共查询到20条相似文献,搜索用时 15 毫秒
1.
Kirsten A. Bielefeld Saeid Amini-Nik Benjamin A. Alman 《Cellular and molecular life sciences : CMLS》2013,70(12):2059-2081
Following a skin injury, the damaged tissue is repaired through the coordinated biological actions that constitute the cutaneous healing response. In mammals, repaired skin is not identical to intact uninjured skin, however, and this disparity may be caused by differences in the mechanisms that regulate postnatal cutaneous wound repair compared to embryonic skin development. Improving our understanding of the molecular pathways that are involved in these processes is essential to generate new therapies for wound healing complications. Here we focus on the roles of several key developmental signaling pathways (Wnt/β-catenin, TGF-β, Hedgehog, Notch) in mammalian cutaneous wound repair, and compare this to their function in skin development. We discuss the varying responses to cutaneous injury across the taxa, ranging from complete regeneration to scar tissue formation. Finally, we outline how research into the role of developmental pathways during skin repair has contributed to current wound therapies, and holds potential for the development of more effective treatments. 相似文献
2.
The goal of periodontal regenerative therapy is to predictably restore the tooth’s supporting periodontal tissues and form a new connective tissue attachment of periodontal ligament (PDL) fibers and new alveolar bone. Periostin is a matricellular protein so named for its expression primarily in the periosteum and PDL of adult mice. Its biological functions have been widely studied in areas such as cardiovascular physiology and oncology. Despite being initially identified in the dental tissues and bone, investigations of Periostin functions in PDL and alveolar-bone-related physiopathology are less abundant. Recently, several studies have suggested that Periostin may be an important regulator of periodontal tissue formation. By promoting collagen fibrillogenesis and the migration of fibroblasts and osteoblasts, Periostin might play a pivotal part in regeneration of the PDL and alveolar bone following periodontal surgery. The aim of this article is to provide an extensive review of the implications of Periostin in periodontal tissue biology and its potential use in periodontal tissue regeneration. 相似文献
3.
Investigations into mechanisms that restrict the recovery of functions after an injury to the brain or the spinal cord have
led to the discovery of specific neurite growth inhibitory factors in the adult central nervous system (CNS) of mammals. Blocking
their growth-suppressive function resulted in disinhibition of axonal growth, i.e. growth of cultured neurons on inhibitory
CNS tissue in vitro and regeneration of injured axons in vivo. The enhanced regenerative and compensatory fibre growth was often accompanied by a substantial improvement in the functional
recovery after CNS injury. The first clinical studies to assess the therapeutic potential of compounds that neutralize growth
inhibitors or interfere with their downstream signalling are currently in progress. This review discusses recent advances
in the understanding of how the ‘founder molecule’ Nogo-A and other glialderived growth inhibitors restrict the regeneration
and repair of disrupted neuronal circuits, thus limiting the functional recovery after CNS injuries.
Received 5 April 2007; received after revision 28 September 2007; accepted 1 October 2007 相似文献
4.
Claudia P. Spampinato 《Cellular and molecular life sciences : CMLS》2017,74(9):1693-1709
The genome integrity of all organisms is constantly threatened by replication errors and DNA damage arising from endogenous and exogenous sources. Such base pair anomalies must be accurately repaired to prevent mutagenesis and/or lethality. Thus, it is not surprising that cells have evolved multiple and partially overlapping DNA repair pathways to correct specific types of DNA errors and lesions. Great progress in unraveling these repair mechanisms at the molecular level has been made by several talented researchers, among them Tomas Lindahl, Aziz Sancar, and Paul Modrich, all three Nobel laureates in Chemistry for 2015. Much of this knowledge comes from studies performed in bacteria, yeast, and mammals and has impacted research in plant systems. Two plant features should be mentioned. Plants differ from higher eukaryotes in that they lack a reserve germline and cannot avoid environmental stresses. Therefore, plants have evolved different strategies to sustain genome fidelity through generations and continuous exposure to genotoxic stresses. These strategies include the presence of unique or multiple paralogous genes with partially overlapping DNA repair activities. Yet, in spite (or because) of these differences, plants, especially Arabidopsis thaliana, can be used as a model organism for functional studies. Some advantages of this model system are worth mentioning: short life cycle, availability of both homozygous and heterozygous lines for many genes, plant transformation techniques, tissue culture methods and reporter systems for gene expression and function studies. Here, I provide a current understanding of DNA repair genes in plants, with a special focus on A. thaliana. It is expected that this review will be a valuable resource for future functional studies in the DNA repair field, both in plants and animals. 相似文献
5.
Pajalunga D Mazzola A Franchitto A Puggioni E Crescenzi M 《Cellular and molecular life sciences : CMLS》2008,65(1):8-15
Tissue repair and regeneration are very complex biological events, whose successful attainment requires far more than mere cell division. However, almost unavoidably they entail cell proliferation as a fundamental premise. Full regeneration or repair cannot be achieved without replacing cells lost to disease or injury, replacement that can only take place via proliferation of surviving cells. This review endeavors to outline the molecular bases of exit from and reentry into the cell cycle. In recent years, the decision to proliferate or not has been seen as mostly the concern of cyclins and cyclin-dependent kinases. This account tries to show that cell cycle inhibitors are as important as the positive regulators in the making of this decision. Finally, the authors wish to suggest that the molecular knowledge of the cell cycle can be harnessed to the benefit of many aspects of regenerative medicine. 相似文献
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Marten Szibor Jochen Pöling Henning Warnecke Thomas Kubin Thomas Braun 《Cellular and molecular life sciences : CMLS》2014,71(10):1907-1916
Cardiomyocytes continuously generate the contractile force to circulate blood through the body. Imbalances in contractile performance or energy supply cause adaptive responses of the heart resulting in adverse rearrangement of regular structures, which in turn might lead to heart failure. At the cellular level, cardiomyocyte remodeling includes (1) restructuring of the contractile apparatus; (2) rearrangement of the cytoskeleton; and (3) changes in energy metabolism. Dedifferentiation represents a key feature of cardiomyocyte remodeling. It is characterized by reciprocal changes in the expression pattern of “mature” and “immature” cardiomyocyte-specific genes. Dedifferentiation may enable cardiomyocytes to cope with hypoxic stress by disassembly of the energy demanding contractile machinery and by reduction of the cellular energy demand. Dedifferentiation during myocardial repair might provide cardiomyocytes with additional plasticity, enabling survival under hypoxic conditions and increasing the propensity to enter the cell cycle. Although dedifferentiation of cardiomyocytes has been described during tissue regeneration in zebrafish and newts, little is known about corresponding mechanisms and regulatory circuits in mammals. The recent finding that the cytokine oncostatin M (OSM) is pivotal for cardiomyocyte dedifferentiation and exerts strong protective effects during myocardial infarction highlights the role of cytokines as potent stimulators of cardiac remodeling. Here, we summarize the current knowledge about transient dedifferentiation of cardiomyocytes in the context of myocardial remodeling, and propose a model for the role of OSM in this process. 相似文献
8.
Apart from cancer and mutation induction, radiobiological effects on mammals are mostly attributable to cell 'death', defined as loss of proliferative capacity. Survival curves relate retention of that capacity to radiation dose, and often manifest a quasi-threshold ('shoulder'). The shoulder is attributable to an initial mechanism of repair ('Q-repair') which is gradually depleted as dose increases. Another form of repair, which is not depleted ('P-repair'), increases the dose required to deliver an average of one lethal event per cell (dose 'D0'). Neither form of repair can unambiguously be linked with repair of defects in isolated DNA. An important initial lesion may well be disruption of the complex structural relationship between the DNA, nuclear membrane and associated proteins. One form of P-repair may be restoration of that structural relationship. 相似文献
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Simon J. Conway Kenji Izuhara Yasusei Kudo Judith Litvin Roger Markwald Gaoliang Ouyang Joseph R. Arron Cecile T. J. Holweg Akira Kudo 《Cellular and molecular life sciences : CMLS》2014,71(7):1279-1288
Periostin, also termed osteoblast-specific factor 2, is a matricellular protein with known functions in osteology, tissue repair, oncology, cardiovascular and respiratory systems, and in various inflammatory settings. However, most of the research to date has been conducted in divergent and circumscribed areas meaning that the overall understanding of this intriguing molecule remains fragmented. Here, we integrate the available evidence on periostin expression, its normal role in development, and whether it plays a similar function during pathologic repair, regeneration, and disease in order to bring together the different research fields in which periostin investigations are ongoing. In spite of the seemingly disparate roles of periostin in health and disease, tissue remodeling as a response to insult/injury is emerging as a common functional denominator of this matricellular molecule. Periostin is transiently upregulated during cell fate changes, either physiologic or pathologic. Combining observations from various conditions, a common pattern of events can be suggested, including periostin localization during development, insult and injury, epithelial–mesenchymal transition, extracellular matrix restructuring, and remodeling. We propose mesenchymal remodeling as an overarching role for the matricellular protein periostin, across physiology and disease. Periostin may be seen as an important structural mediator, balancing appropriate versus inappropriate tissue adaption in response to insult/injury. 相似文献
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H. Al-Kharobi R. El-Gendy D. A. Devine J. Beattie 《Cellular and molecular life sciences : CMLS》2014,71(8):1469-1476
The insulin-like growth factor (IGF) axis is a multicomponent molecular network which has important biological functions in the development and maintenance of differentiated tissue function(s). One of the most important functions of the IGF axis is the control of skeletal tissue metabolism by the finely tuned regulation of the process of osteogenesis. To achieve this, the IGF axis controls the activity of several cell types—osteoprogenitor cells, osteoblasts, osteocytes and osteoclasts to achieve the co-ordinated development of appropriate hard tissue structure and associated matrix deposition. In addition, there is an increasing awareness that the IGF axis also plays a role in the process of odontogenesis (tooth formation). In this review, we highlight some of the key findings in both of these areas. A further understanding of the role of the IGF axis in hard tissue biology may contribute to tissue regeneration strategies in cases of skeletal tissue trauma. 相似文献
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Molecular and Cellular Basis of Regeneration and Tissue Repair 总被引:2,自引:0,他引:2
The Xenopus tadpole is a favourable organism for regeneration research because it is suitable for a wide range of micromanipulative procedures and for a wide range of transgenic methods. Combination of these techniques enables genes to be activated or inhibited at specific times and in specific tissue types to a much higher degree than in any other organism capable of regeneration. Regenerating systems include the tail, the limb buds and the lens. The study of tail regeneration has shown that each tissue type supplies the cells for its own replacement: there is no detectable de-differentiation or metaplasia. Signalling systems needed for regeneration include the BMP and Notch signalling pathways, and perhaps also the Wnt and FGF pathways. The limb buds will regenerate completely at early stages, but not once they are fully differentiated. This provides a good opportunity to study the loss of regenerative ability using transgenic methods. 相似文献
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Functional interplay between tetraspanins and proteases 总被引:1,自引:1,他引:0
Yáñez-Mó M Gutiérrez-López MD Cabañas C 《Cellular and molecular life sciences : CMLS》2011,68(20):3323-3335
Several recent publications have described examples of physical and functional interations between tetraspanins and specific
membrane proteases belonging to the TM-MMP and α-(ADAMs) and γ-secretases families. Collectively, these examples constitute
an emerging body of evidence supporting the notion that tetraspanin-enriched microdomains (TEMs) represent functional platforms
for the regulation of key cellular processes including the release of surface protein ectodomains ("shedding"), regulated
intramembrane proteolysis ("RIPing") and matrix degradation and assembly. These cellular processes in turn play a crucial
role in an array of physiological and pathological phenomena. Thus, TEMs may represent new therapeutical targets that may
simultaneously affect the proteolytic activity of different enzymes and their substrates. Agonistic or antagonistic antibodies
and blocking soluble peptides corresponding to tetraspanin functional regions may offer new opportunities in the treatment
of pathologies such as chronic inflammation, cancer, or Alzheimer's disease. In this review article, we will discuss all these
aspects of functional regulation of protease activities by tetraspanins. 相似文献
17.
It has long been thought that astrocytes, like other glial cells, simply provide a support mechanism for neuronal function in the healthy and inflamed central nervous system (CNS). However, recent evidence suggests that astrocytes play an active and dual role in CNS inflammatory diseases such as multiple sclerosis (MS). Astrocytes not only have the ability to enhance immune responses and inhibit myelin repair, but they can also be protective and limit CNS inflammation while supporting oligodendrocyte and axonal regeneration. The particular impact of these cells on the pathogenesis and repair of an inflammatory demyelinating process is dependent upon a number of factors, including the stage of the disease, the type and microenvironment of the lesion, and the interactions with other cell types and factors that influence their activation. In this review, we summarize recent data supporting the idea that astrocytes play a complex role in the regulation of CNS autoimmunity. 相似文献
18.
Helan Xiao Debbie X. Li Mingyao Liu 《Cellular and molecular life sciences : CMLS》2012,69(24):4149-4162
Airway epithelial cell migration is essential for lung development and growth, as well as the maintenance of respiratory tissue integrity. This vital cellular process is also important for the repair and regeneration of damaged airway epithelium. More importantly, several lung diseases characterized by aberrant tissue remodeling result from the improper repair of damaged respiratory tissue. Epithelial cell migration relies upon extracellular matrix molecules and is further regulated by numerous local, neuronal, and hormonal factors. Under inflammatory conditions, cell migration can also be stimulated by certain cytokines and chemokines. Many well-known environmental factors involved in the pathogenesis of chronic lung diseases (e.g., cigarette smoking, air pollution, alcohol intake, inflammation, viral and bacterial infections) can inhibit airway epithelial cell migration. Further investigation of cellular and molecular mechanisms of cell migration with advanced techniques may provide knowledge that is relevant to physiological and pathological conditions. These studies may eventually lead to the development of therapeutic interventions to improve lung repair and regeneration and to prevent aberrant remodeling in the lung. 相似文献
19.
DNA photolyases are highly efficient light-driven DNA repair enzymes which revert the genomedamaging effects caused by ultraviolet
(UV) radiation. These enzymes occur in almost all living organisms exposed to sunlight, the only exception being placental
mammals like humans and mice. Their catalytic mechanism employs the light-driven injection of an electron onto the DNA lesion
to trigger the cleavage of cyclobutane- pyrimidine dimers or 6-4 photoproducts inside duplex DNA. Spectroscopic and structural
analysis has recently yielded a concise view of how photolyases recognize these DNA lesions involving two neighboring bases,
catalyze the repair reaction within a nanosecond and still achieve quantum efficiencies of close to one. Apart from these
mechanistic aspects, the potential of DNA photolyases for the generation of highly UV-resistant organisms, or for skin cancer
prevention by ectopical application is increasingly recognized.
Received 29 September 2005; received after revision 30 November 2005; accepted 15 February 2006 相似文献
20.
Following injury a complex but well-orchestrated cellular response stimulating wound healing and tissue regeneration is induced.
The balance of different cytokines, growth factors and cells is important in regulating tissue reorganisation. The immune
system is critically involved in this process. Toll-like receptors (TLRs) are essential to the innate immune system, recognising
microbial pathogens. The recent identification of endogenous ligands of TLRs suggests that they function not only to induce
defensive antimicrobial immune responses but also as a sensitive detection system to initiate tissue regeneration after injury.
Here we present an overview of TLRs and their endogenous ligands, and also review the roles of TLRs in inducing tissue regeneration
after injury and in maintaining homeostasis. The identification of endogenous TLR ligands and their involvement in inducing
tissue regeneration will provide new options to improve tissue reorganization after injury.
Received 26 April 2006; received after revision 16 June 2006; accepted 24 August 2006 相似文献