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Annexin A2 silencing enhances apoptosis of human umbilical vein endothelial cells in vitro

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Asian Pacific Journal of Tropical Medicine 2015年第11期8卷 929-933页

作者： Shu-Le Jiang Dong-Yan Pan Chao Gu Hai-Feng Qin Shi-Hong Zhao Department of Ophthalmology Affiliated Changhai Hospital of Second Military Medical University

Objective:To study the effects of inhibited Annexin A2(ANXA2) on human umbilical vein endothelial cells(HUVECs) in vitro.Methods:Short hairpin RNA(shRNA) targeting ANXA2 was designed and cloned into double marked lentvirial vector GV248 for RNAi to generate the recombinant expression plasmids,which were stably transfected into HUVECs.The protein and mRNA expression levels of ANXA2 were analyzed by western blotting and realtime polymerase chain reaction,respectively.Cell proliferation(cell counting kit-8 assay),apoptosis(flow cytometry analysis),the expression(western blotting) and the activity of easpases(enzyme-linked immunosorbent assay) were used to assess the effects of silencing ANXA2 on HUVECs in vitro.Results:The plasmids to express ANXA2-specific shRNA were constructed and were infected into HUVEC resulting in the stably transfected experimental(ANXA2-shRNA),control(eontrol-shRNA) and mock(no plasmid) cell lines,which were verified with western blot and real-time PCR.HUVEC/ANXA2-shRNA showed an inhibition rate 91.89%of ANXA2 expression compared to the mock HUVEC.ANXA2 silencing cell strain obviously presented a lower cell proliferation activity compared to the control and mock HUVECs,with an inhibition rate 82.35%on day 7 in vitro.FACS analysis indicated that the HUVEC/ANXA2-shRNA cells undergoing apoptosis increased by 102.61%compared to the mock HUVECs(P<0.01).Moreover,the activity levels of caspase-3,caspase-8 and caspase-9in HUVEC/ANXA2-shRNA cells were increased and the activated cleaved caspase-3,cleaved Caspase-8 and cleaved caspase-9 were upregulated evidently compared with that of the control and mock HUVECs by 56.29%,89.59%and 144.58%(P<0.01).Conclusions:shRNAmediated silencing of ANX A2 could not only be able to suppress HUVECs:proliferation but to upregulate the enzyme activity of easpases,which bring to an increase of cell apoptosis This work suggested that ANX A2 may represent a useful target of future molecular therapies.

关键词： Retinal neovascularization Annexin A2 RNA interfer

Attenuation of periostin in retinal Müller glia by TNF-α and IFN-γ

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International Journal of Ophthalmology(English edition) 2019年第2期12卷 212-218页

作者： Ying-Qian Peng Man-Jing Cao Shigeo Yoshida Lu-Si Zhang Hui-Lan Zeng Jing-Ling Zou Yoshiyuki Kobayashi Takahito Nakama Jing-Ming Shi Song-Bai Jia Ye-Di Zhou Department of Ophthalmology the Second Xiangya Hospital Central South University Hunan Clinical Research Center of Ophthalmic Disease Department of Ophthalmology Kyushu University Graduate School of Medical Sciences Department of Ophthalmology Kurume University School of Medicine

AIM: To investigate the regulation and mechanisms of periostin expression in retinal Müller glia, and to explore the relevance to retinal neovascularization. METHODS: The oxygen-induced retinopathy(OIR) mouse model and the human Moorfield/Institute of Ophthalmology-Müller 1(MIO-M1) cell line were used in the study. Immunofluorescence staining was used to determine the distribution and expression of periostin and a Müller glial cell marker glutamine synthetase(GS). Cytokines TNF-α and IFN-γ were added to stimulate the MIO-M1 cells. ShRNA was used to knockdown periostin expression in MIO-M1 cells. Quantitative real-time reverse transcription polymerase chain reaction(qRT-PCR) was conducted to assess the mRNA expression of periostin. RESULTS: Immunofluorescence staining showed that periostin was expressed by MIO-M1 Müller glia. GS-positive Müller glia and periostin increased in OIR retinas, and were partially overlaid. The stimulation of TNF-α and IFN-γ reduced the mRNA expression of periostin significantly and dose-dependently in MIO-M1 cells. Knockdown of periostin reduced mRNA expression of vascular endothelial growth factor A(VEGFA) in MIO-M1 cells, while VEGFA expression was not changed in periostin knock-out OIR retinas. CONCLUSION: Müller glia could be one of the main sources of periostin in the retina, and might contribute to the pathogenesis of retinal neovascularization. Proinflammatory cytokines TNF-α and IFN-γ attenuate the periostin expression in retinal Müller glia, which provides a potential and novel method in treating retinal neovascular diseases.

关键词： TNF-α IFN-γ periostin Müller glia retinal neovascularization

Clinical correlates of common corneal neovascular diseases: a literature review

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International Journal of Ophthalmology(English edition) 2015年第1期8卷 182-193页

作者： Nizar Saleh Abdelfattah Mohamed Amgad Amira A Zayed Hamdy Salem Ahmed E Elkhanany Heba Hussein Nawal Abd El-Baky Doheny Image Reading Center Doheny Eye InstituteUniversity of California Faculty of Medicine Cairo University Department of Surgery Mayo Clinic Faculty of Medicine University of Alexandria Department of Medical Oncology Mayo Clinic Faculty of Oral and Dental Medicine Cairo University Antibody Laboratory Protein Research DepartmentGenetic Engineering and Biotechnology Research InstituteCity for Scientific Research and Technology Applications

A large subset of corneal pathologies involves the formation of new vessels(neovascularization), leading to compromised visual acuity. This article aims to review the clinical causes and presentations of corneal neovascularization(CNV) by examining the mechanisms behind common CNV-related corneal pathologies, with a particular focus on herpes simplex stromal keratitis,contact lenses-induced keratitis and CNV secondary to keratoplasty. Moreover, we reviewed CNV in the context of different types of corneal transplantation and keratoprosthesis, and summarized the most relevant treatment available so far.

关键词： cornea neovascularization herpes simplex keratitis keratoplasty contact lens keratoprosthesis

LncRNAs in ocular neovascularizations

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International Journal of Ophthalmology(English edition) 2019年第12期12卷 1959-1965页

作者： Yacouba Cissé Lang Bai Min-Ting Chen Department of Ophthalmology Nanfang Hospital Southern Medical University

The prevalence of eye diseases worldwide is dramatically increasing and represents a major concern in underdeveloped and developed regions. Ocular diseases, previously associated with a higher depression risk, also impose a substantial economic burden on affected families, thus early detection and/or accurate treatment in order to avoid and prevent blindness should be emphasized. Ocular neovascularization(NV), the leading cause of blindness in a variety of eye diseases, is a pathologic process characterized by the formation, proliferation and infiltration of anomalous, tiny and leaky fragile blood vessels within the eye. Genetics have been suspected to play an important role in the occurrence of eye diseases, with the detection of a numbers of specific gene mutations. Long non-coding RNA(lnc RNAs) are novel class of regulatory molecules previously associated with various biological processes and diseases, however the nature of the relation and pathways by which they might contribute to the development of corneal, choroidal and retinal NV have not yet been completely elucidated. In this review, we focus on the regulation and characteristics of lncR NAs, summarize results from ocular NV-related studies and discuss the implication of lncR NAs in ocular NV development.

关键词： glaucoma genetics long non-coding RNA neovascularization

Effect of sorafenib in a murine high risk penetrating keratoplasty model

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International Journal of Ophthalmology(English edition) 2017年第6期10卷 834-839页

作者： Yang Kyung Cho Eun Young Shin Hironori Uehara Balamurali K Ambati Department of Ophthalmology St.Vincent’s HospitalCollege of Medicinethe Catholic University of Korea Research Institute of Medical Science St.Vincent's HospitalCollege of Medicinethe Catholic University of Korea Department of Ophthalmology University of UtahSchool of Medicine

AIM： To evaluate the effect of sorafenib in murine high risk keratoplasty model. ~ METHODS： Graft survival, corneal neovascularization, and corneal lymphangiogenesis were compared among the sorafenib, dexamethasone, dimethyl sulfoxide （DMSO）, and phosphate buffered saline （PBS） groups following subconjunctival injection in mice that underwent high risk penetrating keratoplasty （HRPK）. Real-time polymerase chain reaction was performed to quantify the expression of inflammatory cytokines and vascular endothelial growth factor （VEGF）-A, VEGF-C, vascular endothelial growth factor receptor （VEGFR）-2, VEGFR-3. RESULTS： The two-month graft survival rate for HRPK was 42.86% in sorafenib group, 37.50% in dexamethasone group, 0 in DMSO group, and 0 in PBS group. Sorafenib significantly increased graft survival compared to the DMSO and PBS group （P〈0.05）. The sorafenib didn＇t show significant effect in decreasing neovascularization compared with dexamethsone, DMSO, and PBS group. The sorafenib showed less total lymphangiogenesis than the dexamethasone, DMSO, and PBS group （P=0.011, P〈0.001, P〈0.001, respectively）. The sorafenib group showed reduced expression of VEGF-C, tumor necrosis factor （TNF）-alpha, interleukin （IL）-6, VEGFR-2 and VEGFR-3 compared with DMSO group and PBS group （all P〈0.05）. The sorafenib group didn＇t show difference in the expression of VEGF-A compared with DMSO, neither withPBS. The sorafenib group showed reduced expression of VEGFR-3 compared with dexamethasone （/〉=-0.051）. CONCLUSION： The subconjunctivally administered sorafenib shows significant anti-lymphangiogenic effect, resulting in increased transplant survival in a murine high risk keratoplasty model. We suggest that a close linkage between decreased VEGF-C/VEGFR-2 and -3 signaling and increased corneal graft survival by sorafenib seems to exist.

关键词： Sorafenib neovascularization graft survival lymphangiogenesis dexamethasone

Molecular underpinnings of corneal angiogenesis:advances over the past decade

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International Journal of Ophthalmology(English edition) 2016年第5期9卷 768-779页

作者： Nizar Saleh Abdelfattah Mohamed Amgad Amira A.Zayed Heba Hussein Nawal AbdEl-Baky Doheny Image Reading Center Doheny Eye Institute Faculty of Medicine Cairo University Department of Oncology Mayo ClinicRochester Faculty of Oral and Dental Medicine Cairo University Antibody Laboratory Protein Research DepartmentGenetic Engineering and Biotechnology Research InstituteCity for Scientific Research and Technology Applications

The cornea is maintained in an avascular state by maintaining an environment whereby anti-angiogenic factors take the upper hand over factors promoting angiogenesis. Many of the common pathologies affecting the cornea involve the disruption of such equilibrium and the shift towards new vessel formation, leading to corneal opacity and eventually-vision loss. Therefore it is of paramount importance that the molecular underpinnings of corneal neovascularization（CNV） be clearly understood, in order to develop better targeted treatments. This article is a review of the literature on the recent discoveries regarding pro-angiogenic factors of the cornea（such as vascular endothelial growth factors,fibroblast growth factor and matrix metalloproteinases）and anti-angiogenic factors of the cornea（such as endostatins and neostatins）. Further, we review the molecular underpinnings of lymphangiogenesis, a process now known to be almost separate from（yet related to） hemangiogenesis.

关键词： cornea neovascularization angiogenesis lymphangiogenesis vascular endothelial growth factor

Identification of altered microRNAs in retinas of mice with oxygen-induced retinopathy

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International Journal of Ophthalmology(English edition) 2019年第5期12卷 739-745页

作者： Lu-Si Zhang Ye-Di Zhou Ying-Qian Peng Hui-Lan Zeng Shigeo Yoshida Tan-Tai Zhao Department of Ophthalmology the Second Xiangya Hospital of Central South University Hunan Clinical Research Center of Ophthalmic Disease Department of Ophthalmology Kurume University School of Medicine

AIM: To identify disease-related miRNAs in retinas of mice with oxygen-induced retinopathy(OIR), and to explore their potential roles in retinal pathological neovascularization. METHODS: The retinal miRNA expression profile in mice with OIR and room air controls at postnatal day 17(P17) were determined through miRNA microarray analysis. Several miRNAs were significantly up-and down-regulated in retinas of mice with OIR compared to controls by quantitative real-time reverse transcription-polymerase chain reaction(qRT-PCR). Two databases including Targetscan7.1 and MirdbV5 were used to predict target genes that associated with those significantly altered mi RNAs in retinas of mice with OIR. Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway analyses were also conducted to identify possible biological functions of the target genes. RESULTS: In comparison with room air controls, 3 and 8 miRNAs were significantly up-and down-regulated, respectively, in retinas of mice with OIR. The qRT-PCR data confirmed that mmu-miR-350-3 p and mmu-miR-202-3 p were significantly up-regulated, while mmu-miR-711 and mmu-miR-30 c-1-3 p were significantly down-regulated in mice with OIR compared to controls. GO analysis demonstrated that the identified target genes were related to functions such as cellular macromolecule metabolic process. KEGG pathway analysis showed a group of pathways, such as Wnt signaling pathway, transcriptionalmisregulation in cancer, Mucin type O-glycan biosynthesis, and mitogen-activated protein kinase(MAPK) signaling pathway might be involved in pathological process of retinal neovascularization. CONCLUSION: Our findings suggest that the differentially expressed miRNAs in retinas of mice with OIR might provide potential therapeutic targets for treating retinal neovascularization.

关键词： microRNAs retinal neovascularization oxygen-induced retinopathy microarray

Lotus seedpod-inspired internal vascularized 3D printed scaffold for bone tissue repair

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Bioactive Materials 2021年第6期6卷 1639-1652页

作者： Xiaoyu Han Mingjie Sun Bo Chen Qimanguli Saiding Junyue Zhang Hongliang Song Lianfu Deng Peng Wang Weiming Gong Wenguo Cui Department of Orthopedics Jinan Central HospitalShandong First Medical University&Shandong Academy of Medical Sciences105 Jiefang RoadLixia DistrictJinanShandong250013PR China Shanghai Key Laboratory for Prevention and Treatment of Bone and Joint Diseases Shanghai Institute of Traumatology and OrthopedicsRuijin HospitalShanghai Jiao Tong University School of Medicine197 Ruijin 2nd RoadShanghai200025PR China

In the field of bone defect repair,3D printed scaffolds have the characteristics of personalized customization and accurate internal structure.However,how to construct a well-structured vascular network quickly and effectively inside the scaffold is essential for bone repair after transplantation.Herein,inspired by the unique biological structure of“lotus seedpod”,hydrogel microspheres encapsulating deferoxamine(DFO)liposomes were prepared through microfluidic technology as“lotus seeds”,and skillfully combined with a three-dimensional(3D)printed bioceramic scaffold with biomimetic“lotus”biological structure which can internally grow blood vessels.In this composite scaffold system,DFO was effectively released by 36%in the first 6 h,which was conducive to promote the growth of blood vessels inside the scaffold quickly.In the following 7 days,the release rate of DFO reached 69%,which was fundamental in the formation of blood vessels inside the scaffold as well as osteogenic differentiation of bone mesenchymal stem cells(BMSCs).It was confirmed that the composite scaffold could significantly promote the human umbilical vein endothelial cells(HUVECs)to form the vascular morphology within 6 h in vitro.In vivo,the composite scaffold increased the expression of vascularization and osteogenic related proteins Hif1-α,CD31,OPN,and OCN in the rat femoral defect model,significantly cutting down the time of bone repair.To sum up,this“lotus seedpod”inspired porous bioceramic 3D printed scaffold with internal vascularization functionality has broad application prospects in the future.

关键词： 3D scaffolds Drug release neovascularization Osteogenesis Regeneration

Phosphorylation of alphaB-crystallin in epiretinal membrane of human proliferative diabetic retinopathy

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International Journal of Ophthalmology(English edition) 2016年第8期9卷 1100-1105页

作者： Yoko Dong Zhenyu Dong Satoru Kase Ryo Ando Junichi Fukuhara Satoshi Kinoshita Saori Inafuku Yoshiaki Tagawa Erdal Tan Ishizuka Wataru Saito Miyuki Murata Atsuhiro Kanda Kousuke Noda Susumu Ishida Laboratory of Ocular Cell Biology and Visual Science Department of Ophthalmology Hokkaido University Graduate School of Medicine

AIMTo examine phosphorylation of alphaB-crystallin (p-αBC), a vascular endothelial growth factor (VEGF) chaperone, and immunohistochemically investigate relationship between p-αBC, VEGF and phosphorylated p38-mitogen-activated protein kinase (p-p38 MAPK) in the epiretinal membrane of human proliferative diabetic retinopathy (PDR).METHODSEleven epiretinal membranes of PDR surgically excised were included in this study. Two normal retinas were also collected from enucleation tissues due to choroidal melanoma. Paraformaldehyde-fixed, paraffin-embedded tissue sections were processed for immunohistochemistry with anti-p-αBC, VEGF, CD31, and p-p38 MAPK antibodies.RESULTSImmunoreactivity for p-αBC was observed in all of the epiretinal membranes examined, where phosphorylation on serine (Ser) 59 showed strongest immunoreactivity in over 70% of the membranes. The immunolocalization of p-αBC was detected in the CD31-positive endothelial cells, and co-localized with VEGF and p-p38 MAPK in PDR membranes. Immunoreactivity for p-αBC, however, was undetectable in endothelial cells of the normal retinas, where p-p38 MAPK immunoreactivity was less marked than PDR membranes.CONCLUSIONPhosphorylation of αBC, in particular, phosphorylation on Ser59 by p-p38 MAPK may play a potential role as a molecular chaperon for VEGF in the pathogenesis of epiretinal membranes in PDR.

关键词： phosphorylated alphaB-crystallin vascular endothelial growth factor neovascularization proliferative diabetic retinopathy