scholarly journals Fuyuan Xingnao Decoction Promotes Angiogenesis Through the Rab1/AT1R Pathway in Diabetes Mellitus Complicated With Cerebral Infarction

2021 ◽  
Vol 12 ◽  
Author(s):  
Dong Deng ◽  
Yao Qu ◽  
Lihua Sun ◽  
Liyang Jia ◽  
Jianhong Bu ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Cerebral Cortex ◽  
Cerebral Infarction ◽  
Real Time ◽  
Control Group ◽  
Ang Ii ◽  
Cerebral Microvessels ◽  
Expression Levels

Fuyuan Xingnao decoction (FYXN), a traditional Chinese formula comprised of seven herbs, has been utilized to treat diabetes mellitus complicated with cerebral infarction (DMCI) for years. Yet, its protective and regulatory mechanism is poorly understood. The aim of the study is to investigate the effects of FYXN on DMCI in vitro and in vivo, as well as its mechanism in angiogenesis. For in vivo experiments, FYXN was administered to DMCI rats with streptozotocin (STZ) injection-induced diabetes. Then middle cerebral artery occlusion (MCAO) was conducted and the cerebral cortex sections of the rats were obtained. The ultrastructure of cerebral microvessels and new vessel density of ischemic penumbra were evaluated by the transmission electron microscopy (TEM) assay and immunohistochemistry, respectively. Protein and mRNA expression levels of Rab1/AT1R in cortex were assayed by Western blotting and real-time fluorescence quantitative real-time polymerase chain reaction (RT-qPCR). In vitro, FYXN serum was produced in rats on the fourth day 2 h after the last FYXN administration. Green fluorescence was observed after transfection with lentivirus packaged Rab1-WT or siRNA for 24 h. The activity of brain microvascular endothelial cells (BMECs) treated with sera from these rats was tested by MTT assay and Transwell assays, respectively. The expression of AT1R on the cell membrane and endoplasmic reticulum of BMECs was evaluated by immunofluorescence staining. Protein expression levels of signaling molecules in the Rab1/AT1R pathways were also detected. Results showed that in vivo, FYXN treatment significantly intensified CD31 staining in the cortical areas and enhanced the mRNA and protein levels of AT1R, Ang II, Rab1a, Rab1b and VEGF expression in ischemic cerebral cortex tissues. In vitro, the expression levels of AT1R, Ang II, Rab1a, Rab1b and VEGF in the cerebral infarction model group were significantly higher than those in the control group, with further increases after administration of FYXN drug serum. FYXN promoted the proliferation and migration of BMECs by activating the Rab1/AT1R signaling pathway. In conclusion, FYXN exerts a protective effect against DMCI by promoting angiogenesis via the Rab1/AT1R pathway, which provides strong evidence for the therapeutic effect of FYXN on DMCI.

scholarly journals Hypoxia and its possible relationship with endometrial receptivity in adenomyosis: a preliminary study

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Song Guo ◽  
Di Zhang ◽  
Xiaowei Lu ◽  
Qian Zhang ◽  
Ruihuan Gu ◽  
...  
Keyword(s):  
Real Time ◽  
Western Blotting ◽  
Real Time Pcr ◽  
Underlying Mechanism ◽  
Endometrial Receptivity ◽  
Control Group ◽  
Expression Levels ◽  
Preliminary Study

Abstract Background Adenomyosis (AM) is an important cause of female infertility. However, the underlying mechanism remains unclear. This report describes a preliminary study of hypoxia and its possible association with endometrial receptivity in AM. Methods The study was divided into in vitro and in vivo experiments. In vitro, expression levels of the endometrial receptivity markers HOXA10 and HOXA11 in the implantation period were examined using real-time PCR and western blotting. Endometrial expression of hypoxia-inducible factor (HIF)-1α, HIF-2α, and HIF-3α was determined using immunohistochemistry. In vivo, using an AM mouse model established by oral administration of tamoxifen, we inhibited expression of HIF-2α using an HIF-2α antagonist (PT2399; 30 mg/kg body weight, twice daily by oral gavage for 2 days) and then examined expression levels of Hoxa10 and Hoxa11 using real-time PCR and western blotting. Results Endometrial mRNA and protein expression levels of HOXA10 and HOXA11 were significantly lower in patients with AM than in control patients. Expression of HIF-2α was significantly higher in the AM group than in the control group, whereas that of HIF-1α and HIF-3α was equivalent in both groups. In vivo analysis showed that administration of the HIF-2α antagonist resulted in increased expression of Hoxa10 and Hoxa11 at both the mRNA and protein levels in AM model mice. Conclusions HIF-2α overexpression may be one reason for decreased endometrial receptivity in AM. The current findings provide insight into HIF-2α-mediated AM-related infertility and suggest that PT2399 has potential as a treatment for AM. Trial registration This trial was retrospectively registered.

232 EFFECT OF SUPEROVULATION PRETREATMENT ON DEVELOPMENTAL CHARACTERISTICS OF IN VITRO-FERTILIZED BOVINE EMBRYOS TRANSFERRED TO THE OVIDUCT-UTERUS ENVIRONMENT

2016 ◽  
Vol 28 (2) ◽  
pp. 247
Author(s):  
V. Havlicek ◽  
A. Gad ◽  
S. Papp ◽  
K. Stein ◽  
F. Palm ◽  
...  
Keyword(s):  
Real Time ◽  
Embryo Development ◽  
Internal Control ◽  
Real Time Pcr ◽  
Control Group ◽  
Hormonal Changes ◽  
Expression Levels ◽  
In Vivo Culture

Superovulation is a routine procedure to stimulate growth and ovulation of multiple follicles. However, the hormonal changes in the reproductive tract after superovulation treatment affect the environment and subsequently the early embryo development. The aim of the study was to examine the effect of superovulation pretreatment on embryo development and gene expression of IVM/IVF derived embryos subsequently cultured in vivo. The cumulus‐oocyte complexes derived from slaughterhouse ovaries were in vitro matured and fertilized. The denuded presumptive zygotes were cultured in CR1 medium with 5% oestrous cow serum. A total of 788 cleaved embryos at Day 2 were transferred by transvaginal endoscopy into the oviduct of synchronized and superovulated heifers (superstimulated group, SS) and 784 cleaved embryos were transferred into the ipsilateral oviduct of single ovulated synchronized heifers (single ovulation group, SO). In total, 10 Simmental heifers were used for in vivo culture in a crossover design. The in vivo culture was repeated once at an interval of at least 6 weeks in the same animal. At Day 7, embryos were recovered by combined flushing of the oviducts by endoscopy and the adjacent part of the uterine horns by conventional procedure. The numbers of recovered blastocysts were recorded and the embryos were cultured for the following 48 h to determine the blastocyst rate at Days 8 and 9. Simultaneously, 410 cleaved embryos were cultured in vitro for 9 days (control group, C). Triplicate pools of 10 blastocysts recovered at Day 7 from each treatment group were used for RNA isolation. Real-time PCR using sequence specific primers was performed in StepOnePlus™ real time PCR system (Applied Biosystem, Foster City, CA, USA). A comparative threshold cycle method was used to quantify expression levels of the candidate genes compared to the internal control GAPDH gene. The number of recovered embryos after in vivo culture was significantly lower in the SS group compared with the SO group (66.9 v. 79.5%, respectively; P < 0.05). The blastocyst rates at Days 7, 8, and 9 in the SS, SO, and C groups were not significantly different (31.9, 43.3, and 47.1% v. 35.2, 48.5, and 53.5% v. 37.8, 50, and 56.1%, respectively). Molecular analysis of selected genes playing important roles during pre-implantation development revealed significantly lower expression levels of IL6, IL18, and ABCC2 between both experimental in vivo culture groups and the C-group. The IL18 was also significantly down-regulated in the SS-group compared to the SO-group. The transcription factor NFκB was found to be down-regulated in the SS-group compared to the SO and C groups (P < 0.05). In conclusion, we showed that the superovulation pretreatment did not affect blastocyst yield during the culture period but seemed to influence the expression of developmentally important genes in the resulting embryos.

scholarly journals Effects of Naringin on Proliferation and Osteogenic Differentiation of Human Periodontal Ligament Stem Cells In Vitro and In Vivo

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Lihua Yin ◽  
Wenxiao Cheng ◽  
Zishun Qin ◽  
Hongdou Yu ◽  
Zhanhai Yu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Osteogenic Differentiation ◽  
Periodontal Ligament ◽  
Trabecular Structure ◽  
Control Group ◽  
Periodontal Ligament Stem Cells ◽  
Expression Levels ◽  
Proliferation And Differentiation

This study is to explore the osteogenesis potential of the human periodontal ligament stem cells (hPDLSCs) induced by naringin in vitro and in vitro. The results confirmed that 1 μM naringin performs the best effect and a collection of bone-related genes (RUNX2,COL1A2, OPN, and OCN) had significantly higher expression levels compared to the control group. Furthermore, a typical trabecular structure was observed in vivo, surrounded by a large amount of osteoblasts. These results demonstrated that naringin, at a concentration of 1 μM, can efficiently promote the proliferation and differentiation of hPDLSCs both in vitro and in vivo.

DNA damage induced by phenylalanine and its analogue p-chlorophenylalanine in blood and brain of rats subjected to a model of hyperphenylalaninemia

2013 ◽  
Vol 91 (5) ◽  
pp. 319-324 ◽  
Author(s):  
Kellen R. Simon ◽  
Rosane M. dos Santos ◽  
Giselli Scaini ◽  
Daniela D. Leffa ◽  
Adriani P. Damiani ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cerebral Cortex ◽  
Phenylalanine Hydroxylase ◽  
Neurological Dysfunction ◽  
Control Group ◽  
Acute Administration ◽  
Dna Migration ◽  
In Vitro Effects

Phenylketonuria (PKU) is a disease caused by a deficiency of phenylalanine hydroxylase (PAH), resulting in an accumulation of phenylalanine (Phe) in the brain tissue, cerebrospinal fluid, and other tissues of PKU patients. Considering that high levels of Phe are associated with neurological dysfunction and that the mechanisms underlying the neurotoxicity in PKU remain poorly understood, the main objective of this study was to investigate the in vivo and in vitro effects of Phe on DNA damage, as determined by the alkaline comet assay. The results showed that, compared to control group, the levels of DNA migration were significantly greater after acute administration of Phe, p-chlorophenylalanine (p-Cl-Phe, an inhibitor of PAH), or a combination thereof in cerebral cortex and blood, indicating DNA damage. These treatments also provoked increase of carbonyl content. Additionally, when Phe or p-Cl-Phe was present in the incubation medium, we observed an increase in the frequency and index of DNA damage in the cerebral cortex and blood, without affecting lactate dehydrogenase (LDH) release. Our in vitro and in vivo findings indicate that DNA damage occurs in the cerebral cortex and blood of rats receiving Phe, suggesting that this mechanism could be, at least in part, responsible for the neurological dysfunction in PKU patients.

scholarly journals Effects on thrombocytic hemostasis of a new derivate indolinone

2019 ◽  
Vol 18 (3) ◽  
pp. 574-576
Author(s):  
VV Bykov ◽  
V Yu Serebrov ◽  
VV Udut ◽  
EV Udut ◽  
VP Fisenko
Keyword(s):  
Diabetes Mellitus ◽  
Platelet Aggregation ◽  
Acetylsalicylic Acid ◽  
Medical Science ◽  
Antiplatelet Drug ◽  
Control Group ◽  
Antiplatelet Activity ◽  
Wide Range

Objective. Specific activity of an antiplatelet drug of indolinone series (codenamed DI) was studied in vitro in a model of ADP-induced platelet aggregation in vitro and in vivo in a model of streptozotocininduced diabetes mellitus in rats. Material and Methods. Acetylsalicylic acid and dipyridamole were used as reference drugs. In vitro tests have demonstrated that DI exhibits antiplatelet activity in a wide range of concentrations (0,75×10-6 – 1.5×10-5 М, р<0,05), being comparable to acetylsalicylic acid and dipyridamole. In vivo tests have demonstrated dose-dependent antiplatelet activity of DI in doses of 2,5 – 20 mg/kg (21-14 %). Results and Discussion.Increasing the dose of DI above 10 mg/kg doesn’t increase its antiplatelet activity. After multiple oral administration to rats with streptozotocin-induced diabetes mellitus in 10 mg/kg dose, DI has exhibited antiplatelet activity, reducing the platelet aggregation rate to that of the control group (р<0,05). Conclusion. Thus, DI isapromisingcompound for furtherdevelopmentof an antiplatelet drug with new mechanism of action Bangladesh Journal of Medical Science Vol.18(3) 2019 p.574-576

scholarly journals In vivo and in vitro effects of fructose on rat brain acetylcholinesterase activity: an ontogenetic study

2014 ◽  
Vol 86 (4) ◽  
pp. 1919-1926 ◽  
Author(s):  
CARINE A. GUIMARÃES ◽  
MAIRIS S. BIELLA ◽  
ABIGAIL LOPES ◽  
PEDRO F. DEROZA ◽  
MARIANA B. OLIVEIRA ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Ache Activity ◽  
Young Patients ◽  
Brain Structures ◽  
Acetylcholinesterase Activity ◽  
Control Group ◽  
Inherited Disorders ◽  
Old Rats

Increased fructose concentrations are the biochemical hallmark of fructosemia, a group of inherited disorders on the metabolic pathway of this sugar. The main clinical findings observed in patients affected by fructosemia include neurological abnormalities with developmental delay, whose pathophysiology is still undefined. In the present work we investigated the in vitro and in vivo effects of fructose on acetylcholinesterase (AchE) activity in brain structures of developing rats. For the in vitro experiments, fructose was added at increasing concentrations to the incubation medium. It was observed that fructose provoked an inhibition of acetylcholinesterase activity in cerebral cortex of 30-day-old-rats, even at low concentrations (0.1 mM). For the in vivo experiments, rats were killed 1 h after a single fructose administration (5 µmol/g). Control group received the same volume of saline solution. We found that AchE activity was increased in cerebral cortex of 30- and 60-day-old rats receiving fructose administration. Finally, we observed that AchE activity was unaffected by acute fructose administration in cerebral cortex, striatum or hippocampus of 15- and 90-day-old rats. The present data suggest that a disruption in cholinergic homeostasis may be involved in the pathophysiology of brain damage observed in young patients affected by fructosemia.

scholarly journals Intervention of Gastrodin in Type 2 Diabetes Mellitus and Its Mechanism

2021 ◽  
Vol 12 ◽  
Author(s):  
Yu Bai ◽  
Ke Mo ◽  
Guirong Wang ◽  
Wanling Chen ◽  
Wei Zhang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Insulin Receptors ◽  
Control Group ◽  
Sensitivity Index

As a severe metabolic disease, type 2 diabetes mellitus (T2DM) has become a serious threat to human health in recent years. Gastrodin, as a primary chemical constituent in Gastrodia elata Blume, has antidiabetic effects. However, the possible mechanisms are unclear. The aim of the present study was to investigate the effects and possible mechanisms of gastrodin on the treatment of T2DM. In vivo, after treatment with gastrodin for 6 weeks, fasting blood glucose levels, blood lipid metabolism, and insulin sensitivity index values were remarkably reduced compared with those of the diabetic control group. The values of aspartate aminotransferase and alanine aminotransferase also showed that gastrodin alleviates liver toxicity caused by diabetes. Moreover, gastrodin relieved pathological damage to the pancreas in T2DM rats. In vitro, gastrodin alleviated insulin resistance by increasing glucose consumption, glucose uptake, and glycogen content in dexamethasone-induced HepG2 cells. The Western blotting results showed that gastrodin upregulated the expression of insulin receptors and ubiquitin-specific protease 4 (USP4) and increased the phosphorylation of GATA binding protein 1 (GATA1) and protein kinase B (AKT) in vivo and in vitro. Furthermore, gastrodin decreased the ubiquitin level of the insulin receptor via UPS4 and increased the binding of GATA1 to the USP4 promoter. Additionally, administration of the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway inhibitors MK-2206 and LY294002 abolished the beneficial effects of gastrodin. Our results indicate that gastrodin promotes the phosphorylation of GATA1 via the PI3K/AKT pathway, enhances the transcriptional activity of GATA1, and then increases the expression level of USP4, thereby reducing the ubiquitination and degradation of insulin receptors and ultimately improving insulin resistance. Our study provides scientific evidence for the beneficial actions and underlying mechanism of gastrodin in the treatment of T2DM.

scholarly journals The Effects of miR-136-5p-Mediated Regulation of A20 in Astrocytes from Cultured Spinal Cord Cultured Cells In Vitro

2017 ◽  
Vol 41 (4) ◽  
pp. 1596-1604 ◽  
Author(s):  
Xiaoming Peng ◽  
Xiongzhi Shi ◽  
Jinmin Zhao ◽  
Jichen He ◽  
Keke Li ◽  
...  
Keyword(s):  
Real Time ◽  
Real Time Pcr ◽  
Inflammatory Cytokine ◽  
Cultured Cells ◽  
Expression Level ◽  
Control Group ◽  
Interleukin 17 ◽  
Expression Levels ◽  
Inhibition Group

Background/Aims: This study focused on investigating the regulatory mechanism of miR-136-5p in mouse astrocytes stimulated with interleukin-17(IL-17). Methods: C57BL/6 mouse astrocytes were stimulated with IL-17 (100ng/ml) for various periods of time (0-48 hours) and at various doses (0-200 ng), and the expression levels of inflammatory cytokine and chemokine genes (IL-6, TNF-α, MCP-1, MCP-5 and MIP-2) were then detected by real-time PCR. The expression of the A20 gene was measured with real-time PCR in cells that were stimulated with IL-17 (50 ng/ml) for various periods of time (0-48 hours). C57BL/6 mouse astrocytes were transfected with Ctrl-anti-miR-136-5p or LNA -anti-miR-136-5p for 48 h. Thereafter, the cells were stimulated with or without IL-17 (50ng/ml) for 6 h. The level of A20 protein (TNFα-induced protein 3, TNFAIP3) was detected by Western blot analysis. Results: (1) Compared with the DMEM control group, within six hours, IL-17 stimulation significantly increased the expression levels of inflammatory cytokine and chemokine genes and clearly decreased the expression level of the A20 protein. (2) Without IL-17 stimulation, the expression level of the miR-136-5p gene was significantly decreased, whereas in the miR-136-5p-inhibition group, the A20 protein expression was elevated. IL-17 stimulation slightly decreased the expression of the A20 protein in the miR-136-5p-inhibition group, but it was still slightly higher than in the control group. Conclusion: This study demonstrated that miR-136-5p affected the expression of A20 in IL-17-stimulated astrocytes.

scholarly journals AT1R/GSK-3β/mTOR Signaling Pathway Involved in Angiotensin II-Induced Neuronal Apoptosis after HIE Both In Vitro and In Vivo

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Wei Si ◽  
Banghui Li ◽  
Cameron Lenahan ◽  
Shirong Li ◽  
Ran Gu ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cerebral Infarction ◽  
Neuronal Apoptosis ◽  
Caspase 3 ◽  
Neuronal Degeneration ◽  
Ang Ii ◽  
Mtor Signaling Pathway ◽  
Gsk 3Β

Objective. The focus of the present study is to evaluate the effects of Angiotensin II (Ang II) on neuronal apoptosis after HIE and the potential underlying mechanisms. Methods. Primary neonatal rat cortical neurons were used to study the oxygen-glucose deprivation (OGD) cell model. The expressions of Ang II, AT1R, GSK-3β, p-GSK-3β, mTOR, p-mTOR, Bax, Bcl-2, and cleaved caspase-3 were detected via western blot. IF and flow cytometry were used to evaluate neuronal apoptosis. Hypoxic-ischemic encephalopathy (HIE) was established to evaluate the therapeutic effects of Ang II in vivo. Cerebral infarction areas were detected by 2,3,5-Triphenyltetrazolium chloride staining. The righting and geotaxis reflexes were also recorded. In addition, Fluoro-Jade C staining and TUNEL staining were performed to evaluate neuronal degeneration and apoptosis. Results. Ang II significantly increased the rate of neuronal apoptosis, upregulated the expression of cleaved caspase-3, and downregulated Bcl-2/Bax ratio after OGD insult. For vivo assay, the expressions of endogenous Ang II and AT1R gradually increased and peaked at 24 h after HIE. Ang II increased NeuN-positive AT1R cell expression. In addition, Ang II increased the area of cerebral infarction, promoted neuronal degeneration and apoptosis, aggravated neurological deficits on righting and geotaxis reflexes, and was accompanied by increased expressions of phosphorylated GSK-3β and mTOR. The application of valsartan (Ang II inhibitor) or SB216763 (GSK-3β inhibitor) reversed these phenomena triggered by Ang II following HIE. Conclusion. Ang II increased neuronal apoptosis through the AT1R/GSK-3β/mTOR signaling pathway after experimental HIE both in vitro and in vivo, and Ang II may serve as a novel therapeutic target to ameliorate brain injury after HIE.

253 DIFFERENTIAL GENE EXPRESSION IN IN VIVO-DERIVED v. IN VITRO-PRODUCED EQUINE BLASTOCYSTS AS DETERMINED BY RT-qPCR

2010 ◽  
Vol 22 (1) ◽  
pp. 284
Author(s):  
K. Smits ◽  
K. Goossens ◽  
A. Van Soom ◽  
L. Peelman
Keyword(s):  
Gene Expression ◽  
Real Time ◽  
Differential Gene Expression ◽  
Real Time Pcr ◽  
Calf Serum ◽  
Fatty Acid Binding ◽  
Expression Levels ◽  
Differential Gene

Although in vitro production of equine embryos has greatly evolved in recent years, there are still substantial differences between in vitro-produced and in vivo-derived equine embryos. Fundamental insight into these differences could lead to optimization of equine assisted reproductive techniques. Reverse transcription quantitative real-time PCR (RT-qPCR) is a highly specific and sensitive tool to compare mRNA expression levels of specific genes and was used in this study to determine differences in gene expression between equine in vivo and in vitro embryos. In vivo embryos (n = 8) were derived by uterine flushing of artificially inseminated mares at 7 days after ovulation. For the production of the in vitro embryos (n = 8), oocytes from slaughtered mares were matured in DMEM-F12-based medium (Galli et al. 2007 Anim. Reprod. Sci. 98, 39-55) in 5% CO2 in air (maturation rate: 57%), fertilized by intracytoplasmic sperm injection, and cultured in DMEM-F12 with 10% fetal calf serum in 5% CO2, 5% O2, and 90% N2 for 9.5 days (cleavage rate: 74%; blastocyst rate: 7%). RNA was extracted from single early to expanded blastocysts and amplified and converted into cDNA with the WT-Ovation RNA Amplification System (NuGEN, San Carlos, CA, USA). Based on the presumed gene functions and differential gene expression as determined in a previously performed suppression subtractive hybridization (SSH; Smits et al. 2009 Reprod. Dom. Anim. 44, 75), 5 genes [brain expressed X-linked 2 (BEX2), Mps one binder kinase activator-like 3 (MOBKL3), fatty acid binding protein 3 (FABP3), minichromosome maintenance complex component 7 (MCM7), and ornithine decarboxylase (ODC)] were selected for quantification by RT-qPCR with the KAPA SYBR® FAST qPCR Kit (Kapa Biosystems, Belgium) on the iCycler iQ Real-Time PCR Detection System (Bio-Rad, Nazareth, Belgium). All data were normalized with previously determined stable reference genes (beta actin, ubiquitin C, ribosomal protein L32, and glyceraldehyde-3-phosphate dehydrogenase) and statistically analyzed by means of a Mann-Whitney test. The fact that all genes were expressed at greater levels in the in vivo-derived blastocysts than in the in vitro-produced blastocysts confirmed the results of the SSH. This difference was highly significant for MOBKL3, BEX2, and ODC (P < 0.005), significant for FABP3 (P < 0.05), and not significant for MCM7. These genes have already been shown to be important for embryonic cell survival (ODC), oocyte maturation and pre- implantation development (MOBKL3) in mice, regulation during embryonic development (BEX2) and fetal development (FABP3) in human, and genome replication in eukaryotes (MCM7) (Pendeville et al. 2001 Mol. Cell Biol. 21, 6549-6558; Han et al. 2005 Nucleic Acids Res. 33, 6555-6565). In conclusion, 4 genes (MOBKL3, BEX2, ODC, and FABP3) with greater expression levels in in vivo-derived equine blastocysts have been identified. Whether the up-regulation of these genes is important for normal embryonic differentiation in the horse embryo is currently under investigation.

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