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Bone marrow mesenchymal stem cell transplantation combined with perindopril treatment attenuates infarction remodelling in a rat model of acute myocardial infarction

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2006年第8期7卷 641-647页

作者： WANG Jian-an LUO Rong-hua ZHANG Xing XIE Xiao-jie HU Xin-yang HE Ai-na CHEN Jie LI Jia-hui Department of Cardiology the Second Affiliated Hospital School of Medicine Zhejiang University Hangzhou 310009 China Center of Lab Sir Run Run Shaw Hospital School of Medicine Zhejiang University Hangzhou 310016 China

Objective: This study was performed to evaluate whether implantation of mesenchymal stem cell (MSC) would reduce left ventricular remodelling from the molecular mechanisms compared with angiotensin-converting enzyme inhibitors (ACEIs) perindopril into ischemic myocardium after acute myocardial infarction. Methods: Forty rats were divided into four groups: control, MSC, ACEI, MSC+ACEI groups. Bone marrow stem cell derived rat was injected immediately into a zone made ischemic by coronary artery ligation in MSC group and MSC+ACEI group. Phosphate-buffered saline (PBS) was injected into control group. Perindopril was administered p.o. to ACEI group and MSC+ACEI group. Six weeks after implantation, the rats were killed and heart sample was collected. Fibrillar collagen was observed by meliorative Masson’s trichome stain. Western Blotting was employed to evaluate the protein expression of matrix metalloproteinase (MMP)-2, matrix metalloproteinase (MMP)-9 in infarction zone. The transcriptional level of MMP2, MMP9 and tissue inhibitor of matrix metalloproteinase (TIMP)-1 in infarction area was detected by reverse transcriptase PCR (RT-PCR) analysis. Results: The fibrillar collagen area, the protein expression of MMP2, MMP9 and the transcriptional level of MMP2, MMP9 mRNA in infarction zone reduced in MSC group, ACEI group, and MSC+ACEI group. No significant difference was detected in the expression of TIMP1 mRNA among the 4 groups. Conclusion: Both MSC and ACEI could reduce infarction remodelling by altering collagen metabolism.

关键词： remodelling Acute myocardial infarction Perindopril Bone marrow mesenchymal stem cell

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Contribution of mi RNAs to ion-channel remodelling in atrial fibrillation

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World Journal of Hypertension 2015年第1期5卷 6-13页

作者： José Manuel Vilches Diego Franco Amelia E Aránega Cardiac and Skeletal Myogenesis Group Department of Experimental Biology University of Jaén

Atrial fibrillation(AF) is the most commonly encountered clinical arrhythmia associated with pronounced mortality and morbidity, which are related to palpitations, fainting, congestive heart failure, and stroke. Prolonged episodes of AF promote AF persistence mainly due to electrical remodelling that alters ion-channel expression and/or function. Micro RNAs(mi RNAs), a new class of noncoding mR NAs of around 22 nucleotides in length, have recently emerged as one of the key players in the geneexpression regulatory networks. The potential roles of miR NAs in controlling AF have recently been investigated. Several recent studies have provided promising results for a better understanding of the molecular mechanisms of AF. In this review, we summarize the mechanism of miR NAs as regulators of ion-channel gene expression and their role in causing AF through electrical remodelling.

关键词： Atrial fibrillation MicroRNA Ion channels Electrical remodelling

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From Sméagol to Gollum: Mechanical Stress and Bone remodelling

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Open Journal of Orthopedics 2018年第4期8卷 148-167页

作者： Nicole Pace University of Malta Gozo Malta

This imaginary transformation from Sméagol to Gollum is a dramatization of the illusive repercussions of mechanical stress affecting bone. This paper presents the main ideas of mechanical stress and bone remodelling from a novel’s perspective. The object of this study is to provide evidence for new ways to explore bone’s functional adaptation to mechanical stress made through the copious interpretation and integration of new and existing literature. It tackles the underlying biology of bone cells and how they detect and react to strain stimuli. The different types of mechanical demands in daily activities are sifted through and any misconceptions found fallible in literature are refined. A personal experience of a stress fracture is reviewed to parallel the implications that lead to the incident with the findings on the link between mechanical stress and bone remodelling. Some factors regarding age, gender and ethnicity and the interplay with mechanical stress influencing bone remodelling are considered. Brief overviews of three new medical novelties in bone healing are outlined, hoping that these interventions of proper medical techniques can be a change for the better: one from Gollum to Sméagol rather than vice versa.

关键词： Mechanical Stress Bone remodelling Cycle Mechanostat Model Stress Fracture

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Combined blockade of IL-25, IL-33 and TSLP further inhibits airways inflammation and remodelling in a murine surrogate of asthma

Combined blockade of IL-25, IL-33 and TSLP further inhibits ...

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第十三届全国免疫学学术大会

作者： Yan Chen Gao An Xin Zhang Wenjun Wang Qiong Huang Qin Li Shihao Chen Xiaonan Du Chris J Corrigan Wei Wang Ying Sun Capital Medical University Beijing Chao-Yang Hospital Capital Medical University & Beijing Instituteof Respiratory Medicine King's College London

The role of the epithelial cell-derived cytokines IL-25, IL-33 and TSLP in the pathogenesis of human asthma has progressively been *** blockade of any of these cytokines in isolation has been shown to have the potential significantly to inhibit airways inflammation and hyperresponsiveness in a murine surrogates of asthma, the hypothesis that combined blockade of all three cytokines can accomplish this more efficiently has never been *** the present study, we evaluated, using ELISA and quantitative immunohistochemistry, the effects of single or combined blockade of IL-25 and TSLP in vivo on airways inflammatory cellular infiltration, epithelial cell metaplasia, deposition of collagen and other fibrosis-related proteins as well as matrix metalloproteinases, local Th2 cytokine expression and serum total IgE concentration in a murine surrogate of asthma using IL-33 receptor(ST2) gene deleted(St2) mice sensitised and challenged with ovalbumin or saline *** the St2mice, in which IL-33 signalling is deleted, additional combined blockade of these cytokines further significantly reduced airways inflammatory cellular infiltration, lung tissue expression of Th2 cytokines and the serum total concentration of ***, combined blockade of IL-25 and TSLP also effectively reduced expression of immunoreactivity for the fibrosis-related proteins FGFR4, CTGF and matrix metalloproteinases in the *** data show that combined blockade of these three cytokines can better ameliorate airways pathological changes in this murine asthma surrogate, with implications for human asthma.

关键词： IL-25 IL-33 TSLP Asthma remodelling

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How Much Do We Know about Atopic Asthma: Where Are We Now?

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Cellular & Molecular Immunology 2006年第5期3卷 321-332页

作者： Sun Ying Guizhen Zhang Shuyan Gu Jisheng Zhao King＇s College London Division of Asthma Allergy ＆ Lung BiologyMRC ＆ Asthma UK Centre in Allergic Mechanisms of Asthma LondonUK Department of Central Research The Third Clinical College Jilin University Changchun China King＇s College London MRC ＆ Asthma UK Centre in Allergic Mechanisms of Asthma Division of Asthma Allergy ＆ Lung Biology 5th Floor Thomas Guy House Guy＇s Hospital London SEI 9RT UK

Asthma is a common disease in the worldwide and it affects over 3.5 million adults and children in the UK. Asthma is a chronic disease characterized by airway hyperresponsiveness, airway inflammation, airway remodelling and reversible airway obstruction. Inflammatory cells, cytokines, chemokines, adhesion molecules, and mediators are involved in pathogenesis of asthma. Chronic airway inflammation and remodelling are the major characters in asthma, which result in decreased pulmonary function. The precise processes are far understood at moment. Although corticosteroid therapy plus other exiting drugs （bronchodilators and oral leukotriene receptor antagonists） influences many different inflammatory and structural cell types and continues to be as the ＂gold standard＂ of therapy in asthma, many thousands have chronic, severe diseases and suffer daily symptoms which make their lives a misery. There remains a clear need for novel approaches to therapy, which will be informed by a clearer understanding of disease pathogenesis, particularly in the target organ where airway inflammation and remodelling, the hallmarks of asthma occur. Cellular ＆ Molecular Immunology.

关键词： atopy asthma allergic inflammation remodelling therapy

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Gastrointestinal tract modelling in health and disease

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World Journal of Gastroenterology 2009年第2期15卷 169-176页

作者： Dong-Hua Liao Jing-Bo Zhao Hans Gregersen Hans Gregersen Mech-Sense Aalborg Hospital DK-9100 Aalborg Denmark Institute of Health Technology Aalborg University Denmark Haukeland University Hospital Bergen Norway

The gastrointestinal (GI) tract is the system of organs within multi-cellular animals that takes in food, digests it to extract energy and nutrients, and expels the remaining waste. The various patterns of GI tract function are generated by the integrated behaviour of multiple tissues and cell types. A thorough study of the GI tract requires understanding of the interactions between cells, tissues and gastrointestinal organs in health and disease. This depends on knowledge, not only of numerous cellular ionic current mechanisms and signal transduction pathways, but also of large scale GI tissue structures and the special distribution of the nervous network. A unique way of coping with this explosion in complexity is mathematical and computational modelling; providing a computational framework for the multilevel modelling and simulation of the human gastrointestinal anatomy and physiology. The aim of this review is to describe the current status of biomechanical modelling work of the GI tract in humans and animals, which can be further used to integrate the physiological, anatomical and medical knowledge of the GI system. Such modelling will aid research and ensure that medical professionals benefit, through the provision of relevant and precise information about the patient's condition and GI remodelling in animal disease models. It will also improve the accuracy and efficiency of medical procedures, which could result in reduced cost for diagnosis and treatment.

关键词： Gastrointestinal tract Computational modelling Biomechanics remodelling Disease

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Adult myelination: wrapping up neuronal plasticity

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Neural Regeneration Research 2014年第13期9卷 1261-1264页

作者： Megan O’Rourke Robert Gasperini Kaylene M.Young Menzies Research Institute Tasmania University of Tasmania The School of Medicine University of Tasmania

In this review, we outline the major neural plasticity mechanisms that have been identified in the adult central nervous system （CNS）, and offer a perspective on how they regulate CNS function. In particular we examine how myelin plasticity can operate alongside neurogenesis and synaptic plasticity to influence information processing and transfer in the mature CNS.

关键词： oligodendrocyte OPC adult central nerrous system NG2 oligodendrogenesis plasticity remodelling myelination neural stem cells synapse

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Tracheal compliance and limit flow rate changes in a murine model of asthma

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Science China(Life Sciences) 2008年第10期51卷 922-931页

作者： TENG ZhongZhao1, WANG YiQin2, LI FuFeng2, YAN HaiXia2 & LIU ZhaoRong3 1 Department of Mathematical Sciences, Worcester Polytechnic Institute, Worcester, MA, 01609, USA 2 Syndrome Laboratory of TCM, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China 3 Department of Mechanics and Engineering Science, Fudan University, Shanghai 200433, China Department of Mathematical Sciences Worcester Polytechnic Institute Worcester USA Syndrome Laboratory of TCM Shanghai University of Traditional Chinese Medicine Shanghai China Department of Mechanics and Engineering Science Fudan University Shanghai China

Trachea is the unique passage for air to flow in and out. Its tone is of importance for the respiration system. However, investigation on how tracheal tone changes due to asthma is limited. Aiming at studying how the mechanical property changes due to asthma as well as the compliance and flow limitation, the following methods are adopted. Static and passive pressure-volume tests of rats' trachea of the asthmatic and control groups are carried out and a new type of tube law is formulated to fit the experimental data, based on which changes of compliance and limit flow rate are investigated. In order to give explanation to such changes, histological examinations with tracheal soft tissues are made. The results show that compliance, limit flow rate and material constants included in the tube law largely depend on the longitudinal stretching ratio. Compared with the control group, the tracheal compliance of asthmatic animals decreases significantly, which results in an increased limit flow rate. Histological studies indicate that asthma can lead to hyperplasia/hypertrophy of smooth muscle cells, and increase elastin and collagen fibres in the muscular membrane. Though decreasing compliance increases sta- bility, during the onset of asthma, limit flow rate is much smaller due to the lower transmural pressure. Asthma leads to a stiffer trachea and the obtained results reveal some aspects relevant to asthma-induced tracheal remodelling.

关键词： trachea asthma collapse tube law compliance limit flow rate remodelling

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Left Ventricle Postinfarction Pseudoaneurysm: Anatomical Forms and Surgical Management

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Surgical Science 2014年第4期5卷 138-145页

作者： J. M. Garrido A. Ferreiro J. F. Rodríguez-Vázquez P. Prada S. Verdugo J. Silva S. López-Checa I. Sánchez-Montesinos Departamento de Anatomía y Embriología Humana II Facultad de Medicina Universidad Complutense de Madrid Madrid Spain Departamento de Anatomía y Embriología Humana Facultad de Medicina Universidad de Granada Granada Spain Servicio de Cirugía Cardiovascular HU Ramón y Cajal Departamento de Ciencias Morfológicas Universidad Europea de Madrid Madrid Spain Servicio de Cirugía Cardiovascular HU Ramón y Cajal Madrid Spain Servicio de Cirugía Cardiovascular HU Virgen de las Nieves Granada Spain

Introduction: Left Ventricle Postinfarction Pseudoaneurysm (LVPS)—false aneurysm occurs after a free-wall rupture contained by the adjacent pericardium. LVPS lacks the normal structure of the ventricular wall and disrupts the normal chamber anatomy. However, the natural history, clinical presentation and surgical outcome are still unclear. For that reason, it is necessary to describe the most relevant anatomical characteristics of LVPS and the appropriate surgical strategies currently applied. Methods: We reviewed the anatomical characteristics of several patients diagnosed of LVPS and the surgical technique performed. In this work two different anatomical types of LVPS are described in detail, with the surgical and structural implications for left ventricle reconstruction. Results: There are two different anatomical forms of LVPS: 1) Typical pseudoaneurysm, with a small gateway neck between the Left Ventricle and the false aneurysm chamber (Figure 1(A));2) Atypical pseudoaneurysm, in which the anatomical defect is bigger, without well-defined edges, extends over a large segment of infarcted and thinned myocardial tissue. In both cases, the therapeutics targets and the surgical techniques used were directed to restore the normal geometry of Left Ventricle, keeping the optimal mitral valve function. Conclusions: The surgical key-step is to preserve or to remodel the ventricular chamber anatomy. This fact restores the ventricular geometry, not only removing the wall discontinuity that generated the pseudoaneurysm. Nevertheless, final prognosis depends on the underlying ischemic cardiomyopathy and mechanical complications, such us mitral regurgitation or ventricular septal defect.

关键词： Ventricular Anatomy Left Ventricle Pseudoaneurysm Surgical Treatment Ventricular remodelling Restore of Left Ventricle Morphology and Function of Left Ventricle Ischemic Cardiomyopathy

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Critical Role of Protein Kinase C (PKC) in the Onset of Airway Hypersensitivity in Ova-Sensitized Guinea Pig Model of Asthma

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Open Journal of Respiratory Diseases 2014年第1期4卷 1-11页

作者： Rakesh Kumar Mishra Ritu Kulshrestha Sunil Kumar Chhabra Satish K. Srivastav Surendra Kumar Bansal Department of Biochemistry and Molecular Biology The University of Texas Medical Branch Galveston USA Department of Biochemistry V.P. Chest Institute University of Delhi Delhi India Department of Cardiorespiratory Physiology V.P. Chest Institute University of Delhi Delhi India Department of Pathology V.P. Chest Institute University of Delhi Delhi India

Background and Objectives: Protein kinase C (PKC) activation plays an important role in activation of T-lymphocytes in asthma. Airway hypersensitivity is one of the main characteristic features of asthma, the mechanism of onset of which is not clearly understood. Therefore, the objective was to elucidate the role of PKC in etiopathogenesis of airway hypersensitivity in asthma. Methods: Male guinea pigs (n = 30) were sensitized with ovalbumin and day of initial allergen-specific immune response determined by intradermal test, airway hypersensitivity, BALF cytology and lung histopathology. Total PKC activity, PKC isoenzymes and phosphoinositides were assessed in airway smooth muscles (ASM) and peripheral blood lymphocytes. Results: Intradermal test revealed that day 9 was the earliest time of allergen-specific response and onset of airway hypersensitivity to ovalbumin. It was associated with significant increase in total and differential (lymphocytes and eosinophils) BALF counts and grade I peribronchiolar chronic lymphocytic inflammation in lung. On day 14, grade II infiltration of lymphocytes and eosinophils with onset ofstructural remodelingofproximal and distal airways was seen. Total PKC activity, expression of PKCα, PKCε and phosphoinositides increased significantly in ASM and lymphocytes on day 9 and were maximum on day 14. There was no change in PKC-τ expression. Conclusions: Activation of PKC, particularly PKCα and PKCε, mediated signal transduction pathway plays a critical role in lymphocyte infiltration and onset of airway hypersensitivity, airway remodeling and asthma pathophysiology. The present study is the first one on the mechanism of the etiopathogenesis of the disease, which shows a direct evidence of the role of PKC mediated pathway in the initiation and onset of airway hypersensitivity in ovalbumin sensitized guinea pig model.

关键词： Asthma Airway Hypersensitivity Protein Kinase C Airway remodelling

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