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| 1 | CCM3 and cerebral cavernous malformation disease显示文摘Cerebral cavernous malformations(CCMs)are vascular lesions characterised by enlarged and irregular structure of small blood vessels in the brain,which can result in increased risk of stroke,focal neurological defects and seizures.Three different genes,CCM1/Krev/Rap1 Interacting Trapped 1,CCM2/MGC4607 and CCM3/PDCD10,are associated with the CCMs’progression,and mutations in one of three CCM genes cause CCM disease.These three CCM proteins have similar function in maintaining the normal structure of small blood vessels.However,CCM3 mutation results in a more severe form of the disease which may suggest that CCM3 has unique biological function in the vasculature.The current review focuses on the signalling pathways mediated by CCM3 in regulating endothelial cell junction,proliferation,migration and permeability.These findings may offer potential therapeutic strategies for the treatment of CCMs. | Kang Wang Huanjiao Jenny Zhou Min Wang | 2019 | Stroke & Vascular Neurology2019，4，2： | 3 |
| 2 | Tetramethylpyrazine protects CoCl2-induced apoptosis in human umbilicalvein endothelial cells by regulating the PHD2/HIF/1α-VEGF pathway显示文摘 | Cheng Yang Yue Xu Huanjiao Zhou Lu Yang Shanshan Yu Yi Gao Yongsheng Huang Lin Lu Xiaoling Liang | 2016 | Molecular Medicine Reports2016，，2： | 1 |
| 3 | Gene knockdown by structure defined single-stem loop small non-coding RNAs with programmable regulatory activities显示文摘Gene regulation by trans-acting small RNAs(sRNAs)has considerable advantages over other gene regulation strategies.However,synthetic sRNAs mainly take natural sRNAs(MicC or SgrS)as backbones and comprise three functional elements folding into two or more stem-loop structures:an mRNA base pairing region,an Hfq-binding structure,and a rho-independent terminator.Due to limited numbers of natural sRNAs and complicated backbone structures,synthetic sRNAs suffer from low activity programmability and poor structural modularity.Moreover,natural sRNA backbone sequences may increase the possibility of unwanted recombination.Here,we present a bottom-up approach for creating structure defined single-stem loop small non-coding RNAs(ssl-sRNAs),which contain a standardized scaffold of a 7 bp-stem-4 nt-loop-polyU-tail and a 24 nt basing pairing region covering the first eight codons.Particularly,ssl-sRNA requires no independent Hfq-binding structure,as the polyU tail fulfills the roles of binding Hfq.A thermodynamic-based scoring model and a web server sslRNAD(http://gffzz5b632577293c4c46hb0cvcqpkwk9f6on0.ffgz.tsg.suse.edu.cn/)were developed for automated design of ssl-sRNAs with well-defined structures and programmable activities.ssl-sRNAs displayed weak polar effects when regulating polycistronic mRNAs.The ssl-sRNA designed by sslRNAD showed regulatory activities in both Escherichia coli and Bacillus subtilis.A streamlined workflow was developed for the construction of customized ssl-sRNA and ssl-sRNA libraries.As examples,the E.coli cell morphology was easily modified and new target genes of ergothioneine biosynthesis were quickly identified with ssl-sRNAs.ssl-sRNA and its designer sslRNAD enable researchers to rapidly design sRNAs for knocking down target genes. | Yang Wang Guobin Yin Huanjiao Weng Luyao Zhang Guocheng Du Jian Chen Zhen Kang | 2023 | Synthetic and Systems Biotechnology2023，8，1： | 0 |
| 4 | Smooth muscle cell differentiation: Mechanisms and models for vascular diseases显示文摘BACKGROUND: Vascular smooth muscle cells (VSMCs) are mature cells that play critical roles in both normal and aberrantcardiovascular conditions. In response to various environmental cues, VSMCs can dedifferentiate from a contractile state to ahighly proliferative synthetic state through the so-called 'phenotypic switching' process. Changes in VSMC phenotypecontribute to numerous vascular-related diseases, including atherosclerosis, calcification, and restenosis following angioplasty.Adventitial VSMC progenitor cells also contribute to formation of the neointima.METHODS/RESULTS: Herein, we review both, the roles of VSMC differentiation in vascular diseases, and the in vitromodels used to investigate the molecular mechanisms involved in the regulation of VSMC differentiation and phenotypemodulation.CONCLUSION: A comprehensive understanding of VSMC behavior in vascular diseases is essential to identify newtherapeutic targets for the prevention and treatment of cardiovascular diseases. | Yujie Deng Caixia Lin Huanjiao Jenny Zhou Wang Min | 2017 | Frontiers in Biology2017，12，6： | 0 |
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