Kallikrein and kinin receptor expression in inflammation and cancer
Kallikrein and kinin receptor expression in inflammation and cancer
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DOI：
10.1515/bc.2001.013
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发表时间：
2001-01-01
影响因子：
3.7
通讯作者：
Naicker, S
中科院分区：
文献类型：
--
作者：
Bhoola, K;Ramsaroop, R;Naicker, S
随着激肽受体基因的分子定位、基因表征和克隆实验的展开，丝氨酸蛋白酶的激肽激酶家族在许多炎症疾病中得到了研究。在炎症反应的分子事件中，小肽激肽级联起着重要作用，因为它被认为是启动和维持全身炎症反应和免疫调节紊乱。一个主要的事件是中性粒细胞的趋化吸引，它将钾化钾素-激肽级联传递到细胞损伤和细胞致癌转化的部位。本研究确立了钾化因子级联在感染、炎症性关节疾病、急性移植排斥、肾小球疾病、血管生成和癌症中的偶然参与。我们提供了强有力的证据，证明炎症中新的或增强的激肽B1受体表达，以及血管生成和癌中激肽激酶基因的诱导。该结果为激肽受体拮抗剂和激肽激酶抑制剂的可能作用提供了见解。
The kallikrein family of serine proteases has been investigated in many inflammatory disorders as molecular mapping, gene characterisation and cloning of kinin receptor genes have unfolded experimentally. In the molecular events of the inflammatory response the kallikrein cascade plays a significant role, since it is considered to initiate and maintain systemic inflammatory responses and immune-modulated disorders. A primary event is the chemotactic attraction of neutrophils which deliver the kallikrein-kinin cascade to sites of cellular injury and carcinogenic transformation of cells. The present study establishes the casual involvement of the kallikrein cascade in infection, inflammatory joint disease, acute transplant rejection, renal glomerular diseases, angiogenesis and carcinoma. We provide strong evidence for new or enhanced expression of kinin B1 receptors in inflammation, and additionally the induction of kallikrein genes in angiogenesis and carcinoma. The results provide insights into possible roles of kallikrein inhibitors and kinin receptor antagonists.