Magnetochemistry and chemical synthesis

High magnetic field is one of the effective tools to control a chemical reaction and materials synthesis. In this review,we summarized the magnetic field effects on chemical reactions, such as reaction pathway, growth behavior of nanomaterials, product phase, and magnetic domain of materials. The surface spins and activity of catalysts under magnetic fields were also discussed.

LSD1调控颗粒细胞自噬并抑制Wt1参与FSH调节的有腔卵泡形成

In a growing follicle,the survival and maturation of the oocyte largely depend on support from somatic cells to facilitate FSH-induced mutual signaling and chemical communication.Although apoptosis and autophagy in somatic cells are involved in the process of FSH-induced follicular development,the underlying mechanisms require substantial study.According to our study,along with FSH-induced antral follicles(AFs)formation,both lysine-specific demethylase 1(LSD1)protein levels and autophagy increased simultaneously in granulosa cells(GCs)in a time-dependent manner,we therefore evaluated the importance of LSD upon facilitating the formation of AFs correlated to autophagy in GCs.Conditional knockout of Lsdl in GCs resulted in significantly decreased AF number and subfertility in females,accompanied by marked suppression of the autophagy in GCs.On the one hand,depletion of Lsd1 resulted in accumulation of Wilms tumor 1 homolog(WT1),at both the protein and mRNA levels.WT1 prevented the expression of FSH receptor(Fshr)in GCs and thus reduced the responsiveness of the secondary follicles to FSH induction.On the other hand,depletion of LSD1 resulted in suppressed level of autophagy by upregulation of ATG16L2 in GCs.We finally approved that LSD1 contributed to these sequential activities in GCs through its H3K4me2 demethylase activity.Therefore,the importance of LSD1 in GCs is attributable to its roles in both accelerating autophagy and suppressing WT1 expression to ensure the responsiveness of GCs to FSH during AFs formation.

Sequential activation of uterine epithelial IGF1R by stromal IGF1 and embryonic IGF2 directs normal uterine preparation for embryo implantation

Embryo implantation in both humans and rodents is initiated by the attachment of a blastocyst to the uterine epithelium.For blastocyst attachment,the uterine epithelium needs to transform at both the structural and molecular levels first,and then initiate the interaction with trophectoderm.Any perturbation during this process will result in implantation failure or long-term adverse pregnancy outcomes.Endocrine steroid hormones,which function through nuclear receptors,combine with the local molecules produced by the uteri or embryo to facilitate implantation.The insulin-like growth factor(IGF)signaling has been reported to play a vital role during pregnancy.However,its physiological function during implantation remains elusive.This study revealed that mice with conditional deletion of Igflr gene in uteri suffered from subfertility,mainly due to the disturbed uterine receptivity and abnormal embryo implantation.Mechanistically,we uncovered that in response to the nidatory estrogen on D4 of pregnancy,the epithelial IGF1R,stimulated by the stromal cell-produced IGF1,facilitated epithelial STAT3 activation to modulate the epithelial depolarity.Furthermore,embryonic derived IGF2 could activate both the epithelial ERK1/2 and STAT3 signaling through IGF1R,which was critical for the transcription of Cox2 and normal attachment reaction.In brief,our data revealed that epithelial IGF1R was sequentially activated by the uterine stromal IGF1 and embryonic IGF2 to guarantee normal epithelium differentiation during the implantation process.

Analyzing the cellular and molecular atlas of ovarian mesenchymal cells provides a strategy against female reproductive aging

Ovarian mesenchymal cells(oMCs)constitute a distinct microenvironment that supports folliculogenesis under physiological conditions.Supplementation of exogenous non-ovarian mesenchymal-related cells has been reported to be an efficient approach to improve ovarian functions.However,the development and cellular and molecular characteristics of endogenous oMCs remain largely unexplored.In this study,we surveyed the single-cell transcriptomic landscape to dissect the cellular and molecular changes associated with the aging of oMCs in mice.Our results showed that the oMCs were composed of five ovarian differentiatedMC(odMC)populations and one ovarian mesenchymal progenitor(oMP)cell population.These cells could differentiate into various odMCs via an oMP-derived route to construct the ovarian stroma structures.Comparative analysis revealed that ovarian aging was associated with decreased quantity of oMP cells and reduced quality of odMCs.Based on the findings of bioinformatics analysis,we designed different strategies involving supplementation with young oMCs to examine their effects on female fertility and health.Our functional investigations revealed that oMCs supplementation prior to ovarian senescence was the optimal method to improve female fertility and extend the reproductive lifespan of aged females in the longterm.

SP1 governs primordial folliculogenesis by regulating pregranulosa cell development in mice

Establishment of the primordial follicle(PF)pool is pivotal for the female reproductive lifespan;however,the mechanism of primordial folliculogenesis is poorly understood.Here,the transcription factor SP1 was shown to be essential for PF formation in mice.Our results showed that SP1 is present in both oocytes and somatic cells during PF formation in the ovary.Knockdown of Sp1 expression,especially in pregranulosa cells,significantly suppressed nest breakdown,oocyte apoptosis,and PF formation,suggesting that SP1 expressed by somatic cells functions in the process of primordial folliculogenesis.We further demonstrated that SP1 governs the recruitment and maintenance of Forkhead box L2-positive(FOXL2^+)pregranulosa cells using an Lgr5-EGFP-IRES-CreER^T2(Lgr5-KI)reporter mouse model and a FOXL2^+ cell-specific knockdown model.At the molecular level,SP1 functioned mainly through manipulation of NOTCH2 expression by binding directly to the promoter of the Notch2 gene.Finally,consistent with the critical role of granulosa cells in follicle survival in vitro,massive loss of oocytes in SP1 knockdown ovaries was evidenced before puberty after the ovaries were tranSP1anted under the renal capsules.Conclusively,our results reveal that SP1 controls the establishment of the ovarian reserve by regulating pregranulosa cell development in the mammalian ovary.

Follicles were reconstituted from dissociated mouse fetal ovarian cells in vitro

Early folliculogenesis involved in the interaction of germ cells and somatic cells is a complicated physiological event. Female germ cells are committed to differentiate into oocytes and finish complete development in the functional units of follicles. Thus there will be great significance in basal research and practices to evaluate the possibility of ovarian cells to reconstitute into follicles in vitro. In the present research, 12-16 dpc (days post coitum) mouse fetal ovarian cells were respectively isolated using collagenase digestion and cultured in droplets in vitro. The results revealed that the fetal ovarian cells of 12-16 dpc appeared to form multiple cell aggregates and tissue-like pieces in vitro. However, 12-13 dpc ovarian cells failed to form the follicles. 14-15 dpc ovarian cells were competent to form a few follicle-like complexes. Furthermore many small typical follicles were reconstituted from 16 dpc ovarian cells in vitro. The results showed for the first time that mouse embryonic