Pancreatic stellate cells: a starring role in normal and diseased pancreas.
Pancreatic stellate cells: a starring role in normal and diseased pancreas.
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DOI：
10.3389/fphys.2012.00344
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发表时间：
2012
影响因子：
4
通讯作者：
Wilson JS
中科院分区：
文献类型：
--
作者：
Apte MV;Pirola RC;Wilson JS
虽然外分泌胰腺和内分泌胰腺细胞的形态和功能已经被研究了几个世纪，但胰腺中的一种重要细胞类型——胰腺星状细胞（PSC）直到20年前才被发现。即使在1982年首次被描述之后，又过了16年其生物学特性才得以开始被研究，因为直到1998年才开发出从啮齿动物和人类胰腺中分离和培养PSC的方法。现在已知PSC在胰腺纤维化中起着关键作用，胰腺纤维化是两种主要胰腺疾病——慢性胰腺炎和胰腺癌的一个一贯的组织学特征。在健康状态下，PSC通过调节细胞外基质（ECM）蛋白的合成和降解来维持正常的组织结构。最近的研究还暗示PSC在人类中具有祖细胞、免疫细胞或外分泌胰腺分泌中介等其他功能。在胰腺损伤期间，PSC从其静止期转变为活化的、肌成纤维细胞样表型，分泌过量的ECM蛋白，导致慢性胰腺炎和胰腺癌的纤维化。越来越多通过旁分泌和自分泌途径刺激和/或抑制PSC活化的因子正在被识别和鉴定。现在也已经确定PSC与胰腺癌细胞密切相互作用以促进癌症进展。基于这些发现，在慢性胰腺炎以及胰腺癌的实验模型中已经研究了几种治疗策略，试图抑制/延缓PSC活化，从而缓解慢性胰腺炎或减少胰腺癌中的肿瘤生长。仍然面临的挑战是将这些临床前的研究进展转化为对慢性胰腺炎和胰腺癌患者临床适用的治疗方法。
While the morphology and function of cells of the exocrine and endocrine pancreas have been studied over several centuries, one important cell type in the gland, the pancreatic stellate cell (PSC), had remained undiscovered until as recently as 20 years ago. Even after its first description in 1982, it was to be another 16 years before its biology could begin to be studied, because it was only in 1998 that methods were developed to isolate and culture PSCs from rodent and human pancreas. PSCs are now known to play a critical role in pancreatic fibrosis, a consistent histological feature of two major diseases of the pancreas—chronic pancreatitis and pancreatic cancer. In health, PSCs maintain normal tissue architecture via regulation of the synthesis and degradation of extracellular matrix (ECM) proteins. Recent studies have also implied other functions for PSCs as progenitor cells, immune cells or intermediaries in exocrine pancreatic secretion in humans. During pancreatic injury, PSCs transform from their quiescent phase into an activated, myofibroblast-like phenotype that secretes excessive amounts of ECM proteins leading to the fibrosis of chronic pancreatitis and pancreatic cancer. An ever increasing number of factors that stimulate and/or inhibit PSC activation via paracrine and autocrine pathways are being identified and characterized. It is also now established that PSCs interact closely with pancreatic cancer cells to facilitate cancer progression. Based on these findings, several therapeutic strategies have been examined in experimental models of chronic pancreatitis as well as pancreatic cancer, in a bid to inhibit/retard PSC activation and thereby alleviate chronic pancreatitis or reduce tumor growth in pancreatic cancer. The challenge that remains is to translate these pre-clinical developments into clinically applicable treatments for patients with chronic pancreatitis and pancreatic cancer.
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