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角质形成细胞生长因子由增生诱导药物硝苯地平上调。

Keratinocyte growth factor is upregulated by the hyperplasia-inducing drug nifedipine.

作者信息

Das S J, Olsen I

机构信息

Department of Periodontology, Eastman Dental Institute for Oral Health Care Sciences, University College London, University of London, 256 Gray's Inn Road, London, WC1X 8LD, UK.

出版信息

Cytokine. 2000 Oct;12(10):1566-9. doi: 10.1006/cyto.2000.0756.

Abstract

Keratinocyte growth factor (KGF) is the seventh member of the fibroblast growth factor (FGF) family. It is produced by mesenchymal cells and its activity is specific for epithelial cells, controlling epithelial homeostasis and wound repair in a paracrine manner. Although KGF has been implicated in a number of hyperplastic pathologies, it has not previously been investigated in gingival hyperplasia (GH), an adverse side-effect of three pharmacologically different types of drugs, including the anti-hypertensive drug nifedipine (NIF). The mechanism by which NIF causes GH is not yet known, but we have recently shown that KGF mRNA transcripts are elevated in drug-induced GH in vivo (manuscript submitted). It is therefore possible that the action of NIF is mediated via KGF and, in the present study, using the enzyme-linked immunosorbent assay (ELISA) and the semi-quantitative reverse transcribed-polymerase chain reaction (RT-PCR), we found that NIF upregulates KGF secretion and gene transcription by gingival fibroblasts in vitro. Our results thus suggest that KGF may have an important role in the molecular pathology of GH in vivo.

摘要

角质形成细胞生长因子(KGF)是成纤维细胞生长因子(FGF)家族的第七个成员。它由间充质细胞产生,其活性对上皮细胞具有特异性,以旁分泌方式控制上皮内环境稳定和伤口修复。尽管KGF已被认为与多种增生性病变有关,但此前尚未在牙龈增生(GH)中进行研究,牙龈增生是包括抗高血压药物硝苯地平(NIF)在内的三种药理作用不同的药物的一种不良副作用。NIF导致GH的机制尚不清楚,但我们最近发现,在体内药物诱导的GH中,KGF mRNA转录物水平升高(已提交论文)。因此,NIF的作用可能是通过KGF介导的,在本研究中,我们使用酶联免疫吸附测定(ELISA)和半定量逆转录聚合酶链反应(RT-PCR)发现,NIF在体外上调牙龈成纤维细胞的KGF分泌和基因转录。因此,我们的结果表明,KGF可能在体内GH的分子病理学中起重要作用。

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