On the Determination of the Pattern of Vascular Tissue in Peas

This work is concerned with the rules determining the placeof joining of two vascular strands. Auxin can induce the differentiationof vascular tissue, and this fact is used here for an experimentalstudy of the spatial interactions of vascular strands. Differentiated vascular tissue whose source of auxin has beenremoved attracts newly induced vascular strands. This attractionis expressed in the joining of the new strands to the pre-existingvascular tissue. Differentiated vascular tissue which is wellsupplied with auxin inhibits rather than attracts the formationof new vascular strands in its vicinity. Experiments on pea apices have extended these results to naturallyinduced vascular strands. It is shown that when a leaf primordiumis damaged at an early age its vascular strands are joined bythe strands induced by new leaves, and the contacts may be formedacross the leaf gap. The joining of the vascular strands is,therefore, much closer to the leaf than is normal and this isprobably due to the reduction in the supply of auxin from thedamaged leaf to its vascular traces. It is also shown that whena lateral bud grows its vascular traces join preferentiallythe vascular system leading to organs which have been removed.These vascular traces of a bud specifically avoid the vascularsystem of a leaf or a shoot which is still growing and producingauxin. These results are discussed in reference to the relation betweenthe vascular system and phyllotaxis and to the existence ofleaf gaps.     

Transformation of the collateral vascular bundles into amphivasal vascular bundles in an Arabidopsis mutant.

Arabidopsis inflorescence stems develop a vascular pattern similar to that found in most dicots. The arrangement of vascular tissues within the bundle is collateral, and vascular bundles in the stele are arranged in a ring. Although auxin has been shown to be an inducer of vascular differentiation, little is known about the molecular mechanisms controlling vascular pattern formation. By screening ethyl methanesufonate-mutagenized populations of Arabidopsis, we have isolated an avb1 (amphivasal vascular bundle) mutant with a novel vascular pattern. Unlike the collateral vascular bundles seen in the wild-type stems, the vascular bundles in the avb1 stems were similar to amphivasal bundles, i.e. the xylem completely surrounded the phloem. Furthermore, branching vascular bundles in the avb1 stems abnormally penetrated into the pith, which resulted in a disruption in the ring-like arrangement of vascular bundles in the stele. The avb1 mutation did not affect leaf venation pattern and root vascular organization. Auxin polar transport assay indicated that the avb1 mutation did not disrupt the auxin polar transport activity in inflorescence stems. The avb1 mutation also exhibited pleiotropic phenotypes, including curled stems and extra cauline branches. Genetic analysis indicated that the avb1 mutation was monogenic and partially dominant. The avb1 locus was mapped to a region between markers mi69 and ASB2, which is covered by a yeast artificial chromosome clone, CIC9E2, on chromosome 5. Isolation of the avb1 mutant provides a novel means to study the evolutionary mechanisms controlling the arrangement of vascular tissues within the bundle, as well as the mechanisms controlling the arrangement of vascular bundles in the stele.     

Endothelial Cell Senescence and Age-Related Vascular Diseases

Advanced age is an independent risk factor for ageing-related complex diseases,such as coronary artery disease,stroke,and hypertension,which are common but life threatening and related to the ageing-associated vascular dysfunction.On the other hand,patients with progeria syndromes suffer from serious atherosclerosis,suggesting that the impaired vascular functions may be critical to organismal ageing,or vice versa.However,it remains largely unknown how vascular cells,particularly endothelial cell,become senescent and how the senescence impairs the vascular functions and contributes to the age-related vascular diseases over time.Here,we review the recent progress on the characteristics of vascular ageing and endothelial cell senescence in vitro and in vivo,evaluate how genetic and environmental factors as well as autophagy and stem cell influence endothelial cell senescence and how the senescence contributes to the agerelated vascular phenotypes.such as atherosclerosis and increased vascular stiffness,and explore the possibility whether we can delay the age-related vascular diseases through the control of vascular ageing.     

Nanotechnology in vascular tissue engineering: from nanoscaffolding towards rapid vessel biofabrication

The existing methods of biofabrication for vascular tissue engineering are still bioreactor-based, extremely expensive, laborious and time consuming and, furthermore, not automated, which would be essential for an economically successful large-scale commercialization. The advances in nanotechnology can bring additional functionality to vascular scaffolds, optimize internal vascular graft surface and even help to direct the differentiation of stem cells into the vascular cell phenotype. The development of rapid nanotechnology-based methods of vascular tissue biofabrication represents one of most important recent technological breakthroughs in vascular tissue engineering because it dramatically accelerates vascular tissue assembly and, importantly, also eliminates the need for a bioreactor-based scaffold cellularization process.     

A Simple Clear Technique in Observing Vascular Development of Grape Ovary

The vascular system of the grapevine (Vitis vinifera L.) flower is a channel for transporting water and nutrients to the ovary. It plays an important role in the development of the ovary and fertilization through pollination. However, the vascular bundles in the flower are so tiny that they are difficult to sample and observe by traditional slicing techniques. In this study, ‘Summer Black’ grape flowers were selected as the test materials, and the tissue samples were treated by the optical clearing technique. After simple compaction, the structure and development of the vasculature were observed by common microscopy, fluorescence microscopy and laser confocal microscopy. The results showed that the transparency effects of 3% NaOH and a saturated trichloroacetaldehyde composite agreed well with the observations of the vascular structure and the developmental process of the flower in different periods. Moreover, the samples after optical clearing could be reconstructed in 3D, which helped us know more about its development and function. According to these observations, the vasculature of the ‘Summer Black’ flower can be divided into ovule vascular bundles, peripheral vascular bundles and central vascular bundles. The peripheral vascular bundles were composed of the first-order vascular bundles and the inferior vascular bundles which branched from the superior vascular bundles. These bundles branched in different directions with no discernible pattern. The two different branching methods were as follows. First, the inferior vascular bundle was directly connected to a superior vascular bundle. Secondly, some of the superior vascular bundles bent in different ways, forming the inferior vascular bundle connecting the superior vascular bundles by a metamorphosed vessel with a triangular shape. In a comparison of the developmental changes in various periods, the growth of vascular bundles at each period was directly proportional to the growth of the flower. Laser confocal scanning was used to explore the three-dimensional morphology of the peripheral vascular bundle and showed that the peripheral vascular bundle of grapes was not completely parallel to the flower’s epidermal cells. As a result, the optical clearing technique was convenient and authentic compared with the traditional slicing operation for tiny flower organs. With these advantages according to the observations, this study provides a feasible technique and useful information for the study of vascular bundle development in grape flower organs.     

Interaction of myeloperoxidase with vascular NAD(P)H oxidase-derived reactive oxygen species in vasculature: implications for vascular diseases

Vascular NAD(P)H oxidase-derived reactive oxygen species (ROS) such as hydrogen peroxide (H2O2) have emerged as important molecules in the pathogenesis of atherosclerosis, hypertension, and diabetic vascular complications. Additionally, myeloperoxidase (MPO), a transcytosable heme protein that is derived from leukocytes, is also believed to play important roles in the above-mentioned inflammatory vascular diseases. Previous studies have shown that MPO-induced vascular injury responses are H2O2 dependent. It is well known that MPO can use leukocyte-derived H2O2; however, it is unknown whether the vascular-bound MPO can use vascular nonleukocyte oxidase-derived H2O2 to induce vascular injury. In the present study, ANG II was used to stimulate vascular NAD(P)H oxidases and increase their H2O2 production in the vascular wall, and vascular dysfunction was used as the vascular injury parameter. We demonstrated that vascular-bound MPO has sustained activity in the vasculature. MPO could use the vascular NAD(P)H oxidase-derived H2O2 to produce hypochlorus acid (HOCl) and its chlorinating species. More importantly, MPO derived HOCl and chlorinating species amplified the H2O2-induced vascular injury by additional impairment of endothelium-dependent relaxation. HOCl-modified low-density lipoprotein protein (LDL), a specific biomarker for the MPO-HOCl-chlorinating species pathway, was expressed in LDL and MPO-bound vessels with vascular NAD(P)H oxidase-derived H2O2. MPO-vascular NAD(P)H oxidase-HOCl-chlorinating species may represent a common pathogenic pathway in vascular diseases and a new mechanism involved in exacerbation of vascular diseases under inflammatory conditions.     

Increased pulmonary vascular resistance and permeability due to arachidonate metabolism in isolated rabbit lungs

Liberation and metabolism of arachidonic acid may be the common final pathway of different stimuli on the pulmonary vascular bed. In a model of isolated, ventilated rabbit lungs, perfused with Krebs Henseleit albumin buffer in a recirculating system, changes of pulmonary vascular resistance and of vascular permeability are monitored continuously. The addition of free arachidonic acid or of the Ca-ionophore A 23187 to the perfusion fluid consistently evokes a biphasic increase in vascular resistance as well as an initially reversible increase in vascular permeability, followed by pulmonary edema. Both phases of increased vascular resistance are completely suppressed by inhibition of the cyclooxygenase, decreased to a large degree by inhibitors of thromboxane synthetase, and markedly augmented by short preincubation of arachidonic acid with ram seminal vesicular microsomes and by sulfhydryl reagents. The increased pulmonary vascular permeability is augmented by inhibition of cyclooxygenase and reduced by simultaneous lipoxygenase inhibition. Antagonists of histamine, serotonin and sympathic or parasympathic activity do not have any influence. PG F2alpha., TxB2, PG E2 and PG I2 alter the pulmonary vascular resistance, but do not increase vascular permeability. In conclusion, increased availability of free arachidonic acid evokes a rise in pulmonary vascular resistance, which can be ascribed to cyclooxygenase products, especially to thromboxane, and causes a rise in vascular permeability which can be ascribed to lipoxygenase products. The findings may be related to acute pulmonary lesions with increase in vascular resistance and with vascular leakage.     

Ang-Tie轴在血管和淋巴系统相关疾病中作用的研究进展

形成血管和淋巴管内层的内皮细胞是脉管系统的重要组成部分,并参与血管和淋巴系统疾病的发病机制。内皮细胞上的血管生成素(Angiopoietin,Ang)-具有免疫球蛋白和表皮生长因子同源性结构域的酪氨酸蛋白激酶(Tyrosine kinase receptors with immunoglobulin and EGF homology domains,Tie)轴是除了血管内皮生长因子受体途径外胚胎心血管和淋巴发育所必需的第二种内皮细胞特异性配体-受体信号传导系统。Ang-Tie轴参与调节产后血管生成与重塑、血管通透性和炎症,以维持血管平衡,因此,该系统在许多血管和淋巴系统疾病中发挥重要的作用。针对近年来Ang-Tie轴在血管和淋巴系统相关疾病中作用的研究进展,文中系统论述了Ang-Tie轴在炎症诱导的血管通透性、血管重塑、眼部新生脉管、剪切应力反应、动脉粥样硬化和肿瘤血管生成和转移中的作用,并总结了涉及Ang-Tie轴的相关治疗性抗体、重组蛋白和小分子药物。     

Increased pulmonary vascular resistance and permebility due to arachidonate metabolism in isolated rabbit lungs

Liberation and metabolism of arachidonic acid may be the common final pathway of different stimuli on the pulmunary vascular bed. In a model of isolated, ventilated rabbit lungs, perfused with krebs Henseleit albumin buffer in a recirculating system, changes of pulmonary vascular resistance and of vascular permeability are monitored continously. The addition of free arachidonic acid or of the Ca-ionophore A 23187 to the perfusion fluid consistently evokes a biphasic increases in vascular resistance as well as an initially reversible increase in vascular permeability, followed by pulmonary edema. Both phases of increased vascular resistance are completely suppressed by inhibition of the cyclooxygenase, decreased to a large degree by inhibitors of thromnoxane synthetase, and markedly augmented by short preincubation of arachidonic acid with ram seminal vescular microsomes and by sulfhydryl reagents. The increased pulmonary vascular permeability is augmented by inhibition of cyclooxygenase and reduced by simulteneous lipoxygenase inhibition. Antagonists of histamine, serotonin and sympathic or parasympathic activity do not have any influence.PG F_2α, TxB E₂ and PG I₂ alter the pulmonary vascular resistance, but do not increase vascular permeability.In inclusion, increased availability of free arachidonic acid evokes a rise in pulmonary vascular resistance, which can be ascribed to cyclooxygenase products, especially to thromboxane, and causes a rise in vascular permeability which can be ascribed to lipoxygenase products.The findings may be related to acute pulmonary lesions with increase in vascular resistance and with vascular leakage.     

Genetic regulation of vascular tissue patterning in Arabidopsis

Plants transport water and nutrients through a complex vascular network comprised of interconnected, specialized cell types organized in discrete bundles. To identify genetic determinants of vascular tissue patterning, we conducted a screen for mutants with altered vascular bundle organization in Arabidopsis cotyledons. Mutations in two genes, CVP1 and CVP2 (for cotyledon vascular pattern), specifically disrupt the normal pattern of vascular bundles in cotyledons, mature leaves, and inflorescence stems. The spatial distribution of the procambium, the precursor to mature vascular tissue, is altered in cvp1 and cvp2 embryos, suggesting that CVP1 and CVP2 act at a very early step in vascular patterning. Similarly, in developing stems of cvp1 and leaves of cvp2, the pattern of vascular differentiation is defective, but the maturation of individual vascular cells appears to be normal. There are no discernible alterations in cell morphology in cvp2 mutants. In contrast, cvp1 mutants are defective in directional orientation of the provascular strand, resulting in a failure to establish uniformly aligned vascular cells, and they also show a reduction in vascular cell elongation. Neither cvp1 nor cvp2 mutants displayed altered auxin perception, biosynthesis, or transport, suggesting that auxin metabolism is not generally affected in these mutants.     

Vascular wall extracellular matrix proteins and vascular diseases

Extracellular matrix proteins form the basic structure of blood vessels. Along with providing basic structural support to blood vessels, matrix proteins interact with different sets of vascular cells via cell surface integrin or non-integrin receptors. Such interactions induce vascular cell de novo synthesis of new matrix proteins during blood vessel development or remodeling. Under pathological conditions, vascular matrix proteins undergo proteolytic processing, yielding bioactive fragments to influence vascular wall matrix remodeling. Vascular cells also produce alternatively spliced variants that induce vascular cell production of different matrix proteins to interrupt matrix homeostasis, leading to increased blood vessel stiffness; vascular cell migration, proliferation, or death; or vascular wall leakage and rupture. Destruction of vascular matrix proteins leads to vascular cell or blood-borne leukocyte accumulation, proliferation, and neointima formation within the vascular wall; blood vessels prone to uncontrolled enlargement during blood flow diastole; tortuous vein development; and neovascularization from existing pathological tissue microvessels. Here we summarize discoveries related to blood vessel matrix proteins within the past decade from basic and clinical studies in humans and animals — from expression to cross-linking, assembly, and degradation under physiological and vascular pathological conditions, including atherosclerosis, aortic aneurysms, varicose veins, and hypertension.     

Vascular tone and regular physical exercise

On the basis of the results of rheovasography of the thigh region, the vascular tone was assessed using pulse transit time in subjects regularly playing sports and nonathletes with initial stages of hypertension. An increased rigidity of the vascular wall was observed in subjects with an increased blood pressure. In our opinion, vascular endothelial dysfunction is the main cause of vascular rigidity, and regular dynamic training can improve the endothelium-dependent vascular relaxation.     

Isolation of COV1, a gene involved in the regulation of vascular patterning in the stem of Arabidopsis

The molecular mechanisms that control the ordered patterning of vascular tissue development in plants are not well understood. Several models propose a two-component system for vascular differentiation. These components include an inducer of vascular tissue development and an inhibitor that prevents the formation of vascular bundles near pre-existing bundles. We have identified two recessive allelic mutants in Arabidopsis, designated continuous vascular ring (cov1), that display a dramatic increase in vascular tissue development in the stem in place of the interfascicular region that normally separates the vascular bundles. The mutant plants exhibited relatively normal vascular patterning in leaves and cotyledons. Analysis of the interaction of cov1 with a known auxin signalling mutant and direct analysis of auxin concentrations suggests that cov1 affects vascular pattering by some mechanism that is independent of auxin. The COV1 protein is predicted to be an integral membrane protein of unknown function, highly conserved between plants and bacteria. In plants, COV1 is likely to be involved in a mechanism that negatively regulates the differentiation of vascular tissue in the stem.     

A bioinformatics method for predicting long noncoding RNAs associated with vascular disease

Long noncoding RNAs (lncRNAs) play important roles in human diseases including vascular disease. Given the large number of lncRNAs, however, whether the majority of them are associated with vascular disease remains unknown. For this purpose, here we present a genomic location based bioinformatics method to predict the lncRNAs associated with vascular disease. We applied the presented method to globally screen the human lncRNAs potentially involved in vascular disease. As a result, we predicted 3043 putative vascular disease associated lncRNAs. To test the accuracy of the method, we selected 10 lncRNAs predicted to be implicated in proliferation and migration of vascular smooth muscle cells (VSMCs) for further experimental validation. The results confirmed that eight of the 10 lncRNAs (80%) are validated. This result suggests that the presented method has a reliable prediction performance. Finally, the presented bioinformatics method and the predicted vascular disease associated lncRNAs together may provide helps for not only better understanding of the roles of lncRNAs in vascular disease but also the identification of novel molecules for the diagnosis and therapy of vascular disease.     

Responses of plant vascular systems to auxin transport inhibition.

To assess the role of auxin flows in plant vascular patterning, the development of vascular systems under conditions of inhibited auxin transport was analyzed. In Arabidopsis, nearly identical responses evoked by three auxin transport inhibitor substances revealed an enormous plasticity of the vascular pattern and suggest an involvement of auxin flows in determining the sites of vascular differentiation and in promoting vascular tissue continuity. Organs formed under conditions of reduced auxin transport contained increased numbers of vascular strands and cells within those strands were improperly aligned. In leaves, vascular tissues became progressively confined towards the leaf margin as the concentration of auxin transport inhibitor was increased, suggesting that the leaf vascular system depends on inductive signals from the margin of the leaf. Staged application of auxin transport inhibitor demonstrated that primary, secondary and tertiary veins became unresponsive to further modulations of auxin transport at successive stages of early leaf development. Correlation of these stages to anatomical features in early leaf primordia indicated that the pattern of primary and secondary strands becomes fixed at the onset of lamina expansion. Similar alterations in the leaf vascular responses of alyssum, snapdragon and tobacco plants suggest common functions of auxin flows in vascular patterning in dicots, while two types of vascular pattern alterations in Arabidopsis auxin transport mutants suggest that at least two distinct primary defects can result in impaired auxin flow. We discuss these observations with regard to the relative contributions of auxin transport, auxin sensitivity and the cellular organisation of the developing organ on the vascular pattern.     

血管内皮细胞衰老与血管疾病

细胞衰老是指细胞在各种应激条件下出现周期阻滞,不可逆地丧失增殖能力,其形态、基因表达和功能都发生特定变化的过程。研究表明,血管内皮细胞衰老可以通过削弱血管功能,促进衰老相关血管疾病的发生发展。然而,有关内皮细胞衰老的发生机制以及内皮细胞衰老影响血管功能及衰老相关血管疾病的潜在机制尚待挖掘。本文从血管内皮细胞衰老相关的信号通路,以及血管内皮细胞衰老与血管功能和血管相关疾病（动脉粥样硬化、高血压和糖尿病血管并发症）的最新研究进展进行综述,为进一步认识血管疾病的发病机制,延缓血管衰老提供新的思路。     

Various patterns in the development of the periganglionic vascular bed of respiratory tube ganglia during human embryogenesis

The investigation has been performed in 118 serial sections of human embryos. The development of vascular bed in ganglia of the respiratory tube at early embryogenesis has been studied. The main attention has been paid to the formation of periganglial vascular bed. Loop-like and arc-shaped connections between the developing vessels and galglia and rearrangement of periganglial vascular bed during embryogenesis are described. Three stages in the development of blood supply to the ganglia of the respiratory tube are noted: I stage--avascular (embryos are 17-30 mm long); II stage--formation of periganglial vascular bed (embryos are 33-50 mm long); III stage--formation of intraganglial vascular bed (embryos are 55 mm long and more). Within I and II stages, reorganization phases in the vascular bed are described. A suggestion is made that the vascular factor of the development and differentiation of ganglial elements starts acting since the formation of periganglial vascular bed; before this, the mesenchima surrounding the neuronal plexus performs their trophic.     

Endothelial dysfunction as a cellular mechanism for vascular failure

The regulation of vascular tone, vascular permeability, and thromboresistance is essential to maintain blood circulation and therefore tissue environments under physiological conditions. Atherogenic stimuli, including diabetes, dyslipidemia, and oxidative stress, induce vascular dysfunction, leading to atherosclerosis, which is a key pathological basis for cardiovascular diseases such as ischemic heart disease and stroke. We have proposed a novel concept termed "vascular failure" to comprehensively recognize the vascular dysfunction that contributes to the development of cardiovascular diseases. Vascular endothelial cells form the vascular endothelium as a monolayer that covers the vascular lumen and serves as an interface between circulating blood and immune cells. Endothelial cells regulate vascular function in collaboration with smooth muscle cells. Endothelial dysfunction under pathophysiological conditions contributes to the development of vascular dysfunction. Here, we address the barrier function and microtubule function of endothelial cells. Endothelial barrier function, mediated by cell-to-cell junctions between endothelial cells, is regulated by small GTPases and kinases. Microtubule function, regulated by the acetylation of tubulin, a component of the microtubules, is a target of atherogenic stimuli. The elucidation of the molecular mechanisms of endothelial dysfunction as a cellular mechanism for vascular failure could provide novel therapeutic targets of cardiovascular diseases.     

平滑肌22α蛋白在血管稳态和血管重构中的作用

有关血管稳态和重构的分子机制一直是近年来的研究热点,也被视为治疗血管损伤性疾病的突破点.大量研究证实,血管损伤修复及病理性重构过程与血管平滑肌细胞(vascular smooth muscle cells,VSMCs)的表型转化、异常增殖与迁移、细胞衰老关系密切.平滑肌22α(smooth muscle 22α,SM2...     

A QTL controlling stem morphology and vascular development in Lycopersicon esculentumxLycopersicon hirsutum (Solanaceae) crosses is located on chromosome 2

The vascular tissue of higher plants is organized into a continuous and unified system that undergoes a transition between two highly differentiated structures, the root and the shoot. This transition was studied in tomato by investigating the genetic basis of morphological variation between Lycopersicon esculentum and L. hirsutum LA407. Our analysis concentrated on morphology in stem cross sections, and we detected heritable genetic differences in an inbred backcross population having L. esculentum as the recurrent parent and LA407 as the donor parent. Inbred backcross line (IBL) 2353 contained a donor segment from chromosome 2 and retained features of the LA407 stem vascular morphology. Marker-trait analysis of vascular structure in a cross between IBL 2353 and L. esculentum showed significant (0.0001 ≤ P ≤ 0.0375) associations between markers on chromosome 2 and the size of primary vascular bundles, the shape of the vascular system, and the thickness of the secondary vascular tissue. Families with LA407 DNA for the markers on chromosome 2 had larger primary vascular bundles, more developed secondary vascular tissue, and a triangular vascular shape. These results suggest that the distal portion of chromosome 2 in LA407 contains a locus or loci affecting vascular morphology and development.