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LncRNA MALAT1 affects the progression of endometritis induced by lipopolysaccharide via regulating the expression of
Honglei Chen1, Yuzhen Huang1, Chenxi Yang2
1State Key Laboratory of Reproductive Medicine and Offspring Health, Center for Reproductive Medicine, Institute of Women, Children and Reproductive Health, Shandong University, Jinan, 250012, China; National Research Center for Assisted Reproductive Technology and Reproductive Genetics, Shandong University, Jinan, Shandong, 250012, China; Key Laboratory of Reproductive Endocrinology (Shandong University), Ministry of Education, Jinan, Shandong, 250012, China; Shandong Technology Innovation Center for Reproductive Health, Jinan, Shandong, 250012, China; Shandong Provincial Clinical Research Center for Reproductive Health, Jinan, Shandong, 250012, China; Shandong Key Laboratory of Reproductive Research and Birth Defect Prevention, Jinan, Shandong, 250012, China; Research Unit of Gametogenesis and Health of ART-Offspring, Chinese Academy of Medical Sciences (No.2021RU001), Jinan, Shandong, 250012, China.
Background:
Chronic endometritis (CE) is a common gynecological disorder linked to infertility, but its pathogenesis remains unclear.
Aim:
To investigate the role of lncRNA MALAT1 in lipopolysaccharide (LPS)-induced endometritis and its regulatory mechanism involving the miR-142-3p/PIK3R1 axis.
Methods:
A total of 133 patients with chronic endometritis (CE) and 100 healthy controls were enrolled. Serum and endometrial tissue samples were collected to detect the expression levels of MALAT1, miR-142-3p, and PIK3R1 using RT-qPCR. LPS-treated human endometrial stromal cells (HESCs) were used to establish an endometritis cell model. Cell transfection with MALAT1 siRNA, miR-142-3p mimic/inhibitor, and their negative controls was performed. ELISA was used to measure the concentrations of IL-6, IL-1β, and TNF-α. The CCK-8 assay assessed cell viability. Bioinformatics tools (lncLocator, Starbase, STRING) and dual-luciferase reporter assay validated the targeting relationships among MALAT1, miR-142-3p, and PIK3R1. Western blot assay was performed to measure the protein expression of PIK3R1 and PI3K/Akt pathway.
Results:
MALAT1 and PIK3R1 were upregulated in serum and tissues of CE patients, while miR-142-3p was downregulated. MALAT1 had certain diagnostic value for distinguishing CE from healthy controls. LPS treatment induced inflammatory responses in HESCs, and knockdown of MALAT1 inhibited LPS-induced overexpression of IL-6, IL-1β, and TNF-α. Mechanistically, MALAT1 directly targeted miR-142-3p, and miR-142-3p targeted PIK3R1. Co-transfection of si-MALAT1 and miR-142-3p inhibitor partially reversed the anti-inflammatory effect of MALAT1 knockdown by regulating PI3K/Akt pathway.
Conclusion:
MALAT1 promotes LPS-induced endometritis progression by modulating miR-142-3p to upregulate PIK3R1, suggesting the MALAT1/miR-142-3p/PIK3R1 axis as a potential diagnostic indicator and therapeutic target for CE.
Insights
Long non-coding RNA MALAT1 promotes chronic endometritis (CE) by upregulating PIK3R1 via the miR-142-3p pathway. This axis presents a potential diagnostic and therapeutic target for CE, a common cause of infertility.
Area of Science:
- Gynecology
- Molecular Biology
- Pathogenesis of Endometritis
Background:
- Chronic endometritis (CE) is a prevalent gynecological condition associated with infertility.
- The precise pathogenesis of CE remains incompletely understood.
Purpose of the Study:
- To elucidate the role of the long non-coding RNA MALAT1 in lipopolysaccharide (LPS)-induced endometritis.
- To investigate the regulatory mechanism involving the miR-142-3p/PIK3R1 axis in this process.
Main Methods:
- Expression analysis of MALAT1, miR-142-3p, and PIK3R1 in CE patients and controls.
- Establishment of an LPS-induced endometritis cell model using human endometrial stromal cells (HESCs).
- Validation of molecular interactions using bioinformatics, dual-luciferase reporter assays, and Western blotting.
Main Results:
- MALAT1 and PIK3R1 were upregulated, while miR-142-3p was downregulated in CE patients.
- MALAT1 knockdown suppressed LPS-induced inflammatory responses (IL-6, IL-1β, TNF-α) in HESCs.
- The study confirmed a regulatory axis: MALAT1 targets miR-142-3p, which in turn targets PIK3R1, influencing the PI3K/Akt pathway.
Conclusions:
- The MALAT1/miR-142-3p/PIK3R1 axis plays a crucial role in promoting LPS-induced endometritis.
- This axis demonstrates potential as a diagnostic biomarker and therapeutic target for chronic endometritis.
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