Soluble E-cadherin participates in BLM-induced pulmonary fibrosis by promoting EMT and lung fibroblast migration.

Soluble E-cadherin (sE-cad) is an 80 kDa fragment derived from E-cadherin that is shed from the cell surface through proteolytic cleavage and is a biomarker in various cancers that promotes invasion and migration. Alveolar epithelial destruction, aberrant lung fibroblast migration and inflammation contribute to pulmonary fibrosis. Here, we hypothesized that E-cadherin plays an important role in lung fibrosis. In this study, we found that E-cadherin was markedly increased in the bronchoalveolar lavage fluid (BALF) and serum of mice with pulmonary fibrosis and that blocking sE-cad with HECD-1, a neutralizing antibody targeting the ectodomain of E-cadherin, effectively inhibited myofibroblast accumulation and collagen deposition in the lungs after bleomycin (BLM) exposure. Moreover, transforming growth factor-ß (TGF-ß1) induced the shedding of sE-cad from A549 cells, and treatment with HECD-1 inhibited epithelial-mesenchymal transition (EMT) stimulated by TGF-ß1. Fc-E-cadherin (Fc-Ecad), which is an exogenous form of sE-cad, robustly promoted lung fibroblast migration. E-cadherin participates in bleomycin (BLM)-induced lung fibrosis by promoting EMT in the alveolar epithelium and fibroblast activation. E-cadherin may be a novel therapeutic target for lung fibrosis.

MCU promotes the migration of glioma cells by activating p38 through TFEB-mediated autophagy.

Changes in calcium signalling are crucial for the development of glioma cells. Whether mitochondrial calcium balance is involved in glial cell development is still unknown. Mitochondrial Calcium Uniporter (MCU) plays an important role in regulating glioma progression. In this work, we found that MCU and p38 expression were positively correlated with glioma grade and the degree tumour progression. MCU increases glioma cell migration by upregulating p38. Furthermore, p38 promotes glioma progression by activating Transcription Factor EB (TFEB)-mediated autophagy. Thus, MCU promotes glioma cell migration by activating autophagy in a p38/TFEB pathway-dependent manner, which provides a theoretical basis for new therapeutic targets for gliomas.

Case report: Blood purification effectively relieves multiple system failure in patient with rabies.

Rabies is an infectious disease of animal origin with a high mortality rate. In the early stages of rabies, the rabies virus (RABV) is usually undetectable in saliva and cerebrospinal fluid (CSF). In addition, there are still no effective drugs and treatments. Here, we present a case in which blood purification alleviated multisystem failures. The patient was a 45-year-old woman who presented with the fear of water and wind, restlessness, and hyperactivity. RABV was detected in her saliva by high-throughput sequencing Next Generation Sequencing (NGS) and polymerase chain reaction (PCR). Based on typical clinical symptoms and the result of NGS and PCR, the patient was diagnosed as a confirmed case of rabies. Hemodialysis combined with antiviral therapy and intensive care unit (ICU) treatment can effectively relieve circulatory failure, respiratory failure, and renal failure. Finally, she died of brain death on the 34th day of admission. The case report showed that blood purification was positive for rabies-induced organ failure. Blood purification combined with antiviral therapy can prolong the lives of patients with rabies to some extent.