Experimental lung research · 2026
The downregulation of RAB10 by miR-574-5p alleviates the inflammatory response in neonatal respiratory distress syndrome.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Ji Yanan, Zhou Yangping, Deng Ludan, Hu Ting
Аннотация
AIM: The diagnosis of neonatal respiratory distress syndrome NRDS relies on progressive breathing difficulties after birth, abnormal blood oxygen levels, and typical chest X-ray images. However, this diagnostic method has insufficient specificity and is difficult to make a differential diagnosis. Pulmonary surfactant replacement and respiratory support are the main treatment methods for NRDS, but targeted therapy is still lacking. Serum miRNA detection has high sensitivity and specificity. This study explored the miR-574-5p/RAB10 axis, providing potential molecular targets for the early diagnosis and treatment development of NRDS.
MATERIALS AND METHODS: This study included 110 non-NRDS and 110 NRDS newborns. The NRDS-related alveolar epithelial injury model was established by stimulating HPAEpiCs with LPS to verify the regulatory effect of the miR-574-5p/RAB10 signaling axis on the secretion of inflammatory factors. The level of miR-574-5p and RAB10 in serum and HPAEpiCs was detected by RT-qPCR. The secretion of inflammatory factors was tested by ELISA. The dual luciferase reporter gene assay was employed to investigate the targeting relationship between miR-574-5p and RAB10. The correlation between clinical factors and miR-574-5p expression was analyzed in NRDS by the chi-square test.
RESULTS: The miR-574-5p expression was reduced in NRDS newborns and HPAEpiCs stimulated by LPS, while the RAB10 expression increased. The ELISA indicated that the secretion of inflammatory factors was increased in HPAEpiCs cells stimulated by LPS. The secretion levels of inflammatory factors were decreased after transfection with miR-574-5p mimic, while transfection with the miR-574-5p inhibitor, the secretion levels were increased. Overexpression of RAB10 overturned the anti-inflammatory role of miR-574-5p mimic.
CONCLUSIONS: This study demonstrated that the miR-574-5p/RAB10 signaling axis plays a crucial role in regulating the inflammation in NRDS. This not only provides potential molecular markers for the early diagnosis of NRDS but also identifies miR-574-5p as a potential therapeutic target for NRDS.
MATERIALS AND METHODS: This study included 110 non-NRDS and 110 NRDS newborns. The NRDS-related alveolar epithelial injury model was established by stimulating HPAEpiCs with LPS to verify the regulatory effect of the miR-574-5p/RAB10 signaling axis on the secretion of inflammatory factors. The level of miR-574-5p and RAB10 in serum and HPAEpiCs was detected by RT-qPCR. The secretion of inflammatory factors was tested by ELISA. The dual luciferase reporter gene assay was employed to investigate the targeting relationship between miR-574-5p and RAB10. The correlation between clinical factors and miR-574-5p expression was analyzed in NRDS by the chi-square test.
RESULTS: The miR-574-5p expression was reduced in NRDS newborns and HPAEpiCs stimulated by LPS, while the RAB10 expression increased. The ELISA indicated that the secretion of inflammatory factors was increased in HPAEpiCs cells stimulated by LPS. The secretion levels of inflammatory factors were decreased after transfection with miR-574-5p mimic, while transfection with the miR-574-5p inhibitor, the secretion levels were increased. Overexpression of RAB10 overturned the anti-inflammatory role of miR-574-5p mimic.
CONCLUSIONS: This study demonstrated that the miR-574-5p/RAB10 signaling axis plays a crucial role in regulating the inflammation in NRDS. This not only provides potential molecular markers for the early diagnosis of NRDS but also identifies miR-574-5p as a potential therapeutic target for NRDS.