Fetal growth restriction induced by maternal gal-3 deficiency is associated with altered gut-placenta axis
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Fetal growth restriction induced by maternal gal-3 deficiency is associated with altered gut-placenta axis. / Xie, Yiran; Zhao, Fangqi; Wang, Yiru; Borowski, Sophia; Freitag, Nancy; Tirado-Gonzalez, Irene; Hofsink, Naomi; Matschl, Urte; Plösch, Torsten; Garcia, Mariana G; Blois, Sandra M.
In: CELL DEATH DIS, Vol. 15, No. 8, 08.08.2024, p. 575.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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T1 - Fetal growth restriction induced by maternal gal-3 deficiency is associated with altered gut-placenta axis
AU - Xie, Yiran
AU - Zhao, Fangqi
AU - Wang, Yiru
AU - Borowski, Sophia
AU - Freitag, Nancy
AU - Tirado-Gonzalez, Irene
AU - Hofsink, Naomi
AU - Matschl, Urte
AU - Plösch, Torsten
AU - Garcia, Mariana G
AU - Blois, Sandra M
N1 - © 2024. The Author(s).
PY - 2024/8/8
Y1 - 2024/8/8
N2 - Adverse intrauterine conditions may cause fetal growth restriction (FGR), a pregnancy complication frequently linked to perinatal morbidity and mortality. Although many studies have focused on FGR, the pathophysiological processes underlying this disorder are complex and incompletely understood. We have recently determined that galectin-3 (gal-3), a β-galactoside-binding protein, regulates pregnancy-associated processes, including uterine receptibility, maternal vascular adaptation and placentation. Because gal-3 is expressed at both sides of the maternal-fetal interface, we unraveled the contribution of maternal- and paternal-derived gal-3 on fetal-placental development in the prenatal window and its effects on the post-natal period. Deficiency of maternal gal-3 induced maternal gut microbiome dysbiosis, resulting in a sex-specific fetal growth restriction mainly observed in female fetuses and offspring. In addition, poor placental metabolic adaptions (characterized by decreased trophoblast glycogen content and insulin-like growth factor 2 (Igf2) gene hypomethylation) were only associated with a lack of maternal-derived gal-3. Paternal gal-3 deficiency caused compromised vascularization in the placental labyrinth without affecting fetal growth trajectory. Thus, maternal-derived gal-3 may play a key role in fetal-placental development through the gut-placenta axis.
AB - Adverse intrauterine conditions may cause fetal growth restriction (FGR), a pregnancy complication frequently linked to perinatal morbidity and mortality. Although many studies have focused on FGR, the pathophysiological processes underlying this disorder are complex and incompletely understood. We have recently determined that galectin-3 (gal-3), a β-galactoside-binding protein, regulates pregnancy-associated processes, including uterine receptibility, maternal vascular adaptation and placentation. Because gal-3 is expressed at both sides of the maternal-fetal interface, we unraveled the contribution of maternal- and paternal-derived gal-3 on fetal-placental development in the prenatal window and its effects on the post-natal period. Deficiency of maternal gal-3 induced maternal gut microbiome dysbiosis, resulting in a sex-specific fetal growth restriction mainly observed in female fetuses and offspring. In addition, poor placental metabolic adaptions (characterized by decreased trophoblast glycogen content and insulin-like growth factor 2 (Igf2) gene hypomethylation) were only associated with a lack of maternal-derived gal-3. Paternal gal-3 deficiency caused compromised vascularization in the placental labyrinth without affecting fetal growth trajectory. Thus, maternal-derived gal-3 may play a key role in fetal-placental development through the gut-placenta axis.
KW - Fetal Growth Retardation/metabolism
KW - Pregnancy
KW - Female
KW - Animals
KW - Placenta/metabolism
KW - Mice
KW - Galectin 3/metabolism
KW - Male
KW - Gastrointestinal Microbiome
KW - Mice, Inbred C57BL
KW - Humans
KW - Fetal Development
KW - Insulin-Like Growth Factor II/metabolism
KW - Trophoblasts/metabolism
U2 - 10.1038/s41419-024-06962-6
DO - 10.1038/s41419-024-06962-6
M3 - SCORING: Journal article
C2 - 39117607
VL - 15
SP - 575
JO - CELL DEATH DIS
JF - CELL DEATH DIS
SN - 2041-4889
IS - 8
ER -