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Updated: Jul 8, 2026
Characterization of a Novel Human Organotypic Retinal Culture Technique
Published on: June 9, 2021
METTL14-dependent regulation of HMGB1 attenuates inflammation in diabetic retinopathy
Zhangxin Huang1,2, Jitian Guan1,2, Xue Zhang1,2
1Department of Ophthalmology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Background:
Diabetic retinopathy (DR) is a frequent complication of diabetes, characterized by progressive vision loss, with chronic inflammation being an important contributor in its development. N6-methyladenine (m6A) is a crucial RNA modification within eukaryotes, playing an essential role in different bodily functions and disease states. Nonetheless, the precise mechanism underlying m6A modification in DR remains elusive.
Methods:
BV2 cells were stimulated with high glucose (HG) and mice were injected intraperitoneally with streptozotocin (STZ) to induce inflammation. RT-qPCR, Western blot, ELISA, immunofluorescence, CCK-8, Wound Healing, and RIP assays were used to evaluate the effects of methyltransferase-like 14 (METTL14) in these models.
Results:
Our study indicated significantly decreased levels of METTL14 in HG stimulated BV2 cells and in STZ models. In addition, METTL14 levels were reduced in peripheral venous samples of DR patients. Meanwhile, the inflammatory factors were inhibited by up-regulation of METTL14 in HG stimulated BV2 cells and STZ models. Mechanistically, METTL14 overexpression inhibited high mobility group box 1 (HMGB1), thereby suppressing nuclear factor kappa-B (NF-κB) signaling pathway activation.
Conclusion:
This study suggested that METTL14 may influence inflammation in DR by modulating the HMGB1/NF-κB pathway, providing valuable insights into potential therapeutic approaches for DR.
Insights
Methyltransferase-like 14 (METTL14) levels are reduced in diabetic retinopathy (DR) and influence inflammation by modulating the HMGB1/NF-κB pathway. Upregulating METTL14 may offer therapeutic potential for DR.
Area of Science:
- Molecular Biology
- Immunology
- Ophthalmology
Background:
- Diabetic retinopathy (DR) causes vision loss due to diabetes, with inflammation playing a key role.
- N6-methyladenine (m6A) RNA modification is vital in biological processes, but its role in DR is unclear.
Purpose of the Study:
- To investigate the role of methyltransferase-like 14 (METTL14) in diabetic retinopathy (DR) inflammation.
- To elucidate the underlying molecular mechanisms involving m6A modification in DR pathogenesis.
Main Methods:
- Induced inflammation in BV2 cells with high glucose (HG) and in mice with streptozotocin (STZ).
- Assessed METTL14 expression and inflammatory markers using RT-qPCR, Western blot, ELISA, and immunofluorescence.
- Evaluated cell viability, migration, and RNA-binding protein immunoprecipitation (RIP) assays.
Main Results:
- METTL14 levels were decreased in HG-stimulated cells, STZ models, and DR patients.
- METTL14 upregulation inhibited inflammation in vitro and in vivo.
- METTL14 overexpression suppressed the high mobility group box 1 (HMGB1)/nuclear factor kappa-B (NF-κB) pathway.
Conclusions:
- METTL14 plays a significant role in regulating inflammation in diabetic retinopathy (DR).
- The HMGB1/NF-κB pathway is implicated in METTL14-mediated inflammation in DR.
- METTL14 modulation presents a potential therapeutic strategy for DR.
