• Korean Journal of Environmental Biology
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• v.20 no.4
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• pp.386-390
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• 2002

The opening phenomenon of mature female cone in Pinus densiflora aye observed from the anatomical characteristics. The differentiation of tissue in young cone aye not complete and are going on. In the green cone as large as the adult cone, shrink-age rate of vascular strands and sclerenchyma aye 1.0∼1.5％ and 14.0∼16.0% respectively. The end parts of cone scales are composed of the parenchymatous cell and sclerenchyma. The middle parts in cone scales are composed of the sclerenchyma and vascular strands with the same thickness and more thin than the thickness of the end part and basal one. But thickness of sclerenchyma which compose of scale prop in the basal part of cone scale aye twice than that of vascular strand. In mature cone, the opening phenomenon of the pine cone results from the difference of shrinkage rate between vascular bundle and sclerenchyma. Especially, opening of cone scales are due to larger shrinkage rate of sclerenchyma than vascular strands in the basal part of cone scale.

• Journal of Plant Biology
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• v.31 no.4
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• pp.289-298
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• 1988

The pattern of elongation in the developing hypocotyl of Glycine max shows that the elongation generally proceeds from base to the cotyledonary node in acropetal diredtion, although earlier elongation takes place through the entire hypocotyl. Because the differentiation of the vascular cambium in the hypocotyl advances also acropetally, it can be seen that the acropetal wave of hypocotyl elongation is associated with the acropetal differentiation of the cambium in the hypocotyl elongation is associated with the acropetal differentiation of the cambium in the hypocotyl elongation is associated with the acropetal differentiation of the cambium in the hypocotyl. The elongation of procambial cells occurs not only during active elongation but also after cessation of elongation of the hypocotyl. In tangential view, the procambium of the hypocotyl in early stage has homogeneous structure composed of short cells. Subsequently, these procambial cells elongate actively and then become elongated long cells. These long cells eventually become fusiform initials, while some of elongated long cells are transversely divided and then converted into ray initials. The characteristics of the vascular cambium are entirely acquired some time after hypocotyl elongation is completed, and the transitin from procambium to vascular cambium in the hypocotyl is a rather gradual process.

• Journal of Plant Biology
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• v.26 no.4
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• pp.207-216
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• 1983

Mature embryo and developing seedlings of Ginkgo biloba L. were embedded in a paraplast and serially sectioned at 10${\mu}{\textrm}{m}$ to examine vascular differentiation and vascular transition. Procambium and protophloem formed a continuous system along the epicotylhypocotyl root axis and cotyledons in mature embryo, whereas protoxylem was differentiated discontinuously in the cotyledons and rarely in the upper hypocotyl. The traces of the first and second leaf primordia apeared almost at the same time oppositely to each otehr at the epicotyl and alternately with the cotyledon traces in the upper hypocotyl. The trace differentiated bidirectionally toward the epicotyl and root tips. the young root initially formed a diarch xylem. Then, as the traces of the first and second leaves were superimposed, the diarch xylem. Then, as the traces of the first and second leaves were superimposed, the diarch xylem of the root was changed totriarch and tetrarch xylem, respectively. On the formation of primary vascular system of Ginkgo biloba, it is suggested that the primary phloem forms a continuous system throughout the seedling, whereas the primary xylem of the epicotyl is formed independently from that of the root-hypocotyl cotyledon system.

• Molecules and Cells
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• v.37 no.3
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• pp.196-201
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• 2014

Pulmonary arterial hypertension (PAH) is a progressive disease characterized by the vascular remodeling of the pulmonary arterioles, including formation of plexiform and concentric lesions comprised of proliferative vascular cells. Clinically, PAH leads to increased pulmonary arterial pressure and subsequent right ventricular failure. Existing therapies have improved the outcome but mortality still remains exceedingly high. There is emerging evidence that the seven-transmembrane G-protein coupled receptor APJ and its cognate endogenous ligand apelin are important in the maintenance of pulmonary vascular homeostasis through the targeting of critical mediators, such as Kr$\ddot{u}$ppel-like factor 2 (KLF2), endothelial nitric oxide synthase (eNOS), and microRNAs (miRNAs). Disruption of this pathway plays a major part in the pathogenesis of PAH. Given its role in the maintenance of pulmonary vascular homeostasis, the apelin-APJ pathway is a potential target for PAH therapy. This review highlights the current state in the understanding of the apelin-APJ axis related to PAH and discusses the therapeutic potential of this signaling pathway as a novel paradigm of PAH therapy.

• BMB Reports
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• v.54 no.6
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• pp.285-294
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• 2021

The lymphatic vasculature plays important role in regulating fluid homeostasis, intestinal lipid absorption, and immune surveillance in humans. Malfunction of lymphatic vasculature leads to several human diseases. Understanding the fundamental mechanism in lymphatic vascular development not only expand our knowledge, but also provide a new therapeutic insight. Recently, Hippo-YAP/TAZ signaling pathway, a key mechanism of organ size and tissue homeostasis, has emerged as a critical player that regulate lymphatic specification, sprouting, and maturation. In this review, we discuss the mechanistic regulation and pathophysiological significant of Hippo pathway in lymphatic vascular development.

• Molecules and Cells
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• v.42 no.3
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• pp.218-227
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• 2019

This study was designed to determine the effects of the long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) on vascular smooth muscle cell (VSMC) apoptosis and extracellular matrix (ECM) disruption in a murine abdominal aortic aneurysm (AAA) model. After injection of PVT1-silencing lentiviruses, AAA was induced in Apolipoprotein E-deficient ($ApoE^{-/-}$) male mice by angiotensin II (Ang II) infusion for four weeks. After Ang II infusion, mouse serum levels of pro-inflammatory cytokines were analysed, and aortic tissues were isolated for histological, RNA, and protein analysis. Our results also showed that PVT1 expression was significantly upregulated in abdominal aortic tissues from AAA patients compared with that in controls. Additionally, Ang II treatment significantly increased PVT1 expression, both in cultured mouse VSMCs and in AAA murine abdominal aortic tissues. Of note, the effects of Ang II in facilitating cell apoptosis, increasing matrix metalloproteinase (MMP)-2 and MMP-9, reducing tissue inhibitor of MMP (TIMP)-1, and promoting switching from the contractile to synthetic phenotype in cultured VSMCs were enhanced by overexpression of PVT1 but attenuated by knockdown of PVT1. Furthermore, knockdown of PVT1 reversed Ang II-induced AAA-associated alterations in mice, as evidenced by attenuation of aortic diameter dilation, marked adventitial thickening, loss of elastin in the aorta, enhanced aortic cell apoptosis, elevated MMP-2 and MMP-9, reduced TIMP-1, and increased pro-inflammatory cytokines. In conclusion, our findings demonstrate that knockdown of lncRNA PVT1 suppresses VSMC apoptosis, ECM disruption, and serum pro-inflammatory cytokines in a murine Ang II-induced AAA model.

• BMB Reports
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• v.47 no.6
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• pp.311-317
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• 2014

microRNAs (miRNAs) are a class of small, non-coding RNAs that play critical posttranscriptional regulatory roles typically through targeting of the 3'-untranslated region of messenger RNA (mRNA). Mature miRNAs are known to be involved in global cellular processes, such as differentiation, proliferation, apoptosis, and organogenesis, due to their capacity to target multiple mRNAs. Thus, imbalances in the expression and/or activity of miRNAs are involved in the pathogenesis of numerous diseases, including pulmonary arterial hypertension (PAH). PAH is a progressive disease characterized by vascular remodeling due to excessive proliferation of pulmonary artery endothelial cells (PAECs) and pulmonary artery smooth muscle cells (PASMCs). Recently, studies have evaluated the roles of miRNAs involved in the pathogenesis of PAH in these pulmonary vascular cells. This review provides an overview of recent discoveries on the role of miRNAs in the pathogenesis of PAH and discusses the potential for miRNAs as therapeutic targets and biomarkers of PAH.

• Journal of Plant Biology
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• v.37 no.3
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• pp.371-380
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• 1994

To determine the patterns and the levels of expression of the cauliflower mosaic virus (CaMV 35S) promoter and the rice actin 1 (Act1) promoter in rice, transgenic rice plants containing CaMV 35S-$\beta$-glucuronidase (GUS) and Act1-GUS constructs were generated and examined by fluorometric and histochemical analyses. The fluorometric analysis of stably transformed calluses showed that the activity of the rice Act1 promoter was stronger than that of the CaMV 35S promoter in rice cells. In a histochemcial study of the transgenic rices, it was shown that the GUS activity directed by the CaMV 35S promoter was localized mainly in parenchymal cells of vascular tissues of leaves and roots and mesophyll cells of leaves. These results are similar to those of potato, a dicot plant. In contrast, rice plant transformed with Act1-GUS fusion construct revealed strong GUS activity in parenchymal cells of vascular tissue, mesophyll cells, epidermal cells, bulliform cells, guard subsidiary cells of leaves and most cells of the root, suggesting that the rice Act1 promoter is more constitutive than the CaMV 35S promoter. It was also confirmed that in both types of transgenic rice little or no staining was localized in metaxylen tracheary elements of vascular tissue from leaves or roots. These results indicate that the rice Act1 promoter can be utilized more successfully for expression of a variety of foreign gene in rice than the CaMV 35S promoter.

• The Korean Journal of Ecology
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• v.5 no.4
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• pp.143-153
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• 1982

Distributional pattern of vascular plant species in terms of species-area relationship and distances from their species pool on the 53 islands selected in the South Korea were studied. From the relationship between vascular plant species and area the equation of species-area was established as the follow: S=cA2 c=135.52 z=0.226 S; number of species A; area of island In the equation the Z value 0.226 is lower than those of any other localities reported in the world. Z value increased with the increasing distance from the species pool while C value decreased. The relationships of Z and/or C and distance from species pool, D, were established; Z=0.002D+0.176 C=-39.5logD+178.5 The tendency of common species decrease of them with the increasing islands was fifted to the Fisher's logarithm series. Common species 50% above was 39 species, including the most common species, Pinus thunbergii. Quotient of Similarity value by Sorensen (1948) on common species was relatively low i.e. 0.27∼0.47. It is noticeable for their vegetation conditions that the naturalized plant as a indicator of disturbance, for example Erigeron canadensis, was widely distributed.

• BMB Reports
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• v.55 no.5
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• pp.244-249
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• 2022

Characterized by abnormal proliferation and migration of vascular smooth muscle cells (VSMCs), neointima hyperplasia is a hallmark of vascular restenosis after percutaneous vascular interventions. Vaccinia-related kinase 1 (VRK1) is a stress adaption-associated ser/thr protein kinase that can induce the proliferation of various types of cells. However, the role of VRK1 in the proliferation and migration of VSMCs and neointima hyperplasia after vascular injury remains unknown. We observed increased expression of VRK1 in VSMCs subjected to platelet-derived growth factor (PDGF)-BB by western blotting. Silencing VRK1 by shVrk1 reduced the number of Ki-67-positive VSMCs and attenuated the migration of VSMCs. Mechanistically, we found that relative expression levels of β-catenin and effectors of mTOR complex 1 (mTORC1) such as phospho (p)-mammalian target of rapamycin (mTOR), p-S6, and p-4EBP1 were decreased after silencing VRK1. Restoration of β-catenin expression by SKL2001 and re-activation of mTORC1 by Tuberous sclerosis 1 siRNA (siTsc1) both abolished shVrk1-mediated inhibitory effect on VSMC proliferation and migration. siTsc1 also rescued the reduced expression of β-catenin caused by VRK1 inhibition. Furthermore, mTORC1 re-activation failed to recover the attenuated proliferation and migration of VSMC resulting from shVrk1 after silencing β-catenin. We also found that the vascular expression of VRK1 was increased after injury. VRK1 inactivation in vivo inhibited vascular injury-induced neointima hyperplasia in a β-catenin-dependent manner. These results demonstrate that inhibition of VRK1 can suppress the proliferation and migration of VSMC and neointima hyperplasia after vascular injury via mTORC1/β-catenin pathway.