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      Role of regulator of G-protein signaling 2 (RGS2) in periodontal ligament cells under mechanical stress.

      Cell Biochemistry and Function
      Blotting, Western, Cells, Cultured, Cyclic AMP, antagonists & inhibitors, metabolism, Dideoxyadenosine, analogs & derivatives, pharmacology, Gene Expression Regulation, Humans, Oligonucleotides, Antisense, genetics, Periodontal Ligament, cytology, drug effects, RGS Proteins, physiology, Reverse Transcriptase Polymerase Chain Reaction, Stress, Mechanical, Time Factors

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          Abstract

          Mechanical stress is thought to regulate the expression of genes in the periodontal ligament (PDL) cells. Using a microarray approach, we recently identified a regulator of G-protein signaling 2 (RGS2) as an up-regulated gene in the PDL cells under compressive force. The RGS protein family is known to turn off G-protein signaling. G-protein signaling involves the production of cAMP, which is thought to be one of the biological mediators in response to mechanical stress. Here, we investigated the role of RGS2 in the PDL cells under mechanical stress. PDL cells derived from the ligament tissues of human premolar teeth were cultured in collagen gels and subjected to static compressive force. Compressive force application time-dependently enhanced RGS2 expression and intracellular cAMP levels. To examine the interrelationship between RGS2 and cAMP, the PDL cells were treated with 2',5'-dideoxyadenosine (DDA), an inhibitor of adenyl cyclase, or antisense S-oligonucleotide (S-ODN) to RGS2 under compressive force. DDA dose-dependently inhibited RGS2 stimulated by compressive force. Blockage of RGS2 by antisense S-ODN elevated the cAMP levels compared with controls. These results indicate that cAMP stimulates RGS2 expression, which in turn leads to a decrease in the cAMP production by inactivating the G-protein signaling in the mechanically stressed PDL cells. Copyright (c) 2007 John Wiley & Sons, Ltd.

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