Inflammatory bowel diseases · 2025
Role of lncRNA MGP202 in Modulating B Cell Dynamics and Its Implications in Ulcerative Colitis.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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.
Zhou Runing, Bai Xiaoyin, Zhang Dongdong, Zhu Yashu, Dong Xuyang, Wu Meixu, Guo Mingyue, Yang Liu, Yang Hong, Qian Jiaming
Аннотация
BACKGROUND: The upregulation of long noncoding RNA (lncRNA) MGP202 in ulcerative colitis (UC) patients suggests its potential significance in the disease. Understanding its role in UC pathogenesis and its impact on B cell dynamics is crucial for diagnostic and therapeutic advancements.
METHODS: We investigated the expression and function of MGP202 in UC patients by examining its localization in colon specimens, performing knockdown and overexpression experiments in Raji B cells, and evaluating its interaction with hsa-miR-5590-3p. Furthermore, we explored the downstream effect on interleukin-33 (IL-33) expression.
RESULTS: We found elevated expression of MGP202 in UC patients compared to healthy controls. Knockdown of MGP202 impeded B cell proliferation, while overexpression enhanced it. Direct binding between MGP202 and hsa-miR-5590-3p was confirmed. IL-33 expression decreased with hsa-miR-5590-3p overexpression but increased with MGP202 overexpression. Increased IL-33 levels were detected in the colon mucosa of UC patients.
CONCLUSIONS: Our study reveals the upregulation of MGP202 in UC patients and its regulation of B cell proliferation through sponging hsa-miR-5590-3p and modulating IL-33 expression. These findings highlight MGP202 as a potential diagnostic and therapeutic target for UC, particularly in the context of B cell dynamics. Further investigations are warranted to evaluate clinical applicability and unravel additional mechanisms related to MGP202 modulation of B cell behavior in UC.
METHODS: We investigated the expression and function of MGP202 in UC patients by examining its localization in colon specimens, performing knockdown and overexpression experiments in Raji B cells, and evaluating its interaction with hsa-miR-5590-3p. Furthermore, we explored the downstream effect on interleukin-33 (IL-33) expression.
RESULTS: We found elevated expression of MGP202 in UC patients compared to healthy controls. Knockdown of MGP202 impeded B cell proliferation, while overexpression enhanced it. Direct binding between MGP202 and hsa-miR-5590-3p was confirmed. IL-33 expression decreased with hsa-miR-5590-3p overexpression but increased with MGP202 overexpression. Increased IL-33 levels were detected in the colon mucosa of UC patients.
CONCLUSIONS: Our study reveals the upregulation of MGP202 in UC patients and its regulation of B cell proliferation through sponging hsa-miR-5590-3p and modulating IL-33 expression. These findings highlight MGP202 as a potential diagnostic and therapeutic target for UC, particularly in the context of B cell dynamics. Further investigations are warranted to evaluate clinical applicability and unravel additional mechanisms related to MGP202 modulation of B cell behavior in UC.