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Pluripotent stem cells secrete activin a to improve their epiblast competency after injection into recipient embryos

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Protein & Cell 2018年第8期9卷 717-728页

作者： Jinzhu Xiang Suying Cao Liang Zhong Hanning Wang Yangli Pei Qingqing Wei Bingqiang Wen Haiyuan Mu Shaopeng Zhang Liang Yue Genhua Yue Bing Lim Jianyong Han State Key Laboratory for Agrobiotechnology College of Biological Sciences China Agricultural University Beijing 100193 China Animal Science and Technology College Beijing University of Agriculture Beijing 102206 China Temasek Life Sciences Laboratory National University of Singapore Singapore 117604 Singapore Stem Cell and Developmental Biology Genome Institute of Singapore Singapore 138672 Singapore Beijing Advanced Innovation Center for Food Nutrition and Human Health China Agricultural University Beijing 100193 China State Key Laboratory of Animal Nutrition Institute of Animal Sciences Chinese Academy of Agricultural Sciences Beijing 100193 China

It is not fully clear why there is a higher contribution of pluripotent stem cells （PSCs） to the chimera produced by injection of PSCs into 4-cell or 8-cell stage embryos compared with blastocyst injection. Here, we show that not only embryonic stem cells （ESCs） but also induced pluripotent stem cells （iPSCs） can generate F0 nearly 100% donor cell-derived mice by 4-cell stage embryo injection, and the approach has a ＂dose effect＂. Through an analysis of the PSC-secreted proteins, activin a was found to impede epiblast （EPI） lineage development while promoting trophectoderm （TE） differentiation, resulting in replacement of the EPI lineage of host embryos with PSCs. Interestingly, the injection of ESCs into blastocysts cultured with activin a （cultured from 4-cell stage to early blastocyst at E3.5） could increase the contribution of ESCs to the chimera. The results indicated that PSCs secrete protein activin a to improvetheir EPI competency after injection into recipient embryos through influencing the development of mouse early embryos. This result is useful for optimizing the chimera production system and for a deep understand- ing of PSCs effects on early embryo development.

关键词： pluripotent stem cells 4-cell embryoinjection secreted proteins activin a chimeric mice

Effects of activin a on the Activities of the Mouse Peritoneal Macrophages

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Cellular & Molecular Immunology 2005年第1期2卷 63-67页

作者： XuejunZhang YangLi GuixiangTai GuiyueXu PengyuZhang YuYang FengxueLao ZhonghuiLiu DepartmentofImmunology SchoolofBasicMedicalSciencesJilinUniversityChangchun130021China. TheSecondAffiliatedHospitalofHarbinMedicalUniversity Harbin150086ER.China. Correspondingto：Dr.ZhongHuiLiu DepartmentofImmunologySchoolofBasicMedicalSciencesJilinUniversityChangchun130021China.

activin a is a kind of pre-inflammatory factor that belongs to the transforming growth factor-β(TGF-β) *** investigate the effect and mechanism of activin a on the activities of mouse macrophages,the secretion of NO in the supernatant of cultured mouse peritoneal macrophages was examined by NO assay kit,and the expression of iNOS,ActRIIA and ARIP2 mRNA in mouse peritoneal macrophages was analyzed by RT-PCR. The results showed that activin a stimulated the secretion of NO and the expression of iNOS mRNA in non-activated mouse macrophages in a time-and dose-dependent *** contrast,activin a in the same concentration inhibited the secretion of NO in LPS-activated mouse macrophages in a dose-dependent manner. ActRIIA was highly expressed on macrophages,and activin a upregulated the ActRIIA mRNA expression in ***-ActRIIA antibody can block the secretion of NO from the macrophages stimulated by activin a. Furthermore,RT-PCR analysis revealed that activin a enhanced the ARIP2 mRNA expression in macrophages. These results indicated that activin a may be a weak activator compared with LPS to mouse macrophages,and activin a may modulate the secretion of NO through ActRIIA-ARIP2 signal pathway in mouse macrophages. Cellular & Molecular Immunology.2005;2(1):63-67.

关键词： activin a ActRIIA macrophage RT-PCR NO

Analysis of bacterial spectrum,activin a,and CD64 in chronic obstructive pulmonary disease patients complicated with pulmonary infections

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World Journal of Clinical Cases 2022年第8期10卷 2382-2392页

作者： Zhao-Yang Fei Jiang Wang Jie Liang Xue Zhou Min Guo Experimental Research Centre The First Affiliated Hospital of Chongqing Medical UniversityChongqing 400010China Department of Laboratory Medicine Lianyungang Second People's HospitalLianyungang 222006Jiangsu ProvinceChina

BACKGROUND Pulmonary infections often lead to poor prognoses in patients with chronic obstructive pulmonary disease(COPD).activin a and CD64 play crucial pathological roles in the development of *** To explore the bacterial spectrum via analysis of activing A levels,CD64 index,and related mechanisms in COPD patients complicated with pulmonary *** Between March 2015 and January 2018,a total of 85 patients with COPD,who also suffered from pulmonary infections,were enrolled in this study as the pulmonary infection *** addition,a total of 96 COPD patients,without pulmonary infection,were selected as the control *** samples of patients in the pulmonary infection group were cultivated for bacterial identification prior to administration of *** neutrophil CD64 index was measured using flow cytometry,serum activin a levels were detected via an enzyme-linked immunosorbent assay,and activin a,Smad3,TLR4,My D88,and NFκB protein expression was analyzed by Western *** Gram-negative bacteria were identified in 57.65%of the sputum samples in the pulmonary infection *** most prevalent Gram-negative species were Pseudomonas aeruginosa and Klebsiella ***,Gram-positive bacteria were identified in 41.18%of the sputum samples in the pulmonary infection *** most common Gram-positive species was Streptococcus *** were identified in 1.17%of the sputum samples in the pulmonary infection *** CD64 index was significantly higher in the pulmonary infection group(0.91±0.38)than in the control group(0.23±0.14,Pactivin a levels were significantly higher in the pulmonary infection group(43.50±5.22 ng/m L),compared to the control group(34.82±4.16 ng/m L,Pactivin a,Smad3,TLR4,My D88,and NFκB were all significantly higher in the pulmonary infection group,compared to the control group(all P<0.001).CONCLUSION Pulmonary infections in COPD p

关键词： Chronic obstructive pulmonary disease Infection activin a CD64 index

activin a maintains cerebral cortex neuronal survival and increases voltage-gated Na^+ neuronal current

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Neural Regeneration Research 2010年第19期5卷 1464-1469页

作者： Jingyan Ge Yinan Wang Haiyan Liu Fangfang Chen Xueling Cui Zhonghui Liu Department of Physiology Norman Bethune College of Medicine Jilin University Changchun 130021 Jilin Province China Department of Immunology Norman Bethune College of Medicine Jilin University Changchun 130021 Jilin Province China Department of Anatomy Norman Bethune College of Medicine Jilin University Changchun 130021 Jilin Province China Department of Genetics Norman Bethune College of Medicine Jilin University Changchun 130021 Jilin Province China

activin a, which was first described in 1986, has been shown to maintain hippocampal neuronal survival. activin a increases intracellular free Ca2＋ via L-type Ca2＋ channels. Our previous study showed that activin a promotes neurite growth of dorsal root ganglia in embryonic chickens and inhibits nitric oxide secretion. The present study demonstrated for the first time that activin a could maintain cerebral cortex neuronal survival in vitro for a long period, and that activin a was shown to increase voltage-gated Na＋ current （/Na） in Neuro-2a cells, which was recorded by patch clamp technique. The present study revealed a novel mechanism for activin a, as well as the influence of activin a on neurons by regulating expressions of vasoactive intestine peptide and inducible nitric oxide synthase.

关键词： activin a cerebral cortex neuron voltage-gated sodium current neuro-2a cell neural regeneration

activin a prevents neuron-like PC12 cell apoptosis after oxygen-glucose deprivation

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Neural Regeneration Research 2013年第11期8卷 1016-1024页

作者： Guihua Xu Jinting He Hongliang Guo Chunli Mei Jiaoqi Wang Zhongshu Li Han Chen Jing Mang Hong Yang Zhongxin Xu Department of Neurology China-Japan Union Hospital Jilin University Department of Neurology Changchun Central Hospital

In this study, PC12 cells were induced to differentiate into neuron-like cells using nerve growth factor, and were subjected to oxygen-glucose deprivation. Cells were treated with 0, 10, 20, 30, 50, 100 ng/mL exogenous activin a. The 3-（4,5-dimethyl-2-thiazolyl）-2,5-diphenyl tetrazolium bromide assay and Hoechst 33324 staining showed that the survival percentage of PC12 cells significantly decreased and the rate of apoptosis significantly increased after oxygen-glucose deprivation. Exogenous activin a significantly increased the survival percentage of PC12 cells in a dose-dependent manner. Reverse transcription-PCR results revealed a significant increase in activin receptor IIA, Smad3 and Smad4 mRNA levels, which are key sites in the activin a/Smads signaling pathway, in neuron-like cells subjected to oxygen-glucose deprivation, while mRNA expression of the apoptosis-regulation gene caspase-3 decreased. Our experimental findings indicate that exogenous activin a plays an anti-apoptotic role and protects neurons by means of activating the activin a/Smads signaling pathway.

关键词： neural regeneration brain injury biological factor oxygen-glucose deprivation activin a activinA/Smads signaling pathway caspase-3 apoptosis grants-supported paper neuroregeneration

Lipopolysaccharide induced activin a-follistatin imbalance affects cardiac fibrosis

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Chinese Medical Journal 2012年第12期125卷 2205-2212页

作者： ZHANG Wen-qi YANG Chun-yan LI Shu-mei LIU Miao DING Mei LIU Guo-hui YANG Ping Department of Cardiology Second Hospital Jilin UniversityChangchun Jilin 130041 China Department of Cardiology China-Japan Union Hospital JilinUniversity Changchun Jilin 130033 China

Background Inflammation plays a pivotal role in cardiac remodeling, especially in myocardial fibrosis. Abnormal growth of cardiac fibroblasts is critically involved in the pathophysiology of cardiac hypertrophy/remodeling. Previous study has demonstrated that many inflammation stimulating factors trigger transforming growth factor-β （TGF-β） induction and reactive myocardial fibrosis. activin a （ACT A） is a member of TGF-β superfamily, and follistatin （FS） is an activin-binding protein, i.e. an antagonist of ACT A. Our previous studies have shown that ACT A-FS imbalance occurs in rats with heart failure （HF）, and overexpression of ACT A can lead to ventricular remodeling, and resultant HF. Low expression of FS after myocardial infarction further exacerbated HF. The pathogenic change resulting from overexpression of ACT A is consistent with that of overexpression of angiotensin II （Angll）. Ventricular remodeling includes cardiocyte remodeling and myocardial interstitial collagen deposition and fibrosis, Therefore, the present study was designed to investigate the effects of inflammatory factors on the ACT A-FS and the secretions of cardiac fibroblasts in order to explore in depth the mechanism of myocardial fibrosis. Methods A rat model with HF was established, and the results showed that there was a greater degree of cardiac fibrosis in HF rats. In addition, we found that there was an imbalance of the ACT A/FS system in HF rats, which was characterized by increased levels of ACT A. Further, primary rat cardiac fibroblasts were cultured and the MTT assay was performed to determine the effect of the inflammatory factor-bacterial endotoxin lipopolysaccharide （LPS） on cardiac fibroblast proliferation. Results The results showed that LPS can stimulate the cardiac fibroblasts to proliferate in a dose-dependent manner. Cellular immunohistochemical staining showed that the rat cardiac fibroblasts themselves could express ACT A and FS proteins, and stimulation by LPS could ap

关键词： cardiac remodeling activin a follistatin cardiac fibroblasts lipopolysaccharide

Neuroprotective effects of activin a on endoplasmic reticulum stress-mediated apoptotic and autophagic PC12 cell death

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Neural Regeneration Research 2017年第5期12卷 779-786页

作者： Long-xing Xue Hong-yu Liu Yang Cui Yue Dong Jiao-qi Wang Qiu-ye Ji Jin-ting He Min Yao Ying-ying Wang Yan-kun Shao Jing Mang Zhong-xin Xu Department of Neurology China-Japan Union Hospital lilin University Changchun Jilin province China Research Center China-Japan Union Hospital Jilin University Changchun Jilin Province China

activin a, a member of the transforming growth factor-beta superfamily, plays a neuroprotective role in multiple neurological diseases. Endoplasmic reticulum（ER） stress-mediated apoptotic and autophagic cell death is implicated in a wide range of diseases, including cerebral ischemia and neurodegenerative diseases. Thapsigargin was used to induce PC12 cell death, and activin a was used for intervention. Our results showed that activin a significantly inhibited morphological changes in thapsigargin-induced apoptotic cells, and the expression of apoptosis-associated proteins [cleaved-caspase-12, C/EBP homologous protein（CHOP） and cleaved-caspase-3] and biomarkers of autophagy（Beclin-1 and light chain 3）, and downregulated the expression of thapsigargin-induced ER stress-associated proteins [inositol requiring enzyme-1（IRE1）, tumor necrosis factor receptor-associated factor 2（TRAF2）, apoptosis signal-regulating kinase 1（ASK1）, c-Jun N-terminal kinase（JNK） and p38]. The inhibition of thapsigargin-induced cell death was concentration-dependent. These findings suggest that administration of activin a protects PC12 cells against ER stress-mediated apoptotic and autophagic cell death by inhibiting the activation of the IRE1-TRAF2-ASK1-JNK/p38 cascade.

关键词： nerve regeneration activin a endoplasmic reticulum stress apoptosis autophagy c-Jun N-terminal kinase p38 neural regeneration

Emodin prevents hypoxic-ischemic neuronal injury Involvement of the activin a pathway

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Neural Regeneration Research 2013年第15期8卷 1360-1367页

作者： Hongliang Guo Xiaoran Shen Ye Xu Junliang Yuan Dongming Zhao Wenli Hu Department of Neurology Beijing Chaoyang Hospital Affiliated to Capital Medical University Beihua University Jilin Municipal Central Hospital Jilin Medical College

Emodin, an extract of dried rhizomes and the root of the Rhizoma Polygoni Cuspidati, can protect neurons from hypoxic-ischemic brain damage. This study aimed to verify the underlying mechanism After PC12 cells had differentiated into neuron-like cells under the induction of mouse nerve growth factor, cells were subjected to oxygen-glucose deprivation and treated with emodin. Results shewed that the viability of neuron-like cells cultured under an ischemia-hypoxia environment decreased, while the expression of activin a and caspase-3 in cells increased. Emodin raised the survival rate of oxygen-glucose deprived neuron-like cells~ increased activin a expression, and decreased caspase-3 expression. Experimental findings indicate that emodin can inhibit neuronal apoptosis and alleviate the injury of nerve cells after oxygen-glucose deprivation through the activin a pathway.

关键词： neural regeneration traditional Chinese medicine emodin oxygen-glucose deprivation activin a apoptosis caspase-3 neuroprotection grants-supported paper neuroregeneration

A Critical Role of activin a in Maturation of Mouse Peritoneal Macrophages in vitro and in vivo

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Cellular & Molecular Immunology 2009年第5期6卷 387-392页

作者： Yinan Wang Xueling Cui Guixiang Tai Jingyan Ge Nan Li Fangfang Chen Fang Yu Zhonghui Liu Department of Immunology Norman Bethune College of Medicine JilinUniversity Changchun 130021 China These authors contributed equally to this work Department of Immunology Norman Bethune College of Medicine Jilin University Changchun 130021 China

activin a, a multifunctional factor of the transforming growth factor-beta （TGF-β） superfamily, is mainly produced by microglia and macrophages, and its anti-inflammatory and pro-inflammatory activities are both related to macrophage functions. However the direct effect of activin a on the rest macrophages in vivo remains unclear. In the present study, the results showed that activin a not only increased NO and IL-1β release, but also promoted phagocytic abilities of mouse peritoneal macrophages in vitro and in vivo, whereas it did not influence MHC Ⅰ and MHC Ⅱ expression. Moreover, we found that activin a significantly upregulated the expressions of CD14 and CD68, markers of mature macrophages, on the surface of macrophages in vitro and in vivo. These data suggest that activin a can induce primary macrophage maturation in vitro and in vivo, but may not trigger the acquired immune response via regulating expression of MHC molecules involved in presentation of antigen.

关键词： activin a macrophage maturation CD68 CD14