一氧化氮合成酶在白血病细胞的表达

目的：为了探讨一氧化氮合成酶在ＣＤ２３白血病细胞的表达，以及ＣＤ２３与ＮＯ的关系。方法：采用ＣＲＴ－ＰＣＲ和ＦＡＣＳ技术及Ｗｅｓｔｅｒｎ－ｂｌｏｔｔｉｎｇ放射自显影方法。结果：发现ＣＤ２３白血病细胞株可以表达ｉＮＯＳｍＲＮＡ和ｉＮＯＳ蛋白，同时ＣＤ２３可上调ｉＮＯＳ的表达。结论：ｉＮＯＳ可能与人ＣＤ２３白血病细胞的增殖和凋亡有关。     

Comparative analysis between cyclic GMP and cyclic AMP signalling in human sperm

The principal involvement of cyclic nucleotides in regulating sperm functions is well established, but the factors controlling their generation and actions have not yet been entirely resolved. In particular, specific roles for cyclic (c)GMP in mammalian sperm are poorly understood. In this study, we have characterized comparatively the cAMP and cGMP signalling systems in ejaculated human sperm. Mean concentrations of cGMP (0.1 micromol/l) were found to be 100-fold lower than those of cAMP in non-stimulated cells, and adenylyl cyclase (AC) activities predominate by far guanylyl cyclase (GC) activities in both particulate and soluble protein fractions. By different experimental approaches (photoaffinity labelling, cyclase assays, immunoblotting), we provide evidence for the presence (guanylyl cyclase-A, soluble guanylyl cyclase, regulatory and catalytic subunits of cAMP-dependent protein kinase) or absence (guanylyl cyclase-B, natriuretic peptide clearance receptor, neuronal nitric oxide synthase, cGMP-dependent protein kinase I) of different factors involved in either cAMP or cGMP pathways. Functional studies showed that cGMP, at high concentrations, can enhance sperm protein tyrosine phosphorylation but not serine phosphorylation of glycogen synthase kinase. This study reveals that human sperm are characterized by an exceptional predominance of cAMP signalling and indicates potential roles for cGMP.     

Effects of a nitric oxide donor and nitric oxide synthase inhibitors on luteinizing hormone-induced ovulation in the ex-vivo perfused rat ovary.

The aim of this study was to investigate the role of nitric oxide (NO) in ovulation and ovarian steroidogenesis by the use of NO synthase (NOS) inhibitors and an NO donor administrated to the luteinizing hormone (LH)-stimulated ex-vivo perfused pre-ovulatory rat ovary. The ovaries were stimulated with LH (0.2 microgram/ml) alone or in combination with the phosphodiesterase inhibitor IBMX (200 micromol/l). The presence of both endothelial NOS (eNOS) and inducible NOS (iNOS) in the perfused rat ovary were detected by immunoblotting and a clear increase in amount of iNOS protein was seen after LH+IBMX stimulation. The addition of a non-selective NOS inhibitor, N(G)-monomethyl-L-arginine (L-NMMA; 300 micromol/l), to the perfusate significantly decreased ovulation numbers (median = 4. 0, range = 1-14) as compared with LH + IBMX stimulated control (12.0, 6-17). In contrast, an inhibitor with relative selectivity towards iNOS, aminoguanidine bicarbonate (AG, 300 micromol/l and 1 mmol/l), did not change the ovulation rate (11.5, 6-18 and 11.0, 7-15 respectively). In perfusions with only LH, a lower ovulation rate was seen but with similar effects (0.0, 0-8 for L-NMMA; 7.5, 3-12 for control and 7.0, 1-15 for AG 300 micromol/l). The administration of an NO donor, spermine NONOate, resulted in similar ovulation numbers as in LH-stimulated controls. The NO inhibitors did not affect steroid concentrations in the perfusion media, while 100 micromol/l NONOate increased progesterone production.     

Roles of endogenous nitric oxide synthase inhibitors and endothelin-1 for regulating myometrial contractions during gestation in the rat

This study investigated the roles of endogenous nitric oxide synthase (NOS) inhibitors and endothelin-1 (ET-1) for regulating myometrial contractions during gestation in the rat. Basal and stimulated cyclic GMP production with L-arginine as a NOS substrate or sodium nitroprusside (SNP) as a NO donor were significantly enhanced at the middle of gestation (14th day), while these were greatly decreased at term (22nd day), suggesting the accelerated NO production and/or up-regulation of guanylate cyclase at the middle of gestation. NOS within the myometrium was mainly Ca(2+)dependent and partly Ca(2 + )independent and remained unaffected by aminoguanidine as an inhibitor of inducible NOS in non-pregnant and gestational myometrium. NOS activity per se and endothelial NOS (eNOS) protein expression remained unchanged at the middle and term gestation. Neuronal NOS (nNOS) and inducible NOS (iNOS) proteins were undetectable. SNP at a high concentration of 100 micromol/l failed to modify the spontaneous and ET-1-induced rhythmic contractions in non-pregnant and gestational myometrium. Contents of N(G)-monomethyl-L-arginine (L-NMMA) plus asymmetric N(G),N(G)-dimethyl-L-arginine (ADMA) as endogenous NOS inhibitors and ET-1 within the myometrium were significantly decreased at 14th and 20th days of gestation, whereas these were significantly increased at term gestation (22nd day) and after delivery. There was a significant and positive correlation between endogenous NOS inhibitor content and ET-1. ET-1 within the myometrium was significantly increased with a concomitant decrease in cyclic GMP production after the intraperitoneal application of authentic L-NMMA for 2 weeks, suggesting that the impaired NO production with endogenous NOS inhibitors would result in increased ET-1 content. These results suggest that endogenous NOS inhibitors such as L-NMMA and ADMA play an important role for regulating NO production in rat myometrium. The impaired NO production due to accumulated endogenous NOS inhibitors possibly results in increased ET-1 content within the myometrium, thereby increasing myometrial contractions at term gestation and after delivery.     

Nitric oxide regulates ovarian blood flow in the rat during the periovulatory period

BACKGROUND: The aim of this study was to characterize the roles of nitric oxide (NO) on the rat ovarian blood flow (OBF) during the preovulatory period. METHODS AND RESULTS: Immature Sprague-Dawley rats were primed with pregnant mares' serum gonadotrophin (PMSG, 15 IU) and given hCG (15 IU) 48 h later. The ovary was exposed 48-56 h after PMSG, a laser Doppler probe was attached to the ovarian surface and OBF was measured at two time periods: preovulatory (PO) 48 h after PMSG and ovulatory (OV) 6-8 h after hCG. A non-selective NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), was injected i.v. (4 and 10 mg/kg) or intrabursally (1 mg/kg). Intravenous administration of L-NAME to OV rats rapidly increased blood pressure and reduced OBF by 30%, which returned to the pretreatment level within 30 min. L-NAME given into the ovarian bursa of both PO and OV rats did not affect blood pressure and reduced OBF by nearly 40%, which remained low throughout the experiment. Intravenous injection of hCG to PO rats increased OBF to 116.1% at 5 min and 133.5% at 30 min in relation to the pretreatment level. When L-NAME was given intrabursally, subsequent hCG injection was without effect. CONCLUSIONS: These results indicate that locally produced NO is important for the maintenance and increase of rat OBF during the preovulatory period.     

Targeted disruption of the nitric oxide synthase 2 gene protects against ischaemia/reperfusion injury to skeletal muscle

To provide definitive insight into the complicated roles of the nitric oxide synthase (NOS) enzymes in ischaemia/reperfusion (I/R) injury of skeletal muscle, experiments were undertaken in mice with targeted disruption of the inducible NOS (NOS-2 KO) isoform, compared with the wild-type mouse strain. The degree of I/R injury in the NOS-2 KO mice was attenuated relative to that in the wild-type strain. After 70 min of ischaemia (24 h reperfusion), nitroblue tetrazolium (NBT) staining of skeletal muscle showed significant necrosis (40%) in wild-type mice, whilst in NOS-2 KO mice, ischaemia could be prolonged to 90 min before significant necrosis (38%) was apparent. Specific enzyme activities of the mitochondrial respiratory chain enzymes, measured in skeletal muscle homogenates, suggested that direct inhibition of the enzymes is not causal in the I/R injury. Immunohistological examination of skeletal muscle for NOS-2 showed its induction selectively in mast cells. In vitro experiments using bone marrow-derived mast cells showed that NOS-2 induction was associated with increased degranulation of mast cells. These findings suggest that NO generated by induction of NOS-2 has a deleterious effect in I/R injury of skeletal muscle and that NO exerts its damaging effect through factors released by degranulation of mast cells.     

Association analysis of nitric oxide synthases: NOS1, NOS2A and NOS3 genes,with multiple sclerosis

Abstract

Background: Multiple sclerosis (MS) is a chronic inflammatory autoimmune disorder of the central nervous system.

Aim: To explore the genetic basis of three nitric oxide synthase (NOS) genes: NOS1, NOS2A and NOS3, with susceptibility to MS.

Subjects and methods: A total of 122 MS patients and 118 healthy controls screened for NOS1 (rs2682826, rs41279104), NOS2A (CCTTT)n/(TAAA)n and NOS3 (rs1800783, rs1800779, rs2070744, 27bpVNTR) markers, using TaqMan®SNP Genotyping Assays and fragment analysis were enrolled in this study. QRT-PCR and ELISA were used to analyse the expression of NOS3 mRNA and Nitric Oxide (NO) levels.

Results: Two NOS3 markers were associated with susceptibility to MS and early disease development. The NOS3 rs1800779 G-allele (p?=?0.04) and GG-genotype (p?=?0.02) showed association with susceptibility to MS. Short NOS2 (CCTTT)n (p?=?0.03) and short/long repeat (p?=?0.04) genotypes also showed associations with MS. These associations were intensified by sub-division of patients into Kuwaiti Arabs and Persians (p?<?0.05). The NOS3-27?bp-VNTR a-allele was associated with early MS disease onset ≤26 years (p?=?0.04). The NOS3-27?bp-VNTR a/b-genotype resulted in 23% lower NO production and the NOS3-rs1800779 AA-genotype resulted in lower NOS3 expression. Haplotypes obtained from NOS2A and NOS3 showed increased susceptibility to MS. NOS1 showed no significant association with MS.

Conclusion: This study provides evidence for the association between selected NOS2 and NOS3 markers and MS susceptibility.     

Anatomical and immunohistochemical considerations on the microinnervation of trachea in humans

The anatomy of the tracheal microinnervation is understudied in humans; the purpose of our study was to fill this gap by working on human adult tracheas, to compare the results with those obtained from animal studies, and to checking whether or not these studies are suitable to be translated from comparative to the human anatomy. The study was designed as a qualitative one. The present work was performed on human adult tracheas dissected out in 15 human adult cadavers. Microdissections were performed in eight tracheas and revealed the outer peritracheal plexus, segmentally supplied and distributed to trachea and esophagus, with longitudinal intersegmentary anastomoses but also with bilateral interrecurrential anastomoses previously undescribed in anatomy. Seven different tracheas were transversally cut and paraffin embedded. Histological stains (HE, toluidine blue, luxol fast blue, Giemsa on tissues and trichrome Gieson) and immunohistochemistry using primary antibodies for nNOS, neurofilament, SMA and the cocktail of citokeratines CK AE1-AE3 + 8/18 were done. According to the histological individual variation, the neural layers of the posterior wall of the human trachea could be considered as it follows: (a) an outer neural layer, ganglionated, associated with the connective covering layers, adventitia and the posterior fibroelastic membrane (external elastic lamina); (b) a submucosal ganglionated neural layer, mainly with juxtaglandular microganglia that may expand, as glands do, through the outer covering layers; (c) intrinsic nerves of the transverse trachealis muscle; (d) the neural layer intrinsic to the longitudinal elastic band (internal elastic lamina) and supplied from the inner submucosa; (e) the neural plexus of the lamina propria, with scarcely distributed neurons. We also bring here the first evidences for the in vivo nNOS phenotype of mast cells that were identified, but not exclusively, within the trachealis muscle.     

人参银杏复方制剂对缺氧复氧后大鼠海马CA1区NOS表达的影响

本文旨在观察预防性应用人参银杏复方制剂对缺氧24 h,复氧0、24、72 h时段海马CA1区锥体细胞层神经元Nissl染色变化及海马CA1区一氧化氮合酶(NOS)阳性细胞变化的影响。应用低压氧舱仿海拔8000米高空缺氧模型,以Nissl染色及还原型尼克酰胺腺嘌呤二核苷酸脱氢酶(NADPH-d)组织化学方法并结合图像分析等技术进行研究。结果表明:人参银杏复方制剂能防止缺氧24 h、复氧72 h海马CA1区锥体细胞层神经元的丢失,并能减少缺氧24 h、复氧0、24、72 h时段NOS阳性细胞数量。本研究结果提示:人参银杏复方制剂对缺氧复氧后海马CA1区神经元具有保护作用,其保护作用可能与抑制缺氧复氧后海马CA1区NOS表达有关。     

阿魏酸钠对肿瘤坏死因子诱导人脐静脉内皮细胞NOS基因表达的影响

目的 :探讨阿魏酸钠 (SF)在人脐静脉内皮细胞中对内皮型一氧化氮合酶 (ecNOS)和诱导型一氧化氮合酶 (iNOS)基因表达的影响。方法 :常规培养人脐静脉内皮细胞 (ECV3 0 4) ,分成 5组 :①正常对照组 ,常规培养 ;②肿瘤坏死因子 α(TNF α)Ⅰ组 ,培养液中加入TNF α10 0 0u/ml作用 30min ;③TNF αⅡ组 ,培养液中加入TNF α 10 0 0u/ml作用 6h ;④SF +TNF αⅠ组 ,培养液中先加入SF 1mg/ml孵育 1h ,再加入TNF α 10 0 0u/ml作用 30min ;⑤SF +TNF αⅡ组 ,培养液中先加入SF 1mg/ml孵育 1h ,再加入TNF α 10 0 0u/ml作用 6h。采用原位杂交法检测iNOS和ecNOS的mRNA表达 ,扫描电镜观察细胞形态变化。结果 :①TNF α使内皮细胞iNOSmRNA表达增高而ecNOSmRNA表达降低 ;电镜下内皮细胞破坏较明显 ,细胞皱缩 ,微绒毛断裂 ,分布不规则。以上改变又以 6h为著。②将SF与TNF α共同作用于内皮细胞使内皮细胞iNOSmRNA表达下降 ,ecNOSmRNA表达增高 ;电镜下内皮细胞破坏轻微。结论 :TNF α诱导内皮细胞iNOSmRNA表达增高 ,ecNOSmRNA表达抑制。而SF使内皮细胞iNOSmRNA表达下降 ,ecNOSmRNA表达增高 ,这可能是SF抗动脉粥样硬化 ,抗炎症损伤的机理之一     

Simple enumerations of peripheral blood natural killer (CD56+ NK) cells, B cells and T cells have no predictive value in IVF treatment outcome

BACKGROUND: To evaluate the association between the absolute counts of the peripheral natural killer (NK) cells (including total CD56(+) NK cells, CD56(dim) NK cells and CD56(bright) NK cells), B cells and T cells on the implantation rate and miscarriage rate after IVF treatment. METHODS: This was a prospective observation study. A total of 138 patients who underwent IVF treatment from December 2002 to July 2003 were recruited to the study. Blood samples were obtained on the day of vaginal oocyte retrieval prior to the procedure. The absolute counts of lymphocytes, NK cells, B cells and T cells were identified by flow cytometry. These absolute counts and their relationships to IVF treatment outcome and miscarriage rate were analysed. RESULTS: There were no significant differences with regard the mean values of absolute lymphocyte count, T cell count, B cell count and NK cell count (including total CD56(+) NK, CD56(dim) NK and CD56(bright) NK cells) between the pregnant and non-pregnant groups and also between the ongoing pregnancy and miscarriage groups. The cause of infertility, duration of infertility, basal FSH levels, number of previous failed IVF treatments, number of previous miscarriages and stimulation characteristics were not significantly different between the pregnant and non-pregnant groups. Previous studies have suggested that women with a history of recurrent miscarriage and those with infertility accompanied by recurrent failed IVF treatments are associated with a peripheral blood NK cell percentage >12%, therefore further analysis of peripheral CD56(+) NK cell levels <12% (group A) and >12% (group B) was performed. There was no significant difference in implantation rate (group A: 17.0%; group B: 23.2%), pregnancy rate (group A: 36.6%; group B: 47.7%) or miscarriage rate (group A: 23.3%; group B: 28.6%). CONCLUSION: There were no significant differences between simple enumerations of peripheral blood NK cells (including total CD56(+) NK, CD56(dim) NK and CD56(bright) NK cells), B cells and T cells with IVF treatment outcome and pregnancy outcome. Women who had a peripheral NK cell level >12% did not have higher number of previous pregnancy losses. Importantly their pregnancy rate was not reduced and their miscarriages were not increased compared to women who had a peripheral NK cells level <12%.     

一氧化氮合酶与缺氧复氧所致神经细胞凋亡及银杏叶提取物的保护作用

目的　探讨一氧化氮 (NO)在缺氧复氧诱导神经细胞凋亡中的作用及中药银杏叶提取物的保护机制。方法　实验使用胎龄 16～ 17日Wistar大鼠的大脑皮层神经细胞进行原代分离培养 ;采用Wright Giemsa染色 ,光镜、透射电子显微镜观察 ;原位末端标记法确立缺氧复氧神经细胞凋亡病理模型 ;应用NADPH d组织化学方法检测神经细胞一氧化氮合酶 (NOS)的表达并用计算机图像分析系统进行定量检测。　结果　缺氧复氧可以使大鼠大脑皮层神经细胞发生凋亡 ,随缺氧时间的延长 ,凋亡细胞数渐多 ,至缺氧 8h复氧 18h达高峰 ;在缺氧 2h(H2 R0 组 )和缺氧 8h复氧 18h(R8R1 8)组中神经细胞NOS表达均显著增高 ,与正常对照组比有显著性差异 (P <0 0 1;P <0 0 5 )。EGB能显著抑制此双时相NOS活性的增强 ,并明显降低神经细胞凋亡率。　结论　缺氧复氧损伤可诱导培养的大鼠大脑皮层神经细胞发生凋亡。NOS表达增强从而使NO产生增加可能是缺氧复氧诱导神经细胞凋亡的机制之一。银杏叶提取物 (EGB)经下调NOS表达活性 ,抑制NO的产生保护培养的大鼠大脑皮层神经细胞免于凋亡。     

宫内缺氧对胎鼠大脑皮质神经元c-Fos和NOS表达的影响

目的探讨宫内缺氧对胚胎大鼠大脑皮质神经元内c-Fos和一氧化氮合酶(nitric oxide syntbase,NOS)表达的影响。方法将8只孕期15天的孕鼠随机分为对照组和缺氧组各4只,缺氧组孕鼠采用低张性缺氧模型致鼠胚宫内缺氧1小时,两组鼠胚大脑组织经c-Fos和NOS免疫组化双标染色后,进行观察分析。结果缺氧组大脑皮质c-Fos阳性细胞、NOS阳性细胞和c-Fos/NOS双染阳性细胞均比对照组明显增多(P<0.05)。结论缺氧可刺激鼠胚大脑神经元内c-Fos和NOS的表达。     

脑梗塞患者血清VEGF、NO和NOS测定及其意义

血管内皮生长因子(ｖａｓｃｕｌａｒｅｎｄｏｔｈｅｌｉａｌｇｒｏｗｔｈｆａｃｔｏｒ,ＶＥＧＦ),也称血管通透性因子(ＶＰＦ),由平滑肌细胞等产生和分泌,特异性地作用于血管内皮细胞,是一种强有力的多功能细胞生长因子,可促使血管内皮细胞分裂增生、转移,增加血管通透性并促使新血管形成[1]。为探讨ＶＥＧＦ与缺血性脑血管疾病的关系,本文检测38例脑梗塞患者血清ＶＥＧＦ浓度,同时测定一氧化氮(ＮＯ)、一氧化氮合酶(ＮＯＳ)的水平。1　方法和结果以脑梗塞患者为研究对象,健康献血者为对照组。ＶＥＧＦ采用双抗体夹心ＥＬＩＳＡ法;ＮＯ采用…     

NO/NOS在神经系统中作用的哲学思考

一氧化氮 (NitricOxide ,NO)被称为“明星分子” ,自发现以来一直受到人们广泛关注。NO由L -精氨酸在一氧化氮合酶(nitricoxidesynthase ,NOS)作用下生成 ,是一种在细胞内和细胞间具有高度活性的信使分子 ,广泛分布于生物体内各组织中 ,特别是神经组织中。研究表明NO具有免疫调节、神经传递、血压调控和血小板凝聚抑制等生理功能 ,而且其浓度的变化与机体的生理机能亦紧密相关。同时发现NO参与多种疾病的发生发展 ,尤其表现在神经系统病理损伤的过程。本文用哲学的思想分析NO的认识过程 ,特别是它在神经系统中的作用特点 ,为利用NO…     

Role of the neonatal period of pituitary-testicular activity in germ cell proliferation and differentiation in the primate testis

BACKGROUND: The neonatal period of pituitary-testicular activity (NPTA) in human males has been hypothesized to play a role in germ cell proliferation and differentiation and to be defective in cryptorchid testes. The present study was carried out to establish in the marmoset if suppression of the NPTA, by treatment with a GnRH antagonist, results in impaired germ cell proliferation and/or differentiation. METHODS: Comparison of germ cell (GC) numbers and differentiation from gonocytes to pre-spermatogonia and spermatogonia, at birth (in controls) and at the end of the NPTA in marmoset co-twin males treated from birth to age 14 weeks with vehicle or GnRH antagonist. RESULTS: From birth to age 18-24 weeks, testis weight increased approximately 5-fold and GC number approximately 10-fold, including increased numbers of gonocytes and pre-spermatogonia and the first appearance of spermatogonia. Treatment with GnRH antagonist attenuated the increase in testis weight and GC numbers, but the effect was only partial (24-30% reduction), and the relative proportions of gonocytes, pre-spermatogonia and spermatogonia in the GnRH antagonist-treated group were unchanged from control values. CONCLUSIONS: The NPTA plays only a minor, if any, role in GC proliferation and differentiation in the marmoset. The changes in GnRH antagonist-treated co-twins may reflect impaired GC survival due to withdrawal of gonadotrophin support for Sertoli cells. These findings do not support a pivotal role for the NPTA in neonatal GC development in primates.     

牛磺酸锌对睡眠剥夺大鼠脑认知功能的影响及机理

目的:探索补锌对睡眠剥夺(SD)后大鼠脑认知功能的影响及机制。方法:采用小平台水环境法制作大鼠SD模型,3天后通过Y-型迷宫行为测试结合NADPH-d组化与免疫组化ABC法,分别观察大鼠海马结构不同亚区内一氧化氮合酶(NOS)活性与神经元型一氧化氮合酶(nNOS)蛋白表达水平的变化。结果:SD组大鼠迷宫实验学会次数(89.3±25.3)较正常对照组大鼠(67.1±29.3)增加(t=1.81,P<0.05),补牛磺酸锌(5.9g/kg饲料牛磺酸锌水平)组大鼠的迷宫实验学会次数(71.9±21.4)较SD组减少(t=1.66,P<0.05)。与正常对照组大鼠海马结构的NOS(CA1:32.6±2.1;CA3:20.5±1.8;DG:27.5±1.8)活性和nNOS蛋白(CA1:68.3±4.1;CA3:41.7±2.5;DG:44.4±2.8)表达相比,SD组大鼠海马结构各亚区NOS(CA1:14.8±1.2;CA3:10.6±1.0;DG:13.1±1.3)活性和CA1区与齿状回nNOS蛋白(CA1:51.3±3.6;DG:41.6±2.7)表达减少(P<0.05),CA3区nNOS蛋白变化不明显(38.1±4.8,P>0.05)。与SD组大鼠相比,补牛磺酸锌组大鼠海马结构不同亚区内的NOS表达增加(CA1:27.2±2.8;CA3:15.3±1.6;DG:21.8±1.9,P<0.05),CA1区的nNOS蛋白表达增加(60.1±3.4,P<0.05),CA3和齿状回nNOS表达变化不明显(CA3:39.6±4.9;DG:42.8±3.5,P>0.05)。结论:牛磺酸锌对大鼠学习记忆功能有促进作用,其机理可能与上调海马结构NOS、nNOS表达水平有关。     

Identification, characterization and co-localization of label-retaining cell population in mouse endometrium with typical undifferentiated markers

BACKGROUND: The endometrium, lining of the uterus, is a highly active organ that is remodelled periodically during the lifespan. Different studies suggest the presence of an adult or progenitor stem cell (PSC) population in this tissue because of its cyclic regenerative capacity. METHODS: In this study, we aim at identifying and localizing the putative PSC population in the murine uterus using the 5-bromo-2'-deoxyuridine (BrdU) labelling method to detect label-retaining cells (LRCs) that cycle slowly. Uteri from BrdU-treated mice were analysed via single and double immunohistochemistry to co-localize them with the markers of undifferentiation already described such as c-KIT and POU5F1 (also known as OCT-4). Finally, we confirmed the presence of the indicated markers at mRNA level. RESULTS: We observed the presence and gradual decrease of LRCs in the endometrium during the lifespan of the mice. In adulthood, the LRC population decreased notably and remained in the lower region of the stroma in the murine endometrium. Some of the endometrial LRCs co-localized with c-KIT and POU5F1. PCR and nested-PCR confirmed the presence of these undifferentiated markers. CONCLUSIONS: We demonstrated that the murine endometrium possesses LRCs with the features of a putative PSC population localized at the lower region of the stroma.