Enhanced fibroblast growth factor 5 expression in stromal and exocrine elements of the pancreas in chronic pancreatitis

Enhanced fibroblast growth factor 5 expression in stromal and exocrine elements of the pancreas in chronic pancreatitis
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DOI:
10.1136/gut.43.1.134
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发表时间:
1998-07-01
期刊:
GUT
影响因子:
24.5
通讯作者:
Korc, M
Korc, M
中科院分区:
医学1区
文献类型:
--
作者:
Ishiwata, T;Kornmann, M;Korc, M

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背景-成纤维细胞生长因子5(FGF-5)属于一组促有丝分裂和促血管生成的肝素结合生长因子,但其在慢性炎症状态中的潜在作用尚不清楚。目的-比较FGF-5在正常胰腺和慢性胰腺炎(CP)患者胰腺中的表达,并研究TAKA-1细胞中FGF-5的表达和分泌,方法和结果-Northern印迹显示正常和CP组织样品中存在4.0 kb FGF-5 mRNA转录物。光密度分析表明,转录水平增加了1.44倍的CP组织样品相比,正常组织样品(p=0.039)。免疫组化和原位杂交结果显示,FGF-5在正常胰腺导管和胰岛细胞中有微弱表达。相反,在CP组织样本中,导管、腺泡和胰岛细胞以及导管周围成纤维细胞中FGF-5表达丰富。通过北方印迹法测定,FGF-5也在TAKA-1细胞中表达。通过对肝素-琼脂糖沉淀物进行免疫印迹,TAKA-1细胞显示可将FGF-5分泌到培养基中。结论-外分泌和基质来源的FGF-5有可能参与自分泌和旁分泌途径,这可能有助于慢性胰腺炎的病理生物学。
Background-Fibroblast growth factor 5 (FGF-5) belongs to a group of mitogenic and angiogenic heparin binding growth factors but its potential role in chronic inflammatory conditions is not known.Aims-To compare FGF-5 expression in the normal pancreas and in the pancreas of patients with chronic pancreatitis (CP) and to characterise FGF-5 expression and secretion in TAKA-1 cells, an immortalised Syrian hamster pancreatic duct cell line.Methods and results-Northern blotting revealed the presence of a 4.0 kb FGF-5 mRNA transcript in both normal and CP tissue samples. Densitometric analysis indicated that the transcript levels were increased by a factor of 1.44 in CP tissue samples compared with normal tissue samples (p=0.039). By immunohistochemisty and in situ hybridisation, FGF-5 was faintly expressed in ductal and islet cells in the normal pancreas. In contrast, in CP tissue samples, there was abundant expression of FGF-5 in ductal, acinar, and islet cells, as well as in periductal fibroblasts. FGF-5 was also expressed in TAKA-1 cells as determined by Northern blotting. By immunoblotting of heparin-sepharose precipitates, TAKA-1 cells were shown to secrete FGF-5 into the medium.Conclusion-Exocrine and stromal derived FGF-5 has the potential to participate in autocrine and paracrine pathways that may contribute to the pathobiology of chronic pancreatitis.