Increased expression of transforming growth factor beta s after acute oedematous pancreatitis in rats suggests a role in pancreatic repair.
Increased expression of transforming growth factor beta s after acute oedematous pancreatitis in rats suggests a role in pancreatic repair.
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DOI：
10.1136/gut.40.1.73
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发表时间：
1997-01
期刊：
影响因子：
24.5
通讯作者：
E. Riesle;H. Friess;L. Zhao;Markus Wagner;W. Uhl;K. Baczako;Leslie I. Gold;M. Korc;M. Büchle
中科院分区：
文献类型：
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作者：
E. Riesle;H. Friess;L. Zhao;Markus Wagner;W. Uhl;K. Baczako;Leslie I. Gold;M. Korc;M. Büchle
背景：转化生长因子β亚型（TGF β s）属于细胞生长和分化的多功能调节因子家族。它们对成纤维细胞有丝分裂和趋化作用，是细胞外基质生成（胶原）和沉积的有效刺激物。据报道，在损伤后修复过程中，几种体内系统中TGF - β转录上调。目的：研究TGF β三种哺乳动物亚型（TGF β 1-3）的表达及其与胶原表达的关系，作为急性水肿性胰腺炎大鼠成纤维细胞反应的标志物。方法：采用northern blot和免疫组化方法，观察静脉滴注蛋白实验性诱导急性水肿性胰腺炎大鼠过程中TGF β亚型、胶原和淀粉酶的表达和定位。结果：急性胰腺炎诱导导致TGF β 1、β 2和β 3 mRNA的表达呈双相峰值模式，从第1天到第3天显著增加（分别为6倍、2.5倍、5倍），从第5天到第7天再次显著增加（分别为3倍、2.3倍、3.5倍）。TGF β mRNA在时间上的变化与胶原mRNA的表达一致。相比之下，作为腺泡细胞完整性的一般指标，淀粉酶mRNA的表达在急性胰腺炎诱导后略有下降。胰腺炎组织免疫组化分析显示，TGF β 5主要表达于胰腺腺泡细胞和胰腺导管细胞；这在胰腺炎诱导后一天内表现明显。结论：急性胰腺炎诱导后TGF β 5的过表达提示这些蛋白在胰腺修复和重建中发挥作用。TGF β 5水平的升高可能有助于抑制免疫激活，并可能促进包括胶原在内的细胞外基质的增加和胰腺实质的修复。
BACKGROUND: Transforming growth factor beta isoforms (TGF beta s) belong to a family of multifunctional regulators of cellular growth and differentiation. They are mitogenic and chemotactic for fibroblasts and are potent stimulators of extracellular matrix production (collagen) and deposition. Upregulation of TGF beta transcription has been reported for several in vivo systems during repair after injury. AIMS: To study the expression of the three mammalian isoforms of TGF beta (TGF beta 1-3) and their relation to collagen expression as a marker for fibroblast response in acute oedematous pancreatitis in rats. METHODS: Using northern blot analysis and immunohistochemistry, the expression and localisation of TGF beta isoforms, collagen, and amylase were analysed during the course of acute oedematous pancreatitis in rats, experimentally induced by intravenous caerulein infusion. RESULTS: Induction of acute pancreatitis resulted in a biphasic peak pattern of expression of TGF beta 1, beta 2, and beta 3 mRNA, with a pronounced increase from day 1 to day 3 (sixfold, 2.5-fold, fivefold, respectively) and again from day 5 to day 7 (three-fold, 2.3-fold, 3.5-fold, respectively). The temporal changes in TGF beta mRNA identically paralleled the expression in collagen mRNA. In contrast, amylase mRNA expression, used as a general indicator of acinar cell integrity, was slightly decreased after induction of acute pancreatitis. Immunohistochemical analysis of pancreatitis tissue showed that increased expression of TGF beta s was mainly present in the pancreatic acinar and ductal cells; this was evident within one day after pancreatitis induction. CONCLUSION: Overexpression of TGF beta s after induction of acute pancreatitis suggests a role for these proteins in pancreatic repair and remodelling. The increased levels of TGF beta s may help suppress immune activation, and may contribute to the increase in the extracellular matrix including collagen and to the repair of the pancreatic parenchyma.