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TGF-β signaling in aortic aneurysm: another round of controversy

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Journal of genetics and Genomics 2010年第9期37卷 583-591页

作者： Fuyu Lin Xiao Yang State Key laboratory of Proteomics Genetic Laboratory of Development and Diseases Institute of Biotechnology Beijing 100071 China

Aortic aneurysm （AA） is a common health problem with high mortality and no effective drugs. Transforming growth factor-β （TGF-β） superfamily members regulate various cellular processes, and TGF-β signaling has key roles in development, tissue homeo- stasis, and diseases. Interest in the role of TGF-β signaling in the pathogenesis of AAs has recently emerged, particularly since genetic studies demonstrated an association between gene mutations in components of TGF-β signaling and AAs. However, paradoxical discoveries have implicated dysregulated TGF-β signaling in aneurysm formation, complicating the precise functional role for TGF-β in aneurysm development and progression. Furthermore, interventions targeting towards TGF-β signaling using losartan, which may represent a suitable therapeutic option for AAs, were subject to skepticism especially because of conflicting experimental results obtained from TGF-β antibody treatment without knowledge of the underlying mechanism. We propose a TGF-β aneurysm paradox, which would provide a good opportunity for the development of genetic mouse models of AA. These models would be used to clarify the mechanisms underlying TGF-β signaling, which would translate into novel pharmacologic therapies based on the new molecular discoveries.

关键词： aneurysm TGF-β signaling mouse model

The role of Smad signaling in vascular and hematopoietic development revealed by studies using genetic mouse models

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Science China(Life Sciences) 2010年第4期53卷 485-489页

作者： LAN Yu & YANG Xiao State Key laboratory of Proteomics, genetic laboratory of development and diseases, institute of biotechnology, beijing 100071, China State Key laboratory of Proteomics Genetic Laboratory of Development and Diseases Institute of Biotechnology Beijing China

Smads are intracellular mediators of transforming growth factor β (TGF-β) superfamily signaling. In this review, we focus on the genetic mouse models for Smad pathways, which have provided functional evidence regarding the complex circuitry in angiogenesis and hematopoiesis during development. In the early stages of vascular development, TGF-β signaling is a contri buting factor in angiogenesis and vascular maturation. Whereas in the later embryogenesis, selected molecules of Smad pathways, such as TGF-β type II receptor (TbRII), ALK5, and Smad5, seem to be dispensable for vessel morphogenesis and integrity. TGF-β signaling is not required in the induction of hematopoietic precursors from mesoderm, but inhibits the subsequent expansion of committed hematopoietic precursors. By contrast, bone morphogenetic protein 4 (BMP4) has long been acknowledged pivotal in mesoderm induction and hematopoietic commitment during development. However, recent genetic evidence shows the BMP4-ALK3 axis is not crucial for the formation of hematopoietic cells from FLK1+ mesoderm. Because of the highly redundant mechanisms within the Smad pathways, the precise role of the Smad signaling involved in vascular and hematopoietic development remains nebulous. The generation of novel cell lineage restricted Cre transgenes would shed new light on the future relevant investigations.

关键词： Smad transforming growth factor β (TGF-β) bone morphogenetic protein (BMP) angiogenesis hematopoiesis knockout development

Odontoblast β-catenin signaling regulates fenestration of mouse Hertwig's epithelial root sheath

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Science China(Life Sciences) 2015年第9期58卷 876-881页

作者： ZHANG Ran TENG Yan ZHU Liang LIN JingTing YANG Xiao YANG Guan LI TieJun Department of Oral Pathology Peking University School and Hospital of Stomatology State Key laboratory of Proteomics Genetic Laboratory of Development and Diseases Institute of Biotechnology

The interaction between Hertwig＇s epithelial root sheath （HERS） and the adjacent mesenchyme is vitally important in mouse tooth root development. We previously generated odontoblast-specific Ctnnbl （encodingβ-catenin） deletion mice, and demon- strated that odontoblast β-catenin signaling regulates odontoblast proliferation and differentiation. However, the role of odon- toblast β-catenin signaling in regulation of HERS behavior has not been fully investigated. Here, using the same odonto- blast-specific Ctnnbl deletion mice, we found that ablation of β-catenin signaling in odontoblasts led to aberrant HERS for- mation. Mechanistically, odontoblast-specific Ctnnbl deletion resulted in elevated bone morphogenetic protein 7 （Bmp7） ex- pression and reduced expression of noggin andfollistatin, both of which encode extracellular inhibitors of BMPs. Furthermore, the levels of phosphorylated Smadl/5/8 were increased in HERS cells. In vitro tissue culture confirmed that BMP7 treatment disrupted the HERS structure. Taken together, we demonstrated that odontoblast f3-catenin signaling may act through regula- tion of BMP signaling to maintain the integrity of HERS cells.

关键词： Hertwig's epithelial root sheath β-catenin signaling BMP signaling mesenchyme-epithelium induction

Effect of TGF-β/Smad signaling pathway on lung myofibroblast differentiation

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Acta Pharmacologica Sinica 2007年第3期28卷 382-391页

作者： Li GU~2 Yuan-jue ZHU~(2,4) Xiao YANG~3 Zi-Jian GUO~2 Wen-bing XU~2 Xin-lun TIAN~22 Department of Pulmonary Medicine,Peking Union Medical College Hospital,Chinese Academy of Medical Sciences,beijing 100071 China 3 genetic laboratory of development and diseases,institute of biotechnology,beijing 100070,China Department of Pulmonary Medicine Peking Union Medical College Hospital Chinese Academy of Medical Sciences Beijing China Department of genetic laboratory of development and diseases Institute of Biotechnology Beijing China

Aim:Myofibroblasts play important roles in the pathogenesis of lung *** growth factor（TGF）-β1has been widely recognized as a keyfibrogenic *** major signaling pathway of TGF--β1is through cytoplas-mic Smad *** study investigated the role of individual TGF--β1/Smadsignal proteins in mediating α-smooth muscle actin（α-SMA）gene expression,which is a well-known key marker of myofibroblast ***:Wetransiently cotransfected α-SMA promoter-luciferase fusion plasmid（p895-Luc）and Smad expression plasmids and measured Luc activity in TGF--β1-treated hu-man fetal lung *** induced Smad3 knockout mice lung fibrosis bybleomycin,α-SMA protein expression was assessed by Western ***-lagen protein was analyzed by measuring *** morphol-ogy was assessed by ***:We found that theoverexpression of Smad3,not Smad2 markedly increased TGF--β1-induced α-SMApromoter activity and α-SMA protein expression in vitro,whereas the over-expression of dominant negative mutant Smad3 and Smad7 repressed TGF--β1-induced α-SMA gene *** to wild-type mice,Smad3 knockoutmice showed attenuated lung fibrosis after bleomycin treatment,manifested bylower collagen production and myofibroblast ***:Ourstudy suggested TGF--β1/Smad3 is a major pathway which regulated themyofibroblast *** result indicates a potential significance forfuture attempts of attenuating the progression of human lung fibrosis by theinhibition of the Smad3 cascade.

关键词： myofibroblasts transforming growth factorβ1 Smad

Epigenetics in the modern era of crop improvements

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Science China Life Sciences 2025年

作者： Yan Xue Xiaofeng Cao Xiangsong Chen Xian Deng Xingwang Deng Yong Ding Aiwu Dong Chengguo Duan Xiaofeng Fang Lei Gong Zhizhong Gong Xiaofeng Gu Chongsheng He Hang He Shengbo He Xinjian He Yan He Yuehui He Guifang Jia Danhua Jiang Jianjun Jiang Jinsheng Lai Zhaobo Lang Chenlong Li Qing Li Xingwang Li Bao Liu Bing Liu Xiao Luo Yijun Qi Weiqiang Qian Guodong Ren Qingxin Song Xianwei Song Zhixi Tian Jiawei Wang Yuan Wang Liang Wu Zhe Wu Rui Xia Jun Xiao Lin Xu Zhengyi Xu Wenhao Yan Hongchun Yang Jixian Zhai Yijing Zhang Yusheng Zhao Xuehua Zhong Daoxiu Zhou Ming Zhou Yue Zhou Bo Zhu Jiankang Zhu Qikun Liu College of Life Sciences Institute of Life Science and Green Development Hebei University biotechnology Research institute Chinese Academy of Agricultural Sciences College of Biology Hunan Key Laboratory of Plant Functional Genomics and Developmental Regulation Hunan Engineering and Technology Research Center of Hybrid Rapeseed Hunan University institute of Advanced Agricultural Sciences School of Advanced Agricultural Sciences Peking University State Key laboratory for Conservation and Utilization of Subtropical Agro-Bioresources Guangdong Laboratory for Lingnan Modern Agriculture South China Agricultural University National institute of Biological Sciences Key laboratory of Seed Innovation Institute of Genetics and Developmental Biology Chinese Academy of Sciences School of Advanced Agricultural Sciences Peking-Tsinghua Center for Life Sciences Peking University Synthetic and Functional Biomolecules Center Beijing National Laboratory for Molecular Sciences Key Laboratory of Bioorganic Chemistry and Molecular Engineering of Ministry of Education College of Chemistry and Molecular Engineering Peking University Key laboratory of Seed Innovation State Key Laboratory of Plant Genomics and National Center for Plant Gene Research Institute of Genetics and Developmental Biology Chinese Academy of Sciences State Key laboratory of Wheat Improvement Peking University Institute of Advanced Agricultural Sciences Shandong Laboratory of Advanced Agricultural Sciences in Weifang State Key laboratory of Crop Stress Adaptation and Improvement School of Life Sciences Henan University State Key laboratory of Maize Bio-breeding National Maize Improvement Center Department of Plant Genetics and Breeding China Agricultural University Frontiers Science Center for Molecular Design Breeding China Agricultural University Center for Crop Functional Genomics and Molecular Breeding China Agricultural University Sanya institute of China Agricultural University Hainan Yazhou Bay Seed laboratory institute of Advan

Epigenetic mechanisms are integral to plant growth, development, and adaptation to environmental stimuli. Over the past two decades,our comprehension of these complex regulatory processes has expanded remarkably, producing a substantial body of knowledge on both locus-specific mechanisms and genome-wide regulatory patterns. Studies initially grounded in the model plant Arabidopsis have been broadened to encompass a diverse array of crop species, revealing the multifaceted roles of epigenetics in physiological and agronomic traits. With recent technological advancements, epigenetic regulations at the single-cell level and at the large-scale population level are emerging as new focuses. This review offers an in-depth synthesis of the diverse epigenetic regulations, detailing the catalytic machinery and regulatory functions. It delves into the intricate interplay among various epigenetic elements and their collective influence on the modulation of crop traits. Furthermore, it examines recent breakthroughs in technologies for epigenetic modifications and their integration into strategies for crop improvement. The review underscores the transformative potential of epigenetic strategies in bolstering crop performance, advocating for the development of efficient tools to fully exploit the agricultural benefits of epigenetic insights.

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Collagen1α1 promoter drives the expression of Cre recombinase in osteoblasts of transgenic mice

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Journal of genetics and Genomics 2008年第9期35卷 525-530页

作者： Lagabaiyila Zha Ning Hou Jian Wang Guan Yang Yuanrong Gao Lin Chen Xiao Yang State Key laboratory of Proteomics Genetic Laboratory of Development and Diseases Institute ofBiotechnology Beijing 100071 China laboratory of Trauma Center Daping Hospital The Third Military Medical University Chongqing 400042 China

Osteoblasts participate in bone formation, bone mineralization, osteoclast differentiation and many pathological processes. To study the function of genes in osteoblasts using Cre-LoxP system, we generated a mouse line expressing the Cre recombinase under the control of the rat Collagenlcd （Collα1） promoter （Collα1-Cre）. Two founders were identified by genomic PCR from 16 offsprings, and the integration efficiency is 12.5%. In order to determine the tissue distribution and the activity of Cre recombinase in the transgenic mice, the Coll αl-Cre transgenic mice were bred with the ROSA26 reporter strain and a mouse strain that carries Smad4 conditional alleles （Smad4^Co/Co）. Multiple tissue PCR of Collα1-Cre;Smad4^Co/＋ mice revealed the restricted Cre activity in bone tissues containing osteoblasts and tendon. LacZ staining in the Collα1-Cre;ROSA26 double transgenic mice revealed that the Cre recombinase began to express in the osteoblasts of calvaria at E14.5. Cre activity was observed in the osteoblasts and osteocytes of P10 double transgenic mice. All these data indicated that the Collα1-Cre transgenic mice could serve as a valuable tool for osteoblast lineage analysis and conditional gene knockout in osteoblasts.

关键词： Collagenl osteoblast Cre recombinase transgenic mouse

RNA binding protein 24 deletion disrupts global alternative splicing and causes dilated cardiomyopathy

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Protein & Cell 2019年第6期10卷 405-416页

作者： Jing Liu Xu Kong Mengkai Zhang Xiao Yang Xiuqin Xu The institute of Stem Cell and Regenerative Medicine Medical College Xiamen University Xiamen 361100 China State Key laboratory of Proteomics Genetic Laboratory of Development and Disease Institute of Biotechnology Beijing 100071 China

RNA splicing contributes to a broad spectrum of posttranscriptional gene regulation during normal development, as well as pathological manifestation of heart diseases. However, the functional role and regulation of splicing in heart failure remain poorly understood. RNA binding protein (RBP), a major component of the splicing machinery, is a critical factor in this process. RNA binding motif protein 24 (RBM24) is a tissue-specific RBP which is highly expressed in human and mouse heart. Previous studies demonstrated the functional role of RBM24 in the embryonic heart development. However, the role of RBM24 in postnatal heart development and heart disease has not been investigated. In this paper, using conditional RBM24 knockout mice, we demonstrated that ablation of RBM24 in postnatal heart led to rapidly progressive dilated cardiomyopathy (DCM), heart failure, and postnatal lethality. Global splicing profiling revealed that RBM24 regulated a network of genes related to cardiac function and diseases. Knockout of RBM24 resulted in misregulation of these splicing transitions which contributed to the subsequent development of cardiomyopathy. Notably, our analysis identified RBM24 as a splice factor that determined the splicing switch of a subset of genes in the sacomeric Z-disc complex, including Titin, the major disease gene of DCM and heart failure. Together, this study identifies regulation of RNA splicing by RBM24 as a potent player in remodeling of heart during postnatal development, and provides novel mechanistic insights to the pathogenesis of DCM.

关键词： RNA binding protein RBM24 dilated cardiomyopathy alternative splicing heart failure

Atp4b promoter directs the expression of Cre recombinase in gastric parietal cells of transgenic mice

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Journal of genetics and Genomics 2010年第9期37卷 647-652页

作者： Zengming Zhao Ning Hou Yanxun Sun Yan Teng Xiao Yang genetic laboratory of development and diseases State Key Laboratory of Proteomics Institute ofBiotechnology Beijing 100071 China Model Organism Division E-Institutes of Shanghai Universities Shanghai Jiao Tong University Shanghai 200240 China

Parietal cells are one of the largest epithelium cells of the mucous membrane of the stomach that secrete hydrochloric acid. To study the function of gastric parietal cells during gastric epithelium homeostasis, we generated a transgenic mouse line, namely, Atp4b-Cre, in which the expression of Cre recombinase was controlled by a 1.0 kb promoter of mouse β-subunit of H^＋-, K^＋-ATPase gene （Atp4b）. In order to test the tissue distribution and excision activity of Cre recombinase in vivo, the Atp4b-Cre transgenic mice were bred with the reporter strain ROSA26 and a mouse strain that carries Smad4 conditional alleles （Smad4Ca/Co）. Multiple-tissue PCR of Atp4b-Cre;Smad4Co/＋ mice revealed that the recombination only happened in the stomach. As indicated by LacZ staining, ROSA26;Atp4b-Cre double transgenic mice showed efficient expression of Cre recombinase within the gastric parietal cells. These results showed that this Atp4b-Cre mouse line could be used as a powerful tool to achieve conditional gene knockout in gastric parietal cells.

关键词： parietal cells Cre recombinase transgenic mouse Atp4b

Endothelial Smad4 Restrains the Transition to Hematopoietic Progenitors via Suppression of ERK Activation

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Endothelial Smad4 Restrains the Transition to Hematopoietic ...