Evidence map›Paper›PMID 42286606›Full record

ArticleStem cell research & therapy2026

BDNF secreted by mesenchymal stem cells ameliorates the accelerated meiotic progression in aged mouse oocytes by activating the PI3K/AKT pathway.

Xin Mi, Jiali Zhou, Caiyi Chen, Jing Zhou, Yajuan Yang, Hongyan Wang, Xue Jiao, Yingying Qin, Zi-Jiang Chen, Shidou Zhao

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell research & therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Xin MiState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Reproductive Medicine, Institute of Women, Children and Reproductive Health, Shandong University, Jinan, 250012, Shandong, China.
Jiali ZhouState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Reproductive Medicine, Institute of Women, Children and Reproductive Health, Shandong University, Jinan, 250012, Shandong, China.
Caiyi ChenState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Reproductive Medicine, Institute of Women, Children and Reproductive Health, Shandong University, Jinan, 250012, Shandong, China.
Jing ZhouState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Reproductive Medicine, Institute of Women, Children and Reproductive Health, Shandong University, Jinan, 250012, Shandong, China.
Yajuan YangState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Reproductive Medicine, Institute of Women, Children and Reproductive Health, Shandong University, Jinan, 250012, Shandong, China.
Hongyan WangDivision of Cell, Developmental and Integrative Biology, School of Medicine, South China University of Technology, Guangzhou, 510006, Guangdong, China.
Xue JiaoState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Reproductive Medicine, Institute of Women, Children and Reproductive Health, Shandong University, Jinan, 250012, Shandong, China.
Yingying QinState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Reproductive Medicine, Institute of Women, Children and Reproductive Health, Shandong University, Jinan, 250012, Shandong, China.
Zi-Jiang ChenState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Reproductive Medicine, Institute of Women, Children and Reproductive Health, Shandong University, Jinan, 250012, Shandong, China.
Shidou ZhaoState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Reproductive Medicine, Institute of Women, Children and Reproductive Health, Shandong University, Jinan, 250012, Shandong, China. shidouzhao@sdu.edu.cn.

Funding

CAMS Innovation Fund for Medical Sciences 2021-I2M-5-001National Key Research and Development Program of China 2024YFC2706600National Natural Science Foundation of China 32370906National Natural Science Foundation of China 32588201National Natural Science Foundation of China 82160286National Natural Science Foundation of China 82421004Natural Science Foundation of Shandong Province for Distinguished Young Scholars ZR2023JQ031Specific Research Fund of The Innovation Platform for Academicians of Hainan Province YSPTZX202310Taishan Scholars Program for Young Experts of Shandong Province tsqn202211370
6 · The paper itself

Abstract

backgroundOocyte aneuploidy is a major contributor to age-related fertility decline, but the effective treatments are still unavailable. The spindle assembly checkpoint (SAC), which functions to maintain chromosomal euploidy in oocytes, may become impaired with aging, manifesting primarily as an aberrant acceleration of meiotic progression. In the present study, we investigated the effects, effective components, and molecular mechanisms of the secretome of mesenchymal stem cells (MSC-sec) in reducing aneuploidy by alleviating the accelerated meiotic progression of aged mouse oocytes.

methodsMSC-sec was added to oocyte culture medium and its effects on aged oocytes were evaluated through analysis of meiotic process, chromosome alignment, the expression and localization of SAC proteins BubR1 and ZW10. The critical role of the PI3K/AKT pathway was confirmed by application of the inhibitor LY294002. Exogenous brain-derived neurotrophic factor (BDNF) or BDNF neutralizing antibodies were used to identify the effective components of MSC-sec. The in vitro effects of 7,8-dihydroxyflavone (7,8-DHF), a BDNF receptor agonist, were validated through PI3K/AKT and ERK1/2 pathway activity, meiotic progression and aneuploidy assays, while its in vivo effects were assessed by oocyte quality and early embryo development following intraperitoneal injection.

resultsMSC-sec could ameliorate age-related accelerated meiotic progression and increase the expression of BubR1 and ZW10 at the kinetochore in mouse oocyte. MSC-sec treatment activates the PI3K/AKT pathway in aged oocytes, and its effect on meiotic progression can be blocked by the PI3K inhibitor LY294002. BDNF is identified as the effective component of MSC-sec in decelerating the meiotic progression. In vitro application of 7,8-DHF ameliorated the accelerated meiotic progression and reduced the aneuploidy rate in aged oocytes, effectively mimicking the effects of BDNF. In vivo administration of 7,8-DHF significantly enhanced oocyte quality and early embryo development in aged mice.

conclusionsWe found that BDNF secreted by MSCs ameliorates the accelerated meiotic progression in aged mouse oocytes by activating the PI3K/AKT pathway, which may be attributed to an improvement in SAC function. Our study elucidates the molecular mechanism and effective component of MSC-sec to alleviate aneuploidy of aged oocytes, providing an experimental foundation for the clinical translation of BDNF or its alternative 7,8-DHF in improving the quality and development potential of oocytes from aged women.

Indexed as

Brain-Derived Neurotrophic FactorMeiosisMesenchymal Stem CellsOocytesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAneuploidyAnimalsCell Cycle ProteinsFemaleMiceProtein Serine-Threonine KinasesSignal TransductionBdnf protein, mouseBrain-Derived Neurotrophic FactorBub1b protein, mouseCell Cycle ProteinsPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktAgingBrain-derived neurotrophic factorMesenchymal stem cellsOocyte qualityPI3K/AKT signaling pathway

Identifiers

PMID42286606
PMCPMC13501573

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.