摘要: It is known that social stress could alter oxytocin (OT) and arginine-vasopressin (AVP) expression in specific regions of brains which regulate the aggressive behavior of small rodents, but the effects of density-induced social stress are still unknown. Brandt's voles (Lasiopodomys brandtii) are small herbivores in the grassland of China, but the underlying neurological mechanism of population regulation is still unknown. We tested the effects of housing density of Brandt's voles on OT/AVP system with physical contact (allowing aggression) and without physical contact (not allowing aggression) under laboratory conditions. Then, we tested the effects of paired-aggression (no density effect) of Brandt's voles on OT/AVP system under laboratory conditions. We hypothesized that high density would increase aggression among animals which would then increase AVP but reduce OT in brains of animals. Our results showed that high housing density induced more aggressive behavior. We found high-density-induced social stress (with or without physical contact) and direct aggression significantly increased expression of mRNA and protein of AVP and its receptor, but decreased expression of mRNA and protein of OT and its receptor in specific brain regions of voles. The results suggest that density-dependent change of OT/AVP systems may play a significant role in the population regulation of small rodents by altering density-dependent aggressive behavior.

摘要: As an organophosphorus compound that frequently detected in water samples, triphenyl phosphate (TPhP) has been showed to have multiple toxicological effects on aquatic species. However, no attention has been paid to its potential impact on non-model amphibian species. Here, tadpoles of the Zhenhai brown frog (Rana zhenhaiensis) were exposed to different concentrations of TPhP (0, 0.02 and 0.1 mg/L) throughout the developmental period to assess physiological and metabolic impacts of TPhP exposure on amphibian larvae. After 30-day TPhP exposure, the developmental stage of tadpoles from the high-concentration treatment appeared to be more advanced than that from the other two treatments, but other measured traits (including body size, tail length and liver weight) did not differ among treatments. Metabolite profiles in tadpole livers based on liquid chromatography-mass spectrometry (LC-MS) revealed a distinct metabolic disorder in exposed animals. Specifically, significant changes in various hepatic amino acids (such as glutamine, glutamate, valine and leucine) were observed. Overall, our results indicated that chronic TPhP exposure potentially caused developmental and hepatic physiological changes in R. zhenhaiensis tadpoles, although its impact on tadpole growth appeared to be minor.

摘要: Objectives Mouse embryonic stem cells (ESCs) are derived from the inner cell mass of blastocyst-stage embryos and cultured in different culture media with varied pluripotency. Sporadically, a small population of ESCs exhibit 2-cell stage embryonic features in serum containing medium. However, whether ESCs can transit into 2-cell embryo-like (2C-like) cells in the chemically defined media remains largely unknown. Materials and Methods We established a robust in vitro induction system, based on retinoic acid (RA) containing chemically defined media, which can efficiently increase the subpopulation of 2C-like cells. Further test the pluripotency and 2C features of ESCs cultured in RA. 2C reporter-positive cells were selected by FACS; the level of protein was detected via immunofluorescence staining and western blot; the level gene expressions were measured by RNA-seq. Results Retinoic acid drives a NELFA (negative elongation factor A)-mediated 2C-like state in mouse ESCs, characterized with 2C-specific transcriptional networks and the ability to contribute trophectoderm (TE) when injected into developing embryos. In addition, RA treatment triggers DNA hypomethylation, active histone modification, suppressed glycolysis metabolism and reduced protein synthesis activity of ESCs. Conclusions We showed that RA has a broader role in 2C-like cells state, not only is one of the upstream regulators of the 2C-like state in chemically defined media but also illuminates genetic and epigenetic regulations that govern ESCs to 2C-like transition.

摘要: Objectives Histatin 1(Hst 1) has been proved to promote wound healing. However, there was no specific study on the regulation made by Hst 1 of fibroblasts in the process of wound healing. This research comprehensively studied the regulation of Hst 1 on the function of fibroblasts in the process of wound healing and preliminary mechanism about it. Materials and methods The full-thickness skin wound model was made on the back of C57/BL6 mice. The wound healing, collagen deposition and fibroblast distribution were detected on days 3, 5 and 7 after injury. Fibroblast was cultured in vitro and stimulated with Hst 1, and then, their biological characteristics and functions were detected. Results Histatin 1 can effectively promote wound healing, improve collagen deposition during and after healing and increase the number and function of fibroblasts. After healing, the mechanical properties of the skin also improved. In vitro, the migration ability of fibroblasts stimulated by Hst 1 was significantly improved, and the fibroblasts transformed more into myofibroblasts, which improved the function of contraction and collagen secretion. In fibroblasts, mTOR signalling pathway can be activated by Hst 1. Conclusions Histatin 1 can accelerate wound healing and improve the mechanical properties of healed skin by promoting the function of fibroblasts. The intermolecular mechanisms need to be further studied, and this study provides a direction about mTOR signalling pathway.

摘要: Objectives: Success in pregnancy in mammals predominantly depends on a well-developed placenta. The differentiation of invasive trophoblasts is a fundamental process of placentation, the abnormalities of which are tightly associated with pregnancy disorders including preeclampsia (PE). Monoclonal nonspecific suppressor factor beta (MNSF beta) is an immunosuppressive factor. Its conventional knockout in mice induced embryonic lethality, whereas the underlying mechanism of MNSF beta in regulating placentation and pregnancy maintenance remains to be elucidated. Methods: Trophoblast-specific knockout of MNSF beta was generated using Cyp19-Cre mice. In situ hybridization (ISH), haematoxylin and eosin (HE), immunohistochemistry (IHC) and immunofluorescence (IF) were performed to examine the distribution of MNSF beta and insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) at the foeto-maternal interface. The interaction and expression of MNSF beta, IGF2BP2 and invasion-related molecules were detected by immunoprecipitation (IP), immunoblotting and quantitative real-time polymerase chain reaction (qRT-PCR). The cell invasion ability was measured by the Transwell insert assay. Results: We found that deficiency of MNSF beta in trophoblasts led to embryonic growth retardation by mid-gestation and subsequent foetal loss, primarily shown as apparently limited trophoblast invasion. In vitro experiments in human trophoblasts demonstrated that the conjugation of MNSF beta with IGF2BP2 and thus the stabilization of IGF2BP2 essentially mediated the invasion-promoting effect of MNSF beta. In the placentas from MNSF beta-deficient mice and severe preeclamptic (PE) patients, downregulation of MNSF beta was evidently associated with the repressed IGF2BP2 expression. Conclusions: The findings reveal the crucial role of MNSF beta in governing the trophoblast invasion and therefore foetal development, and add novel hints to reveal the placental pathology of PE.