Hypoxic mesenchymal stem cell-derived exosomal circDennd2a regulates granulosa cell glycolysis by interacting with LDHA

Abstract Background Premature ovarian insufficiency (POI) is an ovarian dysfunction disorder that significantly impacts female fertility. Ovarian granulosa cells (GCs) are crucial somatic components supporting oocyte development that rely on glycolysis for energy production, which is essential for f...

Full description

Saved in:
Bibliographic Details
Main Authors: Wenxin Li, Minjun Lu, Junyu Shang, Jiamin Zhou, Li Lin, Yueqin Liu, Dan Zhao, Xiaolan Zhu
Format: Article
Language:English
Published: BMC 2024-12-01
Series:Stem Cell Research & Therapy
Subjects:
Online Access:https://doi.org/10.1186/s13287-024-04098-0
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1846112768368836608
author Wenxin Li
Minjun Lu
Junyu Shang
Jiamin Zhou
Li Lin
Yueqin Liu
Dan Zhao
Xiaolan Zhu
author_facet Wenxin Li
Minjun Lu
Junyu Shang
Jiamin Zhou
Li Lin
Yueqin Liu
Dan Zhao
Xiaolan Zhu
author_sort Wenxin Li
collection DOAJ
description Abstract Background Premature ovarian insufficiency (POI) is an ovarian dysfunction disorder that significantly impacts female fertility. Ovarian granulosa cells (GCs) are crucial somatic components supporting oocyte development that rely on glycolysis for energy production, which is essential for follicular growth. Hypoxia-induced exosomal circRNAs regulate glycolysis, but their biological functions and molecular mechanisms in POI are largely unexplored. The present comprehensive investigation revealed a substantial reduction in ovarian glycolysis levels in POI rats. Notably, hypoxia-induced exosomes originating from mesenchymal stem cells (HM-Exs) exhibit a remarkable capacity to enhance ovarian glycolysis, mitigate GCs apoptosis, reinstate disrupted estrous cycles, modulate sex hormone levels, and curtail the presence of atretic follicles. These restorative actions collectively contribute to fostering fertility revival in POI-afflicted rats. Methods Cyclophosphamide was administered for 2 weeks to induce POI rat model, and POI rats were randomly divided into three groups and treated with PBS, NM-Exs and HM-Exs, respectively. Ovarian function and fertility were assessed at the end of the study and ovarian tissues were collected for analysis of energy metabolites. The relationship between circDennd2a and POI was explored in vitro by qRT-PCR, Western blotting, CCK-8 assay, EdU staining, TUNEL staining, extracellular acidification rate (ECAR) measurements, and ATP, lactate and pyruvate level assays. Results Our findings revealed depletion of circDennd2a in serum samples and GCs from individuals suffering from POI. The introduction of HM-Exs-derived circDennd2a (HM-Exs-circDennd2a) effectively counteracted GCs apoptosis by enhancing glycolytic processes and driving cellular proliferation. CircDennd2a interacted with lactate dehydrogenase A (LDHA), which served as a catalyst to increase LDHA enzymatic activity and facilitate the conversion of NADH to NAD+. This biochemical cascade worked synergistically to sustain glycolytic function within GCs. Conclusion This study revealed that HM-Exs-circDennd2a promoted LDHA activity and enhanced GCs glycolytic capacity, both of which support its use as a potential clinical diagnostic and therapeutic target for POI.
format Article
id doaj-art-46743d314671403eae6c97f035a4cec8
institution Kabale University
issn 1757-6512
language English
publishDate 2024-12-01
publisher BMC
record_format Article
series Stem Cell Research & Therapy
spelling doaj-art-46743d314671403eae6c97f035a4cec82024-12-22T12:18:53ZengBMCStem Cell Research & Therapy1757-65122024-12-0115111710.1186/s13287-024-04098-0Hypoxic mesenchymal stem cell-derived exosomal circDennd2a regulates granulosa cell glycolysis by interacting with LDHAWenxin Li0Minjun Lu1Junyu Shang2Jiamin Zhou3Li Lin4Yueqin Liu5Dan Zhao6Xiaolan Zhu7Reproductive Medicine Center, The Fourth Affiliated Hospital of Jiangsu UniversityReproductive Medicine Center, The Fourth Affiliated Hospital of Jiangsu UniversityReproductive Medicine Center, The Fourth Affiliated Hospital of Jiangsu UniversityReproductive Medicine Center, The Fourth Affiliated Hospital of Jiangsu UniversityReproductive Medicine Center, The Fourth Affiliated Hospital of Jiangsu UniversityReproductive Medicine Center, The Fourth Affiliated Hospital of Jiangsu UniversityReproductive Medicine Center, The Fourth Affiliated Hospital of Jiangsu UniversityReproductive Medicine Center, The Fourth Affiliated Hospital of Jiangsu UniversityAbstract Background Premature ovarian insufficiency (POI) is an ovarian dysfunction disorder that significantly impacts female fertility. Ovarian granulosa cells (GCs) are crucial somatic components supporting oocyte development that rely on glycolysis for energy production, which is essential for follicular growth. Hypoxia-induced exosomal circRNAs regulate glycolysis, but their biological functions and molecular mechanisms in POI are largely unexplored. The present comprehensive investigation revealed a substantial reduction in ovarian glycolysis levels in POI rats. Notably, hypoxia-induced exosomes originating from mesenchymal stem cells (HM-Exs) exhibit a remarkable capacity to enhance ovarian glycolysis, mitigate GCs apoptosis, reinstate disrupted estrous cycles, modulate sex hormone levels, and curtail the presence of atretic follicles. These restorative actions collectively contribute to fostering fertility revival in POI-afflicted rats. Methods Cyclophosphamide was administered for 2 weeks to induce POI rat model, and POI rats were randomly divided into three groups and treated with PBS, NM-Exs and HM-Exs, respectively. Ovarian function and fertility were assessed at the end of the study and ovarian tissues were collected for analysis of energy metabolites. The relationship between circDennd2a and POI was explored in vitro by qRT-PCR, Western blotting, CCK-8 assay, EdU staining, TUNEL staining, extracellular acidification rate (ECAR) measurements, and ATP, lactate and pyruvate level assays. Results Our findings revealed depletion of circDennd2a in serum samples and GCs from individuals suffering from POI. The introduction of HM-Exs-derived circDennd2a (HM-Exs-circDennd2a) effectively counteracted GCs apoptosis by enhancing glycolytic processes and driving cellular proliferation. CircDennd2a interacted with lactate dehydrogenase A (LDHA), which served as a catalyst to increase LDHA enzymatic activity and facilitate the conversion of NADH to NAD+. This biochemical cascade worked synergistically to sustain glycolytic function within GCs. Conclusion This study revealed that HM-Exs-circDennd2a promoted LDHA activity and enhanced GCs glycolytic capacity, both of which support its use as a potential clinical diagnostic and therapeutic target for POI.https://doi.org/10.1186/s13287-024-04098-0Premature ovarian insufficiency (POI)HypoxiaExosomesCircDennd2aGlycolysis
spellingShingle Wenxin Li
Minjun Lu
Junyu Shang
Jiamin Zhou
Li Lin
Yueqin Liu
Dan Zhao
Xiaolan Zhu
Hypoxic mesenchymal stem cell-derived exosomal circDennd2a regulates granulosa cell glycolysis by interacting with LDHA
Stem Cell Research & Therapy
Premature ovarian insufficiency (POI)
Hypoxia
Exosomes
CircDennd2a
Glycolysis
title Hypoxic mesenchymal stem cell-derived exosomal circDennd2a regulates granulosa cell glycolysis by interacting with LDHA
title_full Hypoxic mesenchymal stem cell-derived exosomal circDennd2a regulates granulosa cell glycolysis by interacting with LDHA
title_fullStr Hypoxic mesenchymal stem cell-derived exosomal circDennd2a regulates granulosa cell glycolysis by interacting with LDHA
title_full_unstemmed Hypoxic mesenchymal stem cell-derived exosomal circDennd2a regulates granulosa cell glycolysis by interacting with LDHA
title_short Hypoxic mesenchymal stem cell-derived exosomal circDennd2a regulates granulosa cell glycolysis by interacting with LDHA
title_sort hypoxic mesenchymal stem cell derived exosomal circdennd2a regulates granulosa cell glycolysis by interacting with ldha
topic Premature ovarian insufficiency (POI)
Hypoxia
Exosomes
CircDennd2a
Glycolysis
url https://doi.org/10.1186/s13287-024-04098-0
work_keys_str_mv AT wenxinli hypoxicmesenchymalstemcellderivedexosomalcircdennd2aregulatesgranulosacellglycolysisbyinteractingwithldha
AT minjunlu hypoxicmesenchymalstemcellderivedexosomalcircdennd2aregulatesgranulosacellglycolysisbyinteractingwithldha
AT junyushang hypoxicmesenchymalstemcellderivedexosomalcircdennd2aregulatesgranulosacellglycolysisbyinteractingwithldha
AT jiaminzhou hypoxicmesenchymalstemcellderivedexosomalcircdennd2aregulatesgranulosacellglycolysisbyinteractingwithldha
AT lilin hypoxicmesenchymalstemcellderivedexosomalcircdennd2aregulatesgranulosacellglycolysisbyinteractingwithldha
AT yueqinliu hypoxicmesenchymalstemcellderivedexosomalcircdennd2aregulatesgranulosacellglycolysisbyinteractingwithldha
AT danzhao hypoxicmesenchymalstemcellderivedexosomalcircdennd2aregulatesgranulosacellglycolysisbyinteractingwithldha
AT xiaolanzhu hypoxicmesenchymalstemcellderivedexosomalcircdennd2aregulatesgranulosacellglycolysisbyinteractingwithldha