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CARMA3 缺乏可减轻博来霉素诱导的肺纤维化的发展。

Deficiency of CARMA3 attenuates the development of bleomycin induced pulmonary fibrosis.

机构信息

Department of Thoracic and Cardiovascular Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.

Department of Thoracic and Cardiovascular Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.

出版信息

Biochem Biophys Res Commun. 2021 Dec 3;581:81-88. doi: 10.1016/j.bbrc.2021.10.013. Epub 2021 Oct 11.

Abstract

BACKGROUND

Pulmonary fibrosis (PF) has attracted more and more attention due to its irreversibility and high mortality rate. Currently, there is no effective treatment option is available to reverse the disease. Caspase recruitment domain-containing membrane-associated guanylate kinase protein (CARMA3) has been recognized as a proinflammatory molecule involved in many lung diseases, such as Allergic airway inflammation and lung cancer. Bleomycin (Bleo), as an alkaline sugar peptide antibiotics, is often used as a first-line anti-tumor agent. Its toxic effect is to induce pulmonary fibrosis (PF) and its clinical symptoms, so it has been widely used in the construction of pulmonary fibrosis model.

METHODS

Wild type mice (WT, n = 20) and CARMA3 knockout mice (CARMA3-KO, n = 20) were generated and injected with bleomycin or saline via trachea. The severity of fibrosis was evaluated by fibrosis markers and lung histological morphology. Furthermore, the amount of alveolar epithelial cells and inflammation in lung tissue were examined. Finally, epithelial-mesenchymal transition was further investigated.

RESULTS

We found CARMA3 expression in the mice alveolar epithelial cells. And compared with WT mice, CARMA3-KO mice showed reduced deposition of collagen fibers, inflammation and destruction of alveolar epithelial cells in lung tissue. In addition, after bleomycin induction, the expressions of proinflammatory factors and collagen-related factors in CARMA3-KO mice were much lower than those in WT mice. The epithelial-mesenchymal transformation phenotype was also improved in CARMA3-KO mice compared to WT mice.

CONCLUSION

Our Results shows that CARMA3 plays an important role in the pathogenesis of bleomycin-induced pulmonary fibrosis. CARMA3 could alleviate the fibrosis by improving inflammation, deposition of collagen and damage of alveolar epithelial cells, which revealed that CARMA3 may be a potential target for pulmonary fibrosis.

摘要

背景

肺纤维化(PF)因其不可逆转和高死亡率而越来越受到关注。目前,尚无有效的治疗方法可以逆转这种疾病。半胱天冬酶募集结构域包含膜相关鸟苷酸激酶蛋白(CARMA3)已被认为是一种参与多种肺部疾病的促炎分子,如过敏性气道炎症和肺癌。博来霉素(Bleo)作为一种碱性糖肽抗生素,常被用作一线抗肿瘤药物。其毒性作用是诱导肺纤维化(PF)及其临床症状,因此被广泛用于肺纤维化模型的构建。

方法

野生型小鼠(WT,n=20)和 CARMA3 敲除小鼠(CARMA3-KO,n=20)通过气管注射博来霉素或生理盐水。通过纤维化标志物和肺组织形态学评估纤维化的严重程度。此外,还检测了肺泡上皮细胞和肺组织中的炎症数量。最后,进一步研究了上皮-间充质转化。

结果

我们发现 CARMA3 在小鼠肺泡上皮细胞中表达。与 WT 小鼠相比,CARMA3-KO 小鼠肺组织中胶原纤维沉积、炎症和肺泡上皮细胞破坏减少。此外,在博来霉素诱导后,CARMA3-KO 小鼠中促炎因子和胶原相关因子的表达明显低于 WT 小鼠。CARMA3-KO 小鼠的上皮-间充质转化表型也比 WT 小鼠有所改善。

结论

我们的结果表明,CARMA3 在博来霉素诱导的肺纤维化发病机制中起重要作用。CARMA3 通过改善炎症、胶原沉积和肺泡上皮细胞损伤来减轻纤维化,这表明 CARMA3 可能是肺纤维化的潜在靶点。

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