Layilin, a talin-binding hyaluronan receptor, is expressed in human articular chondrocytes and synoviocytes and is down-regulated by interleukin-1β
Layilin, a talin-binding hyaluronan receptor, is expressed in human articular chondrocytes and synoviocytes and is down-regulated by interleukin-1β
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DOI：
10.1007/s10165-012-0686-x
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发表时间：
2013-05-01
影响因子：
2.2
通讯作者：
Masuko, Kayo
中科院分区：
文献类型：
--
作者：
Murata, Minako;Yudoh, Kazuo;Masuko, Kayo
Layilin （LAYN）是一种与c型凝集素同源的55-kDa跨膜蛋白，已被确定为透明质酸（HA）的受体。有趣的是，LAYN与主要的HA受体CD44没有任何序列同源性。本研究的主要目的是研究LAYN在人关节软骨细胞和滑膜细胞中的表达和潜在功能。样本取自接受关节置换术的患者。体外培养细胞，用白细胞介素(IL)-1 β或肿瘤坏死因子α (TNF α)刺激24 h，分析LAYN的表达。为了评估LAYN的功能，我们用siRNA转染LAYN软骨细胞，用HA和IL-1 β处理它们，然后分析处理后的软骨细胞中基质金属蛋白酶(MMP)-1和MMP-13的产生。结果表明，LAYN在人关节软骨细胞和滑膜细胞中组成性表达，IL-1 β显著抑制LAYN在这些细胞中的表达。HA抑制IL-1 β诱导的软骨细胞中MMP-1和MMP-13的产生，但在转染了抗LAYN的siRNA的软骨细胞中，这种作用被显著消除。我们的研究结果表明，人软骨细胞表达LAYN，一种新的HA受体，LAYN可能有助于调节关节炎条件下的HA功能。对HA受体的进一步研究可能会导致开发新的治疗方法来调节炎症性关节炎中的HA信号。
Layilin (LAYN), a 55-kDa transmembrane protein with homology to C-type lectins, has been identified as a receptor of hyaluronan (HA). Interestingly, LAYN does not share any sequence homology with CD44, a primary HA receptor. The primary aim of our study was to examine the expression and potential function of LAYN in human articular chondrocytes and synoviocytes.Samples were obtained from patients undergoing joint arthroplasty. Cells were grown in vitro, then stimulated with interleukin (IL)-1 beta or tumor necrosis factor alpha (TNF alpha) for 24 h and the expression of LAYN was analyzed. To assess the function of LAYN, we transfected chondrocytes with siRNA against LAYN, treated them with HA and IL-1 beta, and then analyzed the production of matrix metalloproteinase (MMP)-1 and MMP-13 in the treated chrondrocytes.The results showed that LAYN was constitutively expressed in human articular chondrocytes and synoviocytes and that IL-1 beta significantly suppressed the expression of LAYN in these cells. HA repressed IL-1 beta-induced MMP-1 and MMP-13 production in chondrocytes, but this was significantly abrogated in chondrocytes transfected with siRNA against LAYN.Our results show that human chondrocytes express LAYN, a novel HA receptor, and that LAYN may contribute to the regulation of HA functions in the arthritic condition. Further investigation of the HA receptor may lead to the development of novel therapeutics to regulate HA signaling in inflammatory arthritis.