Helical-Ribbon and Tape Formation of Lipid Packaged [Ru(bpy)3]2+ Complexes in Organic Media

Hatakeda, Miho; Toohara, Souta; Nakashima, Takuya; Sakurai, Shinichi; Kuroiwa, Keita

doi:10.3390/ijms20133298

Cited by 2 publications

(1 citation statement)

References 75 publications

(156 reference statements)

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“…Since autophagy degrades aggregates of damaged organelles or misfolded proteins and manipulates the “regeneration” of cells, it is a vital process for cell survival under stress and inflammation [ 8 , 9 ]. Due to the hypoxic and inflammatory responses associated with PE, placental trophoblasts in individuals with PE are more reliant on autophagy for survival than normal cells [ 10 , 11 ]. Autophagy protects syncytiotrophoblasts from apoptosis, infection, and inflammation in the human placenta [ 12 , 13 ], but many questions remain regarding the exact aetiology and precise pathogenic mechanisms ensuring autophagic flux.…”

Section: Introductionmentioning

confidence: 99%

Chorionic villus-derived mesenchymal stem cell-mediated autophagy promotes the proliferation and invasiveness of trophoblasts under hypoxia by activating the JAK2/STAT3 signalling pathway

et al. 2021

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Background Trophoblast dysfunction during pregnancy is fundamentally involved in preeclampsia. Several studies have revealed that human chorionic villous mesenchymal stem cells (CV-MSCs) could regulate trophoblasts function. Results To understand how human chorionic villous mesenchymal stem cells (CV-MSCs) regulate trophoblast function, we treated trophoblasts with CV-MSC supernatant under hypoxic conditions. Treatment markedly enhanced proliferation and invasion and augmented autophagy. Transcriptome and pathway analyses of trophoblasts before and after treatment revealed JAK2/STAT3 signalling as an upstream regulator. In addition, STAT3 mRNA and protein levels increased during CV-MSC treatment. Consistent with these findings, JAK2/STAT3 signalling inhibition reduced the autophagy, survival and invasion of trophoblasts, even in the presence of CV-MSCs, and blocking autophagy did not affect STAT3 activation in trophoblasts treated with CV-MSCs. Importantly, STAT3 overexpression increased autophagy levels in trophoblasts; thus, it positively regulated autophagy in hypoxic trophoblasts. Human placental explants also proved our findings by showing that STAT3 was activated and that LC3B-II levels were increased by CV-MSC treatment. Conclusion In summary, our data suggest that CV-MSC-dependent JAK2/STAT3 signalling activation is a prerequisite for autophagy upregulation in trophoblasts. Graphic abstract

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