Li Min, Firth James D, Putnins Edward E
Laboratory of Periodontal Biology, Department of Oral Biological and Medical Sciences, The University of British Columbia, Vancouver, British Columbia, Canada.
J Periodontal Res. 2005 Apr;40(2):118-28. doi: 10.1111/j.1600-0765.2004.00780.x.
Keratinocyte growth factor-1 (KGF-1) is up-regulated in chronic inflammation and specifically stimulates epithelial cell proliferation by signaling through the epithelial-specific keratinocyte growth factor receptor (KGFR). We examined KGF-1 and KGFR protein and gene expression in healthy and diseased periodontal tissues.
Tissues were collected from patients with periodontal health or disease, immediately frozen and stained for KGF-1 and KGFR protein expression. Laser capture microdissection of epithelial and connective tissue cells with reverse transcription-polymerase chain reaction (RT-PCR) examined KGF-1 and KGFR gene expression profiles and enzymatic digestion with heparitinase, chondroitinase ABC or pre-treatment with suramin examined epithelial surface molecule interactions with KGF-1.
In tissues collected from healthy patients, KGF-1 protein localized to areas of junctional and basal oral epithelial cells and was significantly increased in periodontal pocket epithelium (p<0.01) and in the oral epithelium (p<0.05) of disease-associated tissues. KGFR localized to the junctional and the parabasal cells of oral epithelium, with the relative staining intensity being increased in disease-associated pocket epithelium (p<0.05). Laser capture microdissection with RT-PCR confirmed KGF-1 and KGFR were specifically expressed by connective tissue and epithelium, respectively. KGF-1 localization to epithelial cells was largely eliminated by suramin pre-treatment, indicating interaction with the KGFR.
KGF-1 and KGFR proteins are expressed in healthy periodontal tissues but significantly increased in diseased periodontal tissues. We hypothesize up-regulation of KGF-1 and KGFR protein associated with disease regulates epithelial cell behavior associated with onset and progression of periodontal pocket formation.
角质形成细胞生长因子-1（KGF-1）在慢性炎症中上调，并通过上皮特异性角质形成细胞生长因子受体（KGFR）信号传导特异性刺激上皮细胞增殖。我们检测了健康和患病牙周组织中KGF-1和KGFR的蛋白及基因表达。
从牙周健康或患病患者处采集组织，立即冷冻并进行KGF-1和KGFR蛋白表达染色。用激光捕获显微切割上皮和结缔组织细胞，通过逆转录聚合酶链反应（RT-PCR）检测KGF-1和KGFR基因表达谱，并用肝素酶、软骨素酶ABC进行酶消化或用苏拉明预处理，检测上皮表面分子与KGF-1的相互作用。
在健康患者采集的组织中，KGF-1蛋白定位于结合上皮和口腔基底上皮细胞区域，在牙周袋上皮（p<0.01）和疾病相关组织的口腔上皮（p<0.05）中显著增加。KGFR定位于口腔上皮的结合上皮和副基底细胞，在疾病相关袋上皮中的相对染色强度增加（p<0.05）。激光捕获显微切割结合RT-PCR证实KGF-1和KGFR分别由结缔组织和上皮特异性表达。苏拉明预处理后，KGF-1在上皮细胞的定位基本消除，表明其与KGFR相互作用。
KGF-1和KGFR蛋白在健康牙周组织中表达，但在患病牙周组织中显著增加。我们推测与疾病相关的KGF-1和KGFR蛋白上调调节了与牙周袋形成的发生和进展相关的上皮细胞行为。
