Mitochondrial dysfunction in placental trophoblast cells experiencing gestational diabetes mellitus.

Tytuł:: Mitochondrial dysfunction in placental trophoblast cells experiencing gestational diabetes mellitus.
Autorzy:: Fisher JJ; School of Medicine and Public Health, University of Newcastle, Hunter Medical Research Institute, New Lambton Heights, New South Wales, Australia.
Vanderpeet CL; School of Biomedical Science, Faculty of Medicine, University of Queensland, St Lucia, Queensland, Australia.
Bartho LA; School of Medical Science, Griffith Health, Griffith University, Gold Coast Campus, Southport, Queensland, Australia.
McKeating DR; School of Medical Science, Griffith Health, Griffith University, Gold Coast Campus, Southport, Queensland, Australia.
Cuffe JSM; School of Biomedical Science, Faculty of Medicine, University of Queensland, St Lucia, Queensland, Australia.
Holland OJ; School of Medical Science, Griffith Health, Griffith University, Gold Coast Campus, Southport, Queensland, Australia.
Perkins AV; School of Medical Science, Griffith Health, Griffith University, Gold Coast Campus, Southport, Queensland, Australia.
Źródło:: The Journal of physiology [J Physiol] 2021 Feb; Vol. 599 (4), pp. 1291-1305. Date of Electronic Publication: 2020 Nov 15.
Typ publikacji:: Journal Article
Język:: English
Imprint Name(s):: Publication: Oxford : Blackwell : Cambridge Univ. Press
Original Publication: London, Cambridge Univ. Press.
MeSH Terms:: Diabetes Mellitus, Type 1*/metabolism
Diabetes Mellitus, Type 2*/metabolism
Diabetes, Gestational*/metabolism
Female ; Humans ; Mitochondria ; Placenta/metabolism ; Pregnancy ; Trophoblasts/metabolism
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Contributed Indexing:: Keywords: cytotrophoblast; gestational diabetes mellitus; mitochondrial dysfunction; mitochondrial isolation; placenta; syncytiotrophoblast
Entry Date(s):: Date Created: 20201102 Date Completed: 20210420 Latest Revision: 20210420
Update Code:: 20240105
DOI:: 10.1113/JP280593
PMID:: 33135816
: Czasopismo naukowe

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Key Points: Mitochondrial dysfunction is known to occur in diabetic phenotypes including type 1 and 2 diabetes mellitus. The incidence of gestational diabetes mellitus (GDM) is increasing and defined as the onset of a diabetic phenotype during pregnancy. The role of placental mitochondria in the aetiology of GDM remains unclear and is an emerging area of research. Differing mitochondrial morphologies within the placenta may influence the pathogenesis of the disorder. This study observed mitochondrial dysfunction in GDM placenta when assessing whole tissue. Upon further investigation into mitochondrial isolates from the cytotrophoblast and syncytiotrophoblast, mitochondrial dysfunction appears exaggerated in syncytiotrophoblast. Assessing mitochondrial populations individually enabled the determination of differences between cell lineages of the placenta and established varying levels of mitochondrial dysfunction in GDM, in some instances establishing significance in pathways previously inconclusive or confounded when assessing whole tissue. This research lays the foundation for future work into mitochondrial dysfunction in the placenta and the role it may play in the aetiology of GDM.
Abstract: Mitochondrial dysfunction has been associated with diabetic phenotypes, yet the involvement of placental mitochondria in gestational diabetes mellitus (GDM) remains inconclusive. This is in part complicated by the different mitochondrial subpopulations present in the two major trophoblast cell lineages of the placenta. To better elucidate the role of mitochondria in this pathology, this study examined key aspects of mitochondrial function in placentas from healthy pregnancies and those complicated by GDM in both whole tissue and isolated mitochondria. Mitochondrial content, citrate synthase activity, reactive oxygen species production and gene expression regulating metabolic, hormonal and antioxidant control was examined in placental tissue, before examining functional differences between mitochondrial isolates from cytotrophoblast (Cyto-Mito) and syncytiotrophoblast (Syncytio-Mito). Our study observed evidence of mitochondrial dysfunction across multiple pathways when assessing whole placental tissue from GDM pregnancies compared with healthy controls. Furthermore, by examining isolated mitochondria from the cytotrophoblast and syncytiotrophoblast cell lineages of the placenta we established that although both mitochondrial populations were dysfunctional, they were differentially impacted. These data highlight the need to consider changes in mitochondrial subpopulations at the feto-maternal interface when studying pregnancy pathologies.
(© 2020 The Authors. The Journal of Physiology © 2020 The Physiological Society.)

Comment in: J Physiol. 2021 Feb;599(4):1019-1020. (PMID: 33337541)

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