Chromatin accessibility memory of donor cells disrupts bovine somatic cell nuclear transfer blastocysts development

Huang, Yite; Zhang, Jingcheng; Li, Xinmei; Wu, Ziping; Xie, Gary; Wang, Yong; Zhengqing, Liu; Jiao, Mei; Zhang, Hexu; Shi, Binqiang; Wang, Yu; Zhang, Yong

doi:10.1096/fj.202300131rrr

Cited by 2 publications

(1 citation statement)

References 82 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…H3K4me3 is a classical epigenetic mediator that acknowledged as an excellent‐tuned pattern for orchestrating genes. 47 …”

Section: Discussionmentioning

confidence: 99%

ARID5B‐mediated LINC01128 epigenetically activated pyroptosis and apoptosis by promoting the formation of the BTF3/STAT3 complex in β2GPI/anti‐β2GPI‐treated monocytes

Tan,

Qiao,

Yang

et al. 2024

Clinical & Translational Med

View full text Add to dashboard Cite

BackgroundAlterations of the trimethylation of histone 3 lysine 4 (H3K4me3) mark in monocytes are implicated in the development of autoimmune diseases. Therefore, the purpose of our study was to elucidate the role of H3K4me3‐mediated epigenetics in the pathogenesis of antiphospholipid syndrome (APS).MethodsH3K4me3 Cleavage Under Targets and Tagmentation and Assay for Transposase‐Accessible Chromatin were performed to determine the epigenetic profiles. Luciferase reporter assay, RNA immunoprecipitation, RNA pull‐down, co‐immunoprecipitation and chromatin immunoprecipitation were performed for mechanistic studies. Transmission electron microscopy and propidium iodide staining confirmed cell pyroptosis. Primary monocytes from patients with primary APS (PAPS) and healthy donors were utilised to test the levels of key molecules. A mouse model mimicked APS was constructed with beta2‐glycoprotein I (β2GPI) injection. Blood velocity was detected using murine Doppler ultrasound.ResultsH3K4me3 signal and open chromatin at the ARID5B promoter were increased in an in vitro model of APS. The epigenetic factor ARID5B directly activated LINC01128 transcription at its promoter. LINC01128 promoted the formation of the BTF3/STAT3 complex to enhance STAT3 phosphorylation. Activated STAT3 interacted with the NLRP3 promoter and subsequently stimulated pyroptosis and apoptosis. ARID5B or BTF3 depletion compensated for LINC01128‐induced pyroptosis and apoptosis by inhibiting STAT3 phosphorylation. In mice with APS, β2GPI exposure elevated the levels of key proteins of pyroptosis and apoptosis pathways in bone marrow‐derived monocytes, reduced the blood velocity of the ascending aorta, increased the thrombus size of the carotid artery, and promoted the release of interleukin (IL)‐18, IL‐1β and tissue factor. Patients with PAPS had the high‐expressed ARID5B and LINC01128, especially those with triple positivity for antiphospholipid antibodies. Moreover, there was a positive correlation between ARID5B and LINC01128 expression.ConclusionThis study indicated that ARID5B/LINC01128 was synergistically upregulated in APS, and they aggravated disease pathogenesis by enhancing the formation of the BTF3/STAT3 complex and boosting p‐STAT3‐mediated pyroptosis and apoptosis, thereby providing candidate therapeutic targets for APS.Highlights The H3K4me3 mark and chromatin accessibility at the ARID5B promoter are increased in vitro model mimicked APS. ARID5B‐mediated LINC01128 induces pyroptosis and apoptosis via p‐STAT3 by binding to BTF3. ARID5B is high‐ expressed in patients with primary APS and positively correlated with LINC01128 expression. OICR‐9429 treatment mitigates pyroptosis and related inflammation in vivo and in vitro models mimicked APS.

show abstract

“…H3K4me3 is a classical epigenetic mediator that acknowledged as an excellent‐tuned pattern for orchestrating genes. 47 …”

Section: Discussionmentioning

confidence: 99%

ARID5B‐mediated LINC01128 epigenetically activated pyroptosis and apoptosis by promoting the formation of the BTF3/STAT3 complex in β2GPI/anti‐β2GPI‐treated monocytes

Tan,

Qiao,

Yang

et al. 2024

Clinical & Translational Med

View full text Add to dashboard Cite

show abstract

Methods of karyoplast cell cycle synchronization for increasing the efficiency of somatic cloning of farm animals

Zhukova

2024

Genes & Cells

View full text Add to dashboard Cite

This article is aimed to the analysis of methods for synchronizing the cell cycle of the somatic cells (karyoplasts) upon somatic cloning of farm animals. To obtain cloned animals, the oocytes at the metaphase of the second meiotic division without prior activation are applied as recipient cells in most experiments. In most experiments to obtain cloned offspring, oocytes are used as recipient cells at metaphase of the second meiotic division without prior activation, which determines the choice of somatic cells as karyoplasts at the G0/G1 stage, the most optimal for subsequent nuclear reprogramming by oocyte cytoplasmic factors. The most commonly used methods for arresting cells in this phase are serum starvation and/or contact inhibition, which allows up to 90% of cells to be stopped at the G0/G1 stage. However, despite the effectiveness of these methods, they have a number of significant limitations, and therefore the addition of components to the culture medium of somatic cells that prevent the progression of cells through the cell cycle stages is becoming widespread. The advantage of using chemical inhibitors is the ability of a number of them to have a protective effect on somatic cells, preventing the induction of apoptotic changes. The efficacy of butyrolactone-I, mimosine and aphidicolin application is controversial but a number of studies attests the possible using of these drugs to synchronize the karyoplasts. Thus, there is a wide range of methods for effective synchronization of the cell cycle of karyoplasts, and when choosing the optimal method, one should pay attention to the type of cells, the species of animals from which they were obtained, the permissible duration of cultivation under given conditions in order to minimize the negative impact of conditions on karyoplast viability.

show abstract

Chromatin accessibility memory of donor cells disrupts bovine somatic cell nuclear transfer blastocysts development

Cited by 2 publications

References 82 publications

ARID5B‐mediated LINC01128 epigenetically activated pyroptosis and apoptosis by promoting the formation of the BTF3/STAT3 complex in β2GPI/anti‐β2GPI‐treated monocytes

ARID5B‐mediated LINC01128 epigenetically activated pyroptosis and apoptosis by promoting the formation of the BTF3/STAT3 complex in β2GPI/anti‐β2GPI‐treated monocytes

Methods of karyoplast cell cycle synchronization for increasing the efficiency of somatic cloning of farm animals

Contact Info

Product

Resources

About