Mitochondrial citrate accumulation triggers senescence of alveolar epithelial cells contributing to pulmonary fibrosis in mice.

Alveolar epithelial cell (AEC) senescence is implicated in the pathogenesis of pulmonary fibrosis (PF). However, the exact mechanism underlying AEC senescence during PF remains poorly understood. Here, we reported an unrecognized mechanism for AEC senescence during PF. We found that, in bleomycin (BLM)-induced PF mice, the expressions of isocitrate dehydrogenase 3α (Idh3α) and citrate carrier (CIC) were significantly down-regulated in the lungs, which could result in mitochondria citrate (citratemt) accumulation in our previous study. Notably, the down-regulation of Idh3α and CIC was related to senescence. The mice with AECs-specific Idh3α and CIC deficiency by adenoviral vector exhibited spontaneous PF and senescence in the lungs. In vitro, co-inhibition of Idh3α and CIC with shRNA or inhibitors triggered the senescence of AECs, indicating that accumulated citratemt triggers AEC senescence. Mechanistically, citratemt accumulation impaired the mitochondrial biogenesis of AECs. In addition, the senescence-associated secretory phenotype from senescent AECs induced by citratemt accumulation activated the proliferation and transdifferentiation of NIH3T3 fibroblasts into myofibroblasts. In conclusion, we show that citratemt accumulation would be a novel target for protection against PF that involves senescence.

Megakaryocytes in pulmonary diseases.

Megakaryocytes (MKs) are typical cellular components in the circulating blood flowing from the heart into the lungs. Physiologically, MKs function as an important regulator of platelet production and immunoregulation. However, dysfunction in MKs is considered a trigger in various diseases. It has been described that the lung is an important site of platelet biogenesis from extramedullary MKs, which may play an essential role in various pulmonary diseases. With detailed studies, there are different degrees of numerical changes of MKs in coronavirus disease 2019 (COVID-19), acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), lung cancer, pulmonary fibrosis (PF), and other pulmonary diseases. Also, MKs inhibit or promote the development of pulmonary diseases through various pathways. Here, we summarize the current knowledge of MKs in pulmonary diseases, highlighting the physiological functions and integrated molecular mechanisms. We aim to shine new light on not only the subsequent study of MKs but also the diagnosis and treatment of pulmonary diseases.

Research ability and research motivation of postgraduate nursing students in traditional Chinese medicine colleges.

AIM: To investigate the relationship between research ability and research motivation of postgraduate nursing students in traditional Chinese medicine colleges and identify other factors that may have an impact on the research ability of postgraduate nursing students. DESIGN: A cross-sectional electronic survey was used to collect data from 191 postgraduate nursing students. METHODS: A total of 191 postgraduate nursing students from seven traditional Chinese medicine colleges were investigated from October to November 2020 using self-rated scales for research ability and research motivation. The relationship between the variables affecting the research ability of postgraduate nursing students in traditional Chinese medicine colleges was determined. RESULTS: There was a positive correlation between the score of self-rated research ability and research motivation among 191 postgraduate nursing students in traditional Chinese medicine colleges. Multiple stepwise regression analysis showed that grade, research motivation, age and active participation in class discussions were the main factors affecting the self-rated research ability. CONCLUSION: The self-rated research ability of postgraduate nursing students in traditional Chinese medicine colleges is positively correlated with research motivation. According to the research motivation orientation, adopting targeted training methods and establishing correct professional understanding may improve the research ability of postgraduate nursing students.

[Effect of superantigen SEA on mitochondrial membrane potential of Molt-4 cell].

AIM: To explore the effect of superantigen staphylococcal enterotoxin A(SEA) on mitochondrial membrane potential of Molt-4 cell. METHODS: Cell counting kit-8(CCK-8) was used to detect the proliferation of T cell in different concentration and time, We employed JC-1 to estimate mitochondrialmembrane potential (δψm) of Molt-4 cell induced by SEA using flow cytometry (FCM). RESULTS: The proliferative activity of T cell treated with SEA(1 mg/L) was changed obviously compared with control.The mitochondrial membrane potential of Molt-4 cell with SEA(1 mg/L) was highest at 10 min by FCM after stimulation of 180, 60, 30 and 10 min. Mitochondrial membrane potential of Molt-4 cell treated with SEA after 10 and 30 min were lower than that with PHA which also have rising effect. CONCLUSION: Superantigen can enhance the mitochondrial membrane potential of Molt-4 cell in the early stage of proliferation.But the effect was weaker than that with mitogen PHA.