SHCBP1 过度表达会引发原发性纤毛缺失,从而加重胰腺炎。

DNA and cell biology Pub Date : 2024-03-01 Epub Date: 2024-01-12 DOI:10.1089/dna.2023.0240
Lianshun Li, Huiming Zhao, Zhengyang Li, Wengui Shi, Zuoyi Jiao
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引用次数: 0

摘要

初级纤毛是以微管为基础的细胞器,可介导各种生物过程。胰腺细胞通常都有纤毛;然而,初级纤毛在急性胰腺炎(AP)中的作用在很大程度上是未知的。在这里,我们报告了由 SHCBP1(SHC1 结合蛋白)介导的原发性纤毛缺失对急性胰腺炎的诱发作用。在体外发炎的胰腺细胞和体内患有 AP 的小鼠组织中,初级纤毛广泛丧失。原发性纤毛的消失加剧了脂多糖(LPS)诱导的胰腺细胞炎症。从机制上讲,AP 会诱导 SHCBP1 有丝分裂因子的过度表达,而 SHCBP1 定位于初级纤毛的基部。通过防止体外和体内初级纤毛的丧失,SHCBP1 的缺乏可缓解 LPS 和神经鞘磷脂诱导的胰腺炎。总之,我们发现炎症诱导的初级纤毛缺失会加重 AP。此外,抑制 SHCBP1 以防止初级纤毛丧失是一种有效的抗 AP 策略。
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SHCBP1 Overexpression Aggravates Pancreatitis by Triggering the Loss of Primary Cilia.

Primary cilia are microtubule-based organelles that mediate various biological processes. Pancreatic cells are typically ciliated; however, the role of primary cilia in acute pancreatitis (AP) is largely unknown. Here, we report that the loss of primary cilia, mediated by SHCBP1 (SHC1 binding protein), exerted a provocative effect on AP. Primary cilia are extensively lost in inflamed pancreatic cells in vitro and in mouse tissues with AP in vivo. Abrogation of primary cilia aggravated lipopolysaccharide (LPS)-induced inflammation in pancreatic cells. Mechanistically, AP induced the overexpression of SHCBP1 mitotic factor, which is localized to the base of primary cilia. SHCBP1 deficiency relieved LPS- and cerulein-induced pancreatitis by preventing the loss of primary cilia in vitro and in vivo. Collectively, we reveal that inflammation-induced loss of primary cilia aggravates AP. Furthermore, abrogating SHCBP1 to prevent primary cilia loss is an efficient strategy to combat AP.

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