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Keratinocyte Growth Factor Receptor is Up-regulated in Cyclosporin A-induced Gingival Hyperplasia
S.J. Das1,2,
H.N. Newman3 and
I. Olsen2,*
1 Department of Periodontology, Regional Dental College, Guwahati-32, India;
2 Eastman Dental Institute for Oral Health Care Sciences, University College London, 256 Gray’s Inn Road, London WCIX 8LD, UK; and
3 Oral Health Research Centre, Parkside National Health Service Trust, London, UK;
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Figure 1. Immunohistochemical analysis of KGFR in gingival tissue. The brown enzyme reaction product indicates the presence of KGFR in gingival tissue. (A) Section of normal gingiva showing the presence of KGFR in the spinous and granular cell layers. Note the absence of KGFR in the basal and cornified cell layers. (B) GH tissue, in which KGFR is seen in the basal as well as the spinous and granular layers of the epithelium, although not in the cornified cell layer. Note the relatively higher staining intensity in the GH section (original magnification, 500x).
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Figure 2. Expression of KGFR mRNA in gingival tissues. (A) Agarose gel showing the PCR products of the GAPDH and KGFR genes. RNA obtained from the normal gingiva (NG), GH, skin, and periodontal ligament (PDL) tissues was reverse-transcribed and amplified with the use of GAPDH- and KGFR-specific oligonucleotide primers. The amplified products were subjected to electrophoresis, and the mobilities of the products were compared with that of the 100-bp DNA ladder used as a size marker (not shown). Note the presence of a band corresponding to the molecular size of GAPDH (600 bp) in all samples, including controls. The band corresponding to KGFR (141 bp) is seen in all samples except the PDL (negative control). (B) Image analysis profile of the agarose gel in (A), showing the presence of bands corresponding to KGFR mRNA in all of the samples except the PDL (negative control). The numbers in brackets are the relative levels of KGFR mRNA in the corresponding samples. Note the relatively greater amounts of transcripts in the GH compared with the normal gingival tissues.
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Figure 3. Effects of CsA on KGFR expression by gingival epithelial cells. (A) Representative fluorescence profiles showing KGFR expression by epithelial cells cultured in the absence and presence of CsA. The dashed lines represent the fluorescence profiles of cells that received no primary antibody. The vertical black line shows the AFI of the non-treated gingival epithelial cells cultured in the absence of CsA. Note the higher AFI of the CsA-treated cells compared with the control cells, as shown in the upper righthand corner. (B) Representative experiment showing RT-PCR analysis of normal gingival epithelial cells cultured in the absence (A) and presence of CsA (B) for 3 days. Each panel shows the electrophoretic mobility of the RT-PCR products and the corresponding image analysis of these bands. Note the presence of GAPDH bands (600 bp) of similar intensities in both panels and the relatively greater amounts of the KGFR gene product (141 bp) in panel B compared with panel A. Numbers in brackets indicate the relative KGFR mRNA level in each panel.
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Journal of Dental Research, Vol. 81, No. 10,
683-687 (2002)
DOI: 10.1177/154405910208101006
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