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MiR-1656 targets GPX4 to trigger pyroptosis in broilers kidney tissues by activating NLRP3 inflammasome under Se
Xuedie Gu1, Yu Wang1, Yujiao He1
1College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, P. R. China.
Abstract:
Selenium (Se) is a vital minor element for the organism. Se deficiency caused inflammation in kidney tissue and regulate the expression of selenoproteins and microRNAs (miRNAs). Pyroptosis involved in the inflammatory response, however, whether microRNA targets GPX4 to regulate Se-deficient kidney tissue pyroptosis is unclear. In this study, broilers were divided into two groups, Control group with 0.3mg/kg Se diet and Se-deficient group with 0.03mg/kg Se diet. The dual luciferase reporter assay system and quantitative real-time PCR (qRT-PCR) were used to screen the specificity of miR-1656 and its target protein in Se-deficient broilers. We tested the pyroptosis-related genes of Se-deficient broilers kidney and miR-1656-transfected primary broilers kidney by qRT-PCR, Western blot (WB) and immunofluorescence staining. Our research indicated that the GPX4 is one of the target genes of miR-1656, and Se deficiency leaded to the overexpression of miR-1656 and the increased expression of pyroptosis-related genes. The overexpression of miR-1656 can induce increased expression of pyroptosis-related genes including NLRP3, Caspase-1, IL-18, and IL-1β by inhibiting the release of GPX4. This study showed that miR-1656 could increase the release of ROS by targeting GPX4, activated the NLRP3 inflammasome, and release the inflammatory factors IL-1β and IL-18 to trigger pyroptosis in the kidney tissue of Se-deficient broilers. This finding may provide new research ideas for kidney injury and cell death due to Se deficiency.
Insights
Selenium deficiency in broilers causes kidney inflammation and pyroptosis. MicroRNA-1656 targets GPX4, promoting this cell death pathway by activating the NLRP3 inflammasome.
Area of Science:
- Biochemistry
- Molecular Biology
- Nutritional Science
Background:
- Selenium (Se) is essential for organismal health, and its deficiency can lead to kidney inflammation.
- MicroRNAs (miRNAs) and selenoproteins are regulated by Se status, and pyroptosis is implicated in inflammatory responses.
- The specific role of miRNAs targeting GPX4 in Se-deficient kidney pyroptosis remains unclear.
Purpose of the Study:
- To investigate the role of miR-1656 in regulating kidney pyroptosis in Se-deficient broilers.
- To identify the target gene of miR-1656 involved in Se deficiency-induced kidney injury.
- To elucidate the molecular mechanism by which miR-1656 influences pyroptosis.
Main Methods:
- Dual luciferase reporter assay and quantitative real-time PCR (qRT-PCR) to identify miR-1656 targets.
- qRT-PCR, Western blot (WB), and immunofluorescence staining to analyze pyroptosis-related genes and proteins.
- Experimental groups included a control (0.3mg/kg Se) and a Se-deficient (0.03mg/kg Se) diet in broilers.
Main Results:
- GPX4 was identified as a direct target gene of miR-1656.
- Se deficiency resulted in the overexpression of miR-1656 and increased expression of pyroptosis markers (NLRP3, Caspase-1, IL-18, IL-1β).
- Overexpression of miR-1656 inhibited GPX4 release, increased reactive oxygen species (ROS), activated the NLRP3 inflammasome, and promoted pyroptosis.
Conclusions:
- miR-1656 plays a critical role in Se-deficient kidney pyroptosis by targeting GPX4.
- The miR-1656/GPX4 axis activates the NLRP3 inflammasome, leading to inflammatory factor release and pyroptosis.
- These findings offer insights into kidney injury mechanisms related to Se deficiency and potential therapeutic targets.
