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( Wonjin Park ),( Yi-yong Baek ),( Joohwan Kim ),( Dong Hyun Jo ),( Seunghwan Choi ),( Jin Hyoung Kim ),( Taesam Kim ),( Suji Kim ),( Minsik Park ),( Ji Yoon Kim ),( Moo-ho Won ),( Kwon-soo Ha ),( Jeo 한국응용약물학회 2019 Biomolecules & Therapeutics(구 응용약물학회지) Vol.27 No.5
Vascular endothelial growth factor (VEGF) plays a pivotal role in pathologic ocular neovascularization and vascular leakage via activation of VEGF receptor 2 (VEGFR2). This study was undertaken to evaluate the therapeutic mechanisms and effects of the tetrapeptide Arg-Leu-Tyr-Glu (RLYE), a VEGFR2 inhibitor, in the development of vascular permeability and choroidal neovascularization (CNV). In cultured human retinal microvascular endothelial cells (HRMECs), treatment with RLYE blocked VEGF-Ainduced phosphorylation of VEGFR2, Akt, ERK, and endothelial nitric oxide synthase (eNOS), leading to suppression of VEGFA- mediated hyper-production of NO. Treatment with RLYE also inhibited VEGF-A-stimulated angiogenic processes (migration, proliferation, and tube formation) and the hyperpermeability of HRMECs, in addition to attenuating VEGF-A-induced angiogenesis and vascular permeability in mice. The anti-vascular permeability activity of RLYE was correlated with enhanced stability and positioning of the junction proteins VE-cadherin, β-catenin, claudin-5, and ZO-1, critical components of the cortical actin ring structure and retinal endothelial barrier, at the boundary between HRMECs stimulated with VEGF-A. Furthermore, intravitreally injected RLYE bound to retinal microvascular endothelium and inhibited laser-induced CNV in mice. These findings suggest that RLYE has potential as a therapeutic drug for the treatment of CNV by preventing VEGFR2-mediated vascular leakage and angiogenesis.
Kim, Suji,Lee, Kyu-Sun,Choi, Seunghwan,Kim, Joohwan,Lee, Dong-Keon,Park, Minsik,Park, Wonjin,Kim, Tae-Hoon,Hwang, Jong Yun,Won, Moo-Ho,Lee, Hansoo,Ryoo, Sungwoo,Ha, Kwon-Soo,Kwon, Young-Guen,Kim, Youn American Society for Biochemistry and Molecular Bi 2018 The Journal of biological chemistry Vol.293 No.49
<P>Inflammatory cytokines, including tumor necrosis factor-α (TNFα), were elevated in patients with cardiovascular diseases and are also considered as crucial factors in the pathogenesis of preeclampsia; however, the underlying pathogenic mechanism has not been clearly elucidated. This study provides novel evidence that TNFα leads to endothelial dysfunction associated with hypertension and vascular remodeling in preeclampsia through down-regulation of endothelial nitric-oxide synthase (eNOS) by NF-κB–dependent biogenesis of microRNA (miR)-31-5p, which targets eNOS mRNA. In this study, we found that miR-31-5p was up-regulated in sera from patients with preeclampsia and in human endothelial cells treated with TNFα. TNFα-mediated induction of miR-31-5p was blocked by an NF-κB inhibitor and NF-κB p65 knockdown but not by mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase inhibitors, indicating that NF-κB is essential for biogenesis of miR-31-5p. The treatment of human endothelial cells with TNFα or miR-31-5p mimics decreased endothelial nitric-oxide synthase (eNOS) mRNA stability without affecting <I>eNOS</I> promoter activity, resulting in inhibition of eNOS expression and NO/cGMP production through blocking of the functional activity of the eNOS mRNA 3′-UTR. Moreover, TNFα and miR-31-5p mimic evoked endothelial dysfunction associated with defects in angiogenesis, trophoblastic invasion, and vasorelaxation in an <I>ex vivo</I> cultured model of human placental arterial vessels, which are typical features of preeclampsia. These results suggest that NF-κB–responsive miR-31-5p elicits endothelial dysfunction, hypertension, and vascular remodeling via post-transcriptional down-regulation of eNOS and is a molecular risk factor in the pathogenesis and development of preeclampsia.</P>
Kim, WonJin,Lee, Hyeongjin,Kim, YongBok,Choi, Chang Hyun,Lee, DaeWeon,Hwang, Heon,Kim, GeunHyung IOP Publishing 2016 Biomedical materials Vol.11 No.5
<P>In recent years, a variety of biomimetic hydrogel scaffolds have been used in tissue engineering because hydrogels can provide reasonable soft-tissue-like environmental conditions for various cell responses. However, although hydrogels can provide an outstanding biofunctional platform, their poor mechanical stability and low processability have been obstacles for their usage as biomedical scaffolds. To overcome this limitation, we propose a simple and versatile method using 3D printing supplemented with a low-temperature working plate and coating process to reinforce the mechanical properties and various cellular activities by accommodating the poly(epsilon-caprolactone) (PCL). To determine the efficiency of the method, we used two typical hydrogels (alginate and collagen), which were deposited in a multi-layer configuration, and PCL as a coating agent. The scaffolds were evaluated in terms of various physical and cellular activities (metabolic activity and osteogenic activity). Throughout the experiments, significant increases in the tensile modulus (> 6-fold), cell proliferation (> 1.2-fold), and calcium deposition (> 1.3-fold) were observed for the hydrogel/PCL scaffolds compared to those for pure hydrogel. Based on the experimental results, we can confirm that the proposed hydrogel scaffold can be a highly promising biomedical scaffold for application in tissue regeneration.</P>
WonJin Kim(김원진),JiUn Lee(이지운),Gi-Hoon Yang(양지훈),Hyeongjin Lee(이형진),YongBok Kim(김용복),Minseong Kim(김민성),YoungWon Koo(구영원),GeunHyung Kim(김근형) 대한기계학회 2016 대한기계학회 춘추학술대회 Vol.2016 No.12
Collagen- based cell-printing technology has provided a new strategy for tissue engineering. However, although collagen-based scaffolds can provide an outstanding biofunctional benefits, their low mechanical strength and poor controllability have been limitation for their usage as hard tissue regeneration. To overcome this limitation, α-tricalcium phosphate (α-TCP) has been used for biomedical scaffolds. α-TCP is biocompatible and soluble material, and hydrolyzed rapidly to calcium-deficient hydroxyapatite which makes α-TCP a useful material for bone tissue regeneration. in this study, we fabricate 3-dimensional (3D) scaffold based on α-TCP/collagen struts coated with collagen-based bioink. To compare the physical and cellular activities, we used a scaffold composed of α-TCP/collagen scaffold coated with cell-embedded collagen. Following fabrication of the cell (MC3T3-E1)-embedded a-TCP/collagen scaffold, the cellular activities were evaluated in vitro.