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Downregulation of miR-491-5p promotes neovascularization after traumatic brain injury

Neural Regeneration Research 2022年第3期17卷 577-586页

作者： Wei Tang Zong-Duo Guo Wei-Na Chai Dong-Lin Du Xiao-Min Yang Lang Cao Hong Chen Chao Zhou Chong-Jie Cheng Xiao-Chuan Sun Zhi-Jian Huang Jian-Jun Zhong Department of Neurosurgery First Affiliated Hospital of Chongqing Medical UniversityChongqingChina Department of Ophthalmology First Affiliated Hospital of Chongqing Medical UniversityChongqingChina

Micro RNA-491-5 p(miR-491-5 p) plays an important role in regulating cell proliferation and migration;however,the effect of miR-491-5 p on neovascularization after traumatic brain injury remains poorly understood.In this study,a controlled cortical injury model in C57 BL/6 mice and an oxygen-glucose deprivation model in microvascular endothelial cells derived from mouse brain were established to simulate traumatic brain injury in vivo and in vitro,respectively.In the in vivo model,quantitative real-time-polymerase chain reaction results showed that the expression of miR-491-5 p increased or decreased following the intracerebroventricular injection of an miR-491-5 p agomir or antagomir,respectively,and the expression of miR-491-5 p decreased slightly after traumatic brain injury.To detect the neuroprotective effects of miR-491-p,neurological severity scores,Morris water maze test,laser speckle techniques,and immunofluorescence staining were assessed,and the results revealed that miR-491-5 p downregulation alleviated neurological dysfunction,promoted the recovery of regional cerebral blood flow,increased the number of lectin-stained microvessels,and increased the survival of neurons after traumatic brain injury.During the in vitro experiments,the potential mechanism of miR-491-5 p on neovascularization was explored through quantitative real-time-polymerase chain reaction,which showed that miR-491-5 p expression increased or decreased in brain microvascular endothelial cells after transfection with an miR-491-5 p mimic or inhibitor,respectively.Dual-luciferase reporter and western blot assays verified that metallothionein-2 was a target gene for miR-491-5 p.Cell counting kit 8(CCK-8) assay,flow cytometry,and 2′,7′-dichlorofluorescein diacetate(DCFH-DA) assay results confirmed that the downregulation of miR-491-5 p increased brain microvascular endothelial cell viability,reduced cell apoptosis,and alleviated oxidative stress under oxygen-glucose deprivation conditions.Cell scratch assay,Transwell assay,tube formation

关键词： brain injury cell migration cell proliferation endothelial cell hypoxia-inducible factor-1 alpha metallothionein 2 microRNA neovascularization neurons vascular endothelial growth factor

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Bioactive extracellular matrix scaffolds engineered with proangiogenic proteoglycan mimetics and loaded with endothelial progenitor cells promote neovascularization and diabetic wound healing

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Bioactive Materials 2022年第4期7卷 460-473页

作者： Siqi He Tanaya Walimbe Hongyuan Chen Kewa Gao Priyadarsini Kumar Yifan Wei Dake Hao Ruiwu Liu Diana L.Farmer Kit S.Lam Jianda Zhou Alyssa Panitch Aijun Wang Department of Burns and Plastic Surgery The Third Xiangya Hospital of Central South UniversityChina Department of Surgery UC DavisUnited States Department of Biomedical Engineering UC DavisUnited States Department of Biochemistry and Molecular Medicine UC DavisUnited States Institute for Pediatric Regenerative Medicine Shriners Hospitals for Children Northern CaliforniaUnited States

Diabetic ischemic wound treatment remains a critical clinical challenge.neovascularization plays a significant role in wound healing during all stages of the tissue repair process.Strategies that enhance angiogenesis and neovascularization and improve ischemic pathology may promote the healing of poor wounds,particularly diabetic wounds in highly ischemic conditions.We previously identified a cyclic peptide LXW7 that specifically binds to integrinαvβ3 on endothelial progenitor cells(EPCs)and endothelial cells(ECs),activates vascular endothelial growth factor(VEGF)receptors,and promotes EC growth and maturation.In this study,we designed and synthesized a multi-functional pro-angiogenic molecule by grafting LXW7 and collagen-binding peptides(SILY)to a dermatan sulfate(DS)glycosaminoglycan backbone,named LXW7-DS-SILY,and further employed this multi-functional molecule to functionalize collagen-based extracellular matrix(ECM)scaffolds.We confirmed that LXW7-DS-SILY modification significantly promoted EPC attachment and growth on the ECM scaffolds in vitro and supported EPC survival in vivo in the ischemic environment.When applied in an established Zucker Diabetic Fatty(ZDF)rat ischemic skin flap model,LXW7-DS-SILY-functionalized ECM scaffolds loaded with EPCs significantly improved wound healing,enhanced neovascularization and modulated collagen fibrillogenesis in the ischemic environment.Altogether,this study provides a promising novel treatment to accelerate diabetic ischemic wound healing,thereby reducing limb amputation and mortality of diabetic patients.

关键词： Diabetic ischemic wound ECM scaffold Endothelial progenitor cells neovascularization Wound healing

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MicroRNAs in laser-induced choroidal neovascularization in mice and rats:their expression and potential therapeutic targets

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Neural Regeneration Research 2021年第4期16卷 621-627页

作者： Bridget Martinez Philip V.Peplow Physical Chemistry and Applied Spectroscopy Chemistry DivisionLos Alamos National LaboratoryLos AlamosNMUSA Department of Medicine St.Georges University School of MedicineGrenada Department of Anatomy University of OtagoDunedinNew Zealand

Choroidal neovascularization characterizes wet age-related macular degeneration.Choroidal neovascularization formation involves a primarily angiogenic process that is combined with both inflammation and proteolysis.A primary cause of choroidal neovascularization pathogenesis is alterations in pro-and anti-angiogenic factors derived from the retinal pigment epithelium,with vascular endothelium growth factor being mainly responsible for both clinical and experimental choroidal neovascularization.MicroRNAs(miRNAs)which are short,non-coding,endogenous RNA molecules have a major role in regulating various pathological processes,including inflammation and angiogenesis.A review of recent studies with the mouse laser-induced choroidal neovascularization model has shown alterations in miRNA expression in choroidal neovascularization tissues and could be potential therapeutic targets for wet age-related macular degeneration.Upregulation of miR-505(days 1 and 3 post-laser),miR-155(day 14)occurred in retina;miR-342-5p(days 3 and 7),miR-126-3p(day 14)in choroid;miR-23a,miR-24,miR-27a(day 7)in retina/choroid;miR-505(days 1 and 3)in retinal pigment epithelium/choroid;downregulation of miR-155(days 1 and 3),miR-29a,miR-29b,miR-29c(day 5),miR-93(day 14),miR-126(day 14)occurred in retinal pigment epithelium/choroid.Therapies using miRNA mimics or inhibitors were found to decrease choroidal neovascularization lesions.Choroidal neovascularization development was reduced by overexpression of miR-155,miR-188-5p,miR-(5,B,7),miR-126-3p,miR-342-5p,miR-93,miR-126,miR-195a-3p,miR-24,miR-21,miR-31,miR-150,and miR-184,or suppression of miR-505,miR-126-3p,miR-155,and miR-23/27.Further studies are warranted to determine miRNA expression in mouse laser-induced choroidal neovascularization models in order to validate and extend the reported findings.Important experimental variables need to be standardized;these include the strain and age of animals,gender,number and position of laser burns to the eye,laser parameters to induce choroidal neovascu

关键词： age-related macular degeneration angiogenesis animal model blood plasma choroid laser microRNAs neovascularization retina retinal pigment epithelium therapeutic targets vascular endothelial growth factor

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Effects of long non-coding RNA myocardial infarction-associated transcript on retinal neovascularization in a newborn mouse model of oxygen-induced retinopathy

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Neural Regeneration Research 2021年第9期16卷 1877-1881页

作者： Yu Di Yue Wang Xue Wang Qing-Zhu Nie Department of Ophthalmology Shengjing Hospital of China Medical UniversityShenyangLiaoning ProvinceChina

Whether long non-coding RNA myocardial infarction-associated transcript is involved in oxygen-induced retinopathy remains poorly understood. To validate this hypothesis, we established a newborn mouse model of oxygen-induced retinopathy by feeding in an oxygen concentration of 75 ± 2% from postnatal day 8 to postnatal day 12, followed by in normal air. On postnatal day 11, the mice were injected with the myocardial infarction-associated transcript siRNA plasmid via the vitreous cavity to knockdown long non-coding RNA myocardial infarction-associated transcript. Myocardial infarction-associated transcript siRNA transcription significantly inhibited myocardial infarctionassociated transcript mRNA expression, reduced the phosphatidylinosital-3-kinase, phosphorylated Akt and vascular endothelial growth factor immunopositivities, protein and mRNA expression, and alleviated the pathological damage to the retina of oxygen-induced retinopathy mouse models. These findings suggest that myocardial infarction-associated transcript is likely involved in the retinal neovascularization in retinopathy of prematurity and that inhibition of myocardial infarction-associated transcript can downregulate phosphatidylinosital-3-kinase, phosphorylated Akt and vascular endothelial growth factor expression levels and inhibit neovascularization. This study was approved by the Animal Ethics Committee of Shengjing Hospital of China Medical University, China(approval No. 2016 PS074 K) on February 25, 2016.

关键词： long non-coding RNA myocardial infarction-associated transcript neovascularization neurovascular prematurity retinopathy vascular development vascular endothelial growth factor

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Tracking the in vivo spatio-temporal patterns of neovascularization via NIR-II fluorescence imaging

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Nano Research 2020年第11期13卷 3123-3129页

作者： Mo Chen Sijia Feng Yimeng Yang Yunxia Li Jian Zhang Shiyi Chen Jun Chen Institute of Sports Medicine of Fudan University Department of Orthopaedic Sports MedicineHuashan HospitalFudan UniversityShanghai200041China

The in vivo spatio-temporal patterns of neovascularization are still poorly understood because it is limited to multi-scale techniques from the cellular level to living animal level.Owing to deep tissue-penetration and zero autofluorescence background,the second near-infrared(NIR-II,1,000–1,700 nm)fluorescence imaging recently shows promise in breaking through this dilemma by dynamically tracking the pathophysiological process of neovascularization in vivo.Here,NIR-II fluorescence imaging was recruited for monitoring blood vessels in order to visualize the vascular injury and quantitively assess neovascularization in mouse models of acute skeleton muscle contusion and hindlimb ischemia.The temporal analysis of real-time NIR-II fluorescence intensity demonstrated that the blood flow perfusion of ischemia area was able to rapidly restore to 96%of pre-ischemic state within one week.Moreover,the spatial analysis revealed that the lower and outer quadrants of ischemia area in the mouse model of hindlimb ischemia always had relatively high blood flow perfusion compared with other quadrants during three weeks post-ischemia,and even exceeded pre-ischemic quantity at 21 days post-ischemia.In conclusion,this in vivo imaging technique has significant potential utility for studying the spatio-temporal patterns of neovascularization in vivo.

关键词： bioimaging second near-infrared(NIR-II)fluorescence nanoprobes spatio-temporal neovascularization

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Therapeutic neovascularization promoted by injectable hydrogels

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Bioactive Materials 2018年第4期3卷 389-400页

作者： Amrita Pal Brent L.Vernon Mehdi Nikkhah School of Biological and Health Systems Engineering Arizona State UniversityArizona 85281USA

The aim of therapeutic neovascularization is to repair ischemic tissues via formation of new blood vessels by delivery of angiogenic growth factors,stem cells or expansion of pre-existing cells.For efficient neovascularization,controlled release of growth factors is particularly necessary since bolus injection of molecules generally lead to a poor outcome due to inadequate retention within the injured site.In this regard,injectable hydrogels,made of natural,synthetic or hybrid biomaterials,have become a promising solution for efficient delivery of angiogenic factors or stem and progenitor cells for in situ tissue repair,regeneration and neovascularization.This review article will broadly discuss the state-of-the-art in the development of injectable hydrogels from natural and synthetic precursors,and their applications in ischemic tissue repair and wound healing.We will cover a wide range of in vitro and in vivo studies in testing the functionalities of the engineered injectable hydrogels in promoting tissue repair and neovascularization.We will also discuss some of the injectable hydrogels that exhibit self-healing properties by promoting neovascularization without the presence of angiogenic factors.

关键词： Injectable hydrogels neovascularization Tissue regeneration Angiogenic factors Cell-therapy

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Complement factor B knockdown by short hairpin RNA inhibits laser-induced choroidal neovascularization in rats

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International Journal of Ophthalmology(English edition) 2020年第3期13卷 382-389页

作者： Xin Wang Qing-Li Shang Jing-Xue Ma Shu-Xia Liu Cai-Xia Wang Cheng Ma Department of Ophthalmology the Second Hospital of Hebei Medical UniversityShijiazhuang 050000Hebei ProvinceChina Department of Pathology Hebei Medical UniversityShijiazhuang 050017Hebei ProvinceChina Department of Ophthalmology Tianjin First Central HospitalTianjin 300192China

AIM:To evaluate whether recombinant complement factor B(CFB)short hairpin RNA(sh RNA)reduces laserinduced choroidal neovascularization(CNV)in rats.METHODS:Laser-induced rat CNV model was established,and then the animals underwent fundus fluorescence angiography(FFA)and hematoxylin and eosin(HE)staining.On day 3 and 7 after photocoagulation,the expression of CFB and membrane attack complex(MAC)was detected by immunhischemistry.A recombinant CFBsh RNA plasmid was constructed.CFB and scrambled sh RNA plasmids were intravenous injected into rats via the tail vein on the day of laser treatment,respectively.On day 7,the incidence of CNV was determined by FFA,and the expression of CFB and vascular endothelial growth factor(VEGF)in retinal pigment epithelium(RPE)/choroidal tissues was detected by immunhischemistry,Western blot and/or semi-quantitative reverse transcription-polymerase chain reaction(RT-PCR)in CFB and scrambled sh RNA groups.The possible adverse effects of CFB-sh RNA injection were assessed by transmission electron microscopy and electroretinography.RESULTS:FFA and HE results indicated that a laserinduced rat CNV model was successfully established on day 7 after photocoagulation.The expression of CFB and MAC was extremely weak in normal retina and choroid,and increased on day 3 after photocoagulation.However,it started to reduce on day 7.CFB sh RNA plasmid was successfully constructed and induced CFB knockdown in the retinal and choroidal tissues.FFA showed CFB knockdown significantly inhibited incidence of CNV in rats.Moreover,CFB knockdown significantly inhibited the expression of VEGF in RPE/choroidal tissues.CFB sh RNA caused no obvious side effects in eyes.CONCLUSION:CFB knockdown significantly inhibits the formation and development of CNV in vivo through reducing the expression of VEGF,which is a potential therapy target.The alternative pathway of complement activation plays an important role in CNV formation.

关键词： choroidal neovascularization complement factor B short hairpin RNA membrane attack complex vascular endothelial growth factor

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Microarray expression profile and functional analysis of circular RNAs in choroidal neovascularization

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The Journal of Biomedical Research 2020年第1期34卷 67-74页

作者： Jiancheng Huang Meng Chen Kai Xu Rongmei Zhou Shujie Zhang Chen Zhao Department of Ophthalmology the First Affiliated Hospital of Nanjing Medical UniversityState Key Laboratory of Reproductive MedicineNanjingJiangsu 210029China Eye Institute Eye and ENT HospitalShanghai Medical CollegeFudan UniversityShanghai 200031China NHC Key Laboratory of Myopia(Fudan University) Key Laboratory of MyopiaChinese Academy of Medical Sciencesand Shanghai Key Laboratory of Visual Impairment and Restoration(Fudan University)Shanghai 200032China.

Choroidal neovascularization(CNV) is a leading cause of visual loss in age-related macular degeneration(AMD). However, the molecular mechanism for CNV progression is still unclear. This study aimed to identify CNV-related circular RNAs(circRNAs), a novel class of non-coding RNAs with diverse functions. A total of 117 circRNAs were differentially expressed in the murine CNV model by microarrays. Gene ontology(GO)enrichment and Kyoto Encyclopedia of Genes and Genomes(KEGG) analysis were performed to identify the functions of selected circRNAs. The host genes of these circRNAs were predicted to be targeted to neurogenesis(ontology: biological process), proteinaceous extracellular matrix(ECM)(ontology: cellular component), and binding(ontology: molecular function). Differentially expressed circRNAs-mediated regulatory networks were enriched in ECM receptor interaction. Most of the dysregulated circRNAs could potentially bind to five different mi RNAs by Target Scan and mi Randa. Specifically, circ_15752 was identified in this circRNAs pool which may facilitate vascular endothelial cell proliferation, migration, and tube formation, suggesting a critical role in endothelial angiogenesis. Our work suggests that dysregulated circRNAs may be involved in CNV pathogenesis and serve as potential biomarkers for CNV.

关键词： circRNAs microarray choroidal neovascularization

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Abrupt visual loss during anti-vascular endothelial growth factor treatment for type 3 neovascularization

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International Journal of Ophthalmology(English edition) 2019年第3期12卷 480-487页

作者： Jae Hui Kim Young Suk Chang Jong Woo Kim Chul Gu Kim Dong Won Lee Department of Ophthalmology Kim's Eye Hospital Konyang University College of Medicine Department of Ophthalmology Konyang University College of Medicine

AIM: To investigate the incidence of abrupt visual loss and its associated factors, during anti-vascular endothelial growth factor(VEGF) treatment for type 3 neovascularization.METHODS: This retrospective study included 137 eyes that were newly diagnosed with type 3 neovascularization. All eyes were treated with anti-VEGF therapy. Abrupt visual loss was defined as loss of 5 or more lines in best-corrected visual acuity(BCVA) in comparison to the previous visit. The incidence and timing of abrupt visual loss as well as the factors associated with it, were determined. In addition, the BCVA at the final follow-up was compared between the eyes with and those without abrupt visual loss.RESULTS: The mean follow-up period was 42.4±18.9 mo after diagnosis, and abrupt visual loss was noted in 22 eyes(16.1%) at a mean of 19.6±13.9 mo. Abrupt visual loss was found to be associated with subretinal hemorrhage in 11 eyes(50.0%), development of or increase in the height of pigment epithelial detachment with fluid in 8 eyes(36.4%), and tears in the retinal pigment epithelium in 3 eyes(13.6%). The logarithm of minimum angle of resolution(logMAR) mean BCVA at the final follow-up was 2.07±0.67(Snellen equivalents: 20/2349) and 1.00±0.55(20/200) in eyes with and without abrupt visual loss, respectively. BCVA was significantly worse in the eyes with abrupt visual loss(Pneovascularization and is associated with poor visual outcome. Additional studies are needed to determine how abrupt visual loss can be prevented.

关键词： age-related macular degeneration type 3 neovascularization retinal angiomatous proliferation hemorrhage tear in retinal pigment epithelium pigment epithelial detachment

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Recombinant Human Erythropoietin Augments neovascularization Responses in a Neonatal Rat Model of Premature Brain Damage by Phosphatidylinositol 3 Kinase/Akt Pathway

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Chinese Medical Journal 2017年第7期130卷 854-858页

作者： Da-Fan Yu Li-Hua Zhu Li Jiang Department of Clinical Medcine Medical School of Southeast University Jiangsu 210009 China 2Department of Pediatrics Zhongda Hospital Southeast University Nanjing Jiangsu 210009 China

Background：Recombinant human-erythropoietin （rh-EPO） has therapeutic efficacy for premature infants with brain damage during the active rehabilitation and anti-inflammation.In the present study,we found that the rh-EPO was related to the promotion ofneovascularization.Our aim was to investigate whether rh-EPO augments neovascularization in the neonatal rat model of premature brain damage through the phosphatidylinositol 3 kinase （PI3K）/protein kinase B （Akt） signaling pathway.Methods：Postnatal day 5 （PD5）,rats underwent permanent ligation of the right common carotid artery and were exposed to hypoxia for 2 h.All the rat pups were randomized into five groups as follows：（1） control group;（2） hypoxia-ischemic （HI） group;（3） HI ＋ LY294002 group;（4） HI ＋ rh-EPO group;and （5） HI ＋ rh-EPO ＋ LY294002 group.The phospho-Akt protein was tested 90 min after the whole operation,and CD34,vascular endothelial growth factor receptor 2 （VEGFR2）,and vascular endothelial growth factor （VEGF） were also tested 2 days after the whole operation.Results：In the hypoxic and ischemic zone of the premature rat brain,the rh-EPO induced CD34＋ cells to immigrate to the HI brain zone （P 〈 0.05） and also upregulated the VEGFR2 protein expression （P 〈 0.05） and VEGF mRNA level （P 〈 0.05） through the PI3K/Akt （P 〈 0.05） signaling pathway when compared with other groups.Conclusions：The rh-EPO treatment augments neovascularization responses in the neonatal rat model of premature brain damage through the PI3K/Akt signaling pathway.Besides,the endogenous EPO may exist in the HI zone of rat brain and also has neovascularization function through the PI3K/Akt signaling pathway.

关键词： Erythropoietin Hypoxia-ischemia neovascularization Premature Brain

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