Scholarlink

Objective <p>The mechanisms underlying the progression of acute pancreatitis (AP) remain incompletely elucidated. This study investigates the expression pattern, diagnostic and prognostic value of miR-1-3p in AP patients, and further elucidates its role in pancreatic acinar cell injury and the underlying molecular mechanisms.</p> Methods <p>miR-1-3p levels were measured via qPCR and correlated with clinical indicators. ROC analysis evaluated diagnostic efficacy, and logistic regression assessed prognostic relevance. A Caerulein-induced injury model was established in MPC-83 cells. Post-transfection with a miR-1-3p inhibitor, cell viability (CCK-8), inflammatory factors (ELISA), and oxidative stress (WST-8/TBA) were evaluated. Bioinformatics-predicted target genes were validated through dual-luciferase reporter and RIP assays, with rescue experiments confirming the targeting relationship.</p> Results <p>miR-1-3p was significantly upregulated in SAP patients and effectively distinguished healthy individuals (AUC = 0.880) and disease severity (AUC = 0.878). Its levels positively correlated with CRP, APACHE II, and BUN (<i>p</i> &lt; 0.0001). High miR-1-3p expression independently predicted poor prognosis (OR = 9.54, <i>p</i> = 0.023). Inhibition of miR-1-3p alleviated Caerulein-induced cellular injury in vitro. GNPTAB was identified as a direct target, showing downregulation and negative correlation with miR-1-3p in patients. Rescue experiments confirmed that GNPTAB downregulation partially reversed the protective effects of miR-1-3p inhibition.</p> Conclusions <p>miR-1-3p, upregulated in SAP, is a potential diagnostic biomarker and predictor of poor prognosis. It exacerbates pancreatic acinar cell injury by targeting GNPTAB, contributing to inflammation, oxidative stress, and AP progression.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

miR-1-3p, as a novel diagnostic and prognostic biomarker, aggravates pancreatic acinar cell injury in acute pancreatitis by targeting GNPTAB

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月10日

查看全文
  • Haibin Huang,
  • Jinyu Liu,
  • Lianjun Wu,
  • Wen Miao

摘要

Objective

The mechanisms underlying the progression of acute pancreatitis (AP) remain incompletely elucidated. This study investigates the expression pattern, diagnostic and prognostic value of miR-1-3p in AP patients, and further elucidates its role in pancreatic acinar cell injury and the underlying molecular mechanisms.

Methods

miR-1-3p levels were measured via qPCR and correlated with clinical indicators. ROC analysis evaluated diagnostic efficacy, and logistic regression assessed prognostic relevance. A Caerulein-induced injury model was established in MPC-83 cells. Post-transfection with a miR-1-3p inhibitor, cell viability (CCK-8), inflammatory factors (ELISA), and oxidative stress (WST-8/TBA) were evaluated. Bioinformatics-predicted target genes were validated through dual-luciferase reporter and RIP assays, with rescue experiments confirming the targeting relationship.

Results

miR-1-3p was significantly upregulated in SAP patients and effectively distinguished healthy individuals (AUC = 0.880) and disease severity (AUC = 0.878). Its levels positively correlated with CRP, APACHE II, and BUN (p < 0.0001). High miR-1-3p expression independently predicted poor prognosis (OR = 9.54, p = 0.023). Inhibition of miR-1-3p alleviated Caerulein-induced cellular injury in vitro. GNPTAB was identified as a direct target, showing downregulation and negative correlation with miR-1-3p in patients. Rescue experiments confirmed that GNPTAB downregulation partially reversed the protective effects of miR-1-3p inhibition.

Conclusions

miR-1-3p, upregulated in SAP, is a potential diagnostic biomarker and predictor of poor prognosis. It exacerbates pancreatic acinar cell injury by targeting GNPTAB, contributing to inflammation, oxidative stress, and AP progression.