
      sTNFR75, are proteolytically shed upon inflammatory stimuli and then modulate 
      various TNF-alpha bioactivities. As human gingival fibroblasts (HGF) can be 
      potential targets for TNF-alpha in inflamed gingiva, we hypothesized that HGF 
      partially modulate the cellular responses to TNF-alpha by regulating their own 
      TNFR. In this study, the kinetics of expression of cell-associated and soluble 
      forms of both receptors from cultured HGF in response to proinflammatory 
      cytokines TNF-alpha and interleukin-1 beta (IL-1 beta) were investigated in 
      vitro. Both TNF-alpha and IL-1 beta upregulated the gene expression of TNFR75 and 
      did not affect that of TNFR55. TNF-alpha and IL-1 beta decreased binding of 
      [(125)I]TNF-alpha to HGF. Moreover, TNF-alpha and IL-1 beta upregulated the 
      release of sTNFR75 from HGF but not that of sTNFR55. These results suggest that 
      HGF under inflammatory conditions may contribute to the inactivation of 
      circulating TNF-alpha through the preferential induction and shedding of TNFR75.
FAU - Ohe, H
AU  - Ohe H
AD  - Department of Periodontology and Endodontology, Okayama University Dental School, 
      Okayama, Japan.
FAU - Takashiba, S
AU  - Takashiba S
FAU - Naruishi, K
AU  - Naruishi K
FAU - Chou, H H
AU  - Chou HH
FAU - Yamada, H
AU  - Yamada H
FAU - Nishimura, F
AU  - Nishimura F
FAU - Arai, H
AU  - Arai H
FAU - Murayama, Y
AU  - Murayama Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Interferon Cytokine Res
JT  - Journal of interferon & cytokine research : the official journal of the 
      International Society for Interferon and Cytokine Research
JID - 9507088
RN  - 0 (Antigens, CD)
RN  - 0 (Interleukin-1)
RN  - 0 (Iodine Radioisotopes)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type II)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Antigens, CD/*metabolism
MH  - Binding, Competitive
MH  - Cells, Cultured
MH  - Fibroblasts/*drug effects/metabolism
MH  - Gingiva/drug effects/metabolism
MH  - Humans
MH  - Immunohistochemistry
MH  - Interleukin-1/*pharmacology
MH  - Iodine Radioisotopes
MH  - Receptors, Tumor Necrosis Factor/*metabolism
MH  - Receptors, Tumor Necrosis Factor, Type I
MH  - Receptors, Tumor Necrosis Factor, Type II
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 2001/01/11 11:00
MHDA- 2001/02/28 10:01
CRDT- 2001/01/11 11:00
PHST- 2001/01/11 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2001/01/11 11:00 [entrez]
AID - 10.1089/107999000750053744 [doi]
PST - ppublish
SO  - J Interferon Cytokine Res. 2000 Dec;20(12):1077-82. doi: 
      10.1089/107999000750053744.