| 1. |
- Ackermann, Paul W, et al.
(author)
-
Neuronal pathways in tendon healing and tendinopathy : update
- 2014
-
In: Frontiers in Bioscience-Landmark. - Stockholm : Karolinska Institutet, Dept of Molecular Medicine and Surgery. - 1093-4715 .- 1093-9946 .- 2768-6698.
-
Journal article (peer-reviewed)abstract
- The regulatory mechanisms involved in tendon homeostasis and repair are not fully understood. Accumulating data, however, demonstrate that the nervous system, in addition to afferent (sensory) functions, through efferent neuronal pathways plays an active role in regulating pain, inflammation, and tissue repair processes. Thus, in normal-, healing- and tendinopathic tendons three major neuronal signalling pathways consisting of autonomic, sensory and glutamatergic neuromediators have been established. In healthy tendons, these neural elements are found in the paratenon, whereas the proper tendon is practically devoid of nerves, reflecting that normal tendon homeostasis is regulated by pro- and anti-inflammatory mediators from the tendon surroundings. During tendon repair, however, there is extensive nerve ingrowth into the tendon proper and subsequent time-dependent appearance of sensory, autonomic and glutamatergic mediators, which amplify and fine-tune inflammation and tendon regeneration. In tendinopathy, excessive and protracted sensory and glutamatergic signalling may be involved in inflammatory, painful and hypertrophic tissue reactions. As our understanding of these processes improves, neuronal mediators may prove to be useful in the development of targeted pharmacotherapy and tissue engineering approaches to painful, degenerative and traumatic tendon disorders.
|
|
| 2. |
- Achour, Cyrinne, et al.
(author)
-
Long non-coding RNA and Polycomb : an intricate partnership in cancer biology
- 2018
-
In: Frontiers in Bioscience. - : IMR Press. - 1093-9946 .- 1093-4715. ; 23, s. 2106-2132
-
Journal article (peer-reviewed)abstract
- High-throughput analyses have revealed that the vast majority of the transcriptome does not code for proteins. These non-translated transcripts, when larger than 200 nucleotides, are termed long non-coding RNAs (lncRNAs), and play fundamental roles in diverse cellular processes. LncRNAs are subject to dynamic chemical modification, adding another layer of complexity to our understanding of the potential roles that lncRNAs play in health and disease. Many lncRNAs regulate transcriptional programs by influencing the epigenetic state through direct interactions with chromatin-modifying proteins. Among these proteins, Polycomb repressive complexes 1 and 2 (PRC1 and PRC2) have been shown to be recruited by lncRNAs to silence target genes. Aberrant expression, deficiency or mutation of both lncRNA and Polycomb have been associated with numerous human diseases, including cancer. In this review, we have highlighted recent findings regarding the concerted mechanism of action of Polycomb group proteins (PcG), acting together with some classically defined lncRNAs including X-inactive specific transcript (XIST), antisense non-coding RNA in the INK4 locus (ANRIL), metastasis associated lung adenocarcinoma transcript 1 (MALAT1), and HOX transcript antisense RNA (HOTAIR).
|
|
| 3. |
- Ackermann, PW, et al.
(author)
-
Neuronal pathways in tendon healing
- 2009
-
In: Frontiers in bioscience (Landmark edition). - : IMR Press. - 2768-6698 .- 1093-9946 .- 1093-4715. ; 14:13, s. 5165-5187
-
Journal article (peer-reviewed)
|
|
| 4. |
- Akusjärvi, Göran
(author)
-
Temporal regulation of adenovirus major late alternative RNA splicing
- 2008
-
In: Frontiers in Bioscience. - : IMR Press. - 1093-9946 .- 1093-4715. ; 13, s. 5006-5015
-
Journal article (peer-reviewed)abstract
- Adenovirus makes extensive use of alternative RNA splicing to produce a complex set of spliced mRNAs during replication. The accumulation of viral mRNAs is subjected to a temporal regulation, a mechanism that ensures that proteins that are needed at certain stages of the virus life cycle are produced in a timely fashion. The complex interactions between the virus and the host cell RNA splicing machinery has been studied in detail during the last decade. These studies have resulted in the characterization of two viral proteins, E4-ORF4 and L4-33K, that adenovirus uses to remodel the host cell RNA splicing machinery. Here I will review the current knowledge of how mRNA expression from the adenovirus major late transcription unit is controlled with a particular emphasis on how cis-acting sequence element, trans-acting factors and mechanisms regulating adenovirus major late L1 alternative RNA splicing is controlled.
|
|
| 5. |
|
|
| 6. |
- Aldskogius, Håkan
(author)
-
Mechanisms and consequences of microglial responses to peripheral axotomy
- 2011
-
In: Frontiers in Bioscience. - : IMR Press. - 1093-9946 .- 1093-4715 .- 1945-0516 .- 1945-0524. ; 3, s. 857-868
-
Journal article (peer-reviewed)abstract
- Microglia respond rapidly to injury of peripheral nerve axons (axotomy). This response is integrated into the responses of the injured neurons, i.e. processes for neuron survival, axon regeneration and restoration of target contact. The microglial response is also integrated in changes in presynaptic terminals on axotomized motor or autonomic neurons and in changes in the central terminals of peripherally axotomized sensory neurons. Microglia also has an established role in interacting with astrocytes to shape their response to peripheral axotomy. Axotomy models in mice have demonstrated a role for microglia in regulating the entry of lymphocytes into motor nuclei or sensory areas following peripheral axotomy. Whether this is a universal component of peripheral nerve injury remains to be determined. Under certain circumstances, microglia activated by axotomy are major contributors to CNS pathology, e.g. in models of neuropathic pain. However, the general roles played by microglia after peripheral nerve injury are still incompletely understood. Early proposals that the microglial reaction to peripheral nerve injury is preparatory for the eventuality of neuron degeneration may still have relevance.
|
|
| 7. |
- Bernhardt, Nadine Rabe, et al.
(author)
-
Genetic analysis of left-right coordination of locomotion
- 2013
-
In: Frontiers in Bioscience. - : IMR Press. - 1093-9946 .- 1093-4715. ; 18, s. 20-35
-
Journal article (peer-reviewed)abstract
- While there is a rather large amount of data from pharmacological and anatomical studies of the murine locomotor CPG network, comprehensive information regarding the cellular and functional properties of the neuronal populations is lacking. Here, we describe concepts arising from genetic studies of the locomotor network with a focus on commissural interneurons regulating left-right coordination. In particular, this involves several families of axon guidance molecules relevant for midline crossing. We also describe recent advances within the field of neural circuit analysis, including imaging, genetic inactivation and optogenetic strategies, which are applicable to locomotor circuits. Such efforts, for example by using available genetic markers, should substantially increase our possibilities to decipher the functionality of spinal cord neuronal networks.
|
|
| 8. |
- Blum, K., et al.
(author)
-
Substance use disorder a bio-directional subset of reward deficiency syndrome
- 2017
-
In: Frontiers in Bioscience-Landmark. - : IMR Press. - 1093-9946 .- 1093-4715. ; 22, s. 1534-1548
-
Journal article (peer-reviewed)abstract
- This commentary is to inform clinicians challenged with an increase in people seeking treatment for Substance Use Disorder (SUD), that the ninety percent revolving door, is, in part, due to post-withdrawal, untreated neurotoxicity. This impairment attenuates neurotransmitter signaling and compromises resting state functional connectivity, leading to unwanted sequelae including depression, sleep disturbances, sensation seeking, lack of satisfaction and impulsivity. Neuroimaging studies indicate that neurobiological recovery can take years. Like a "double edge sword" SUD has a biological bi-directional (bio-directional) effect on the brain reward circuitry. The acute intake of psychoactive drugs results in heightened dopaminergic activity, while, the opposite, hypodopaminergia occurs following chronic abuse. Individuals with SUD can have a genetic predisposition, compounded by stress and neurotoxically induced, epigenetic insults that impact recovery from protracted abstinence. Follow-up post -short-term recovery usually includes supportive therapies and programs like 12 -steps and other fellowships. However, relapse will usually occur if post -short-term recovery hypodopaminergia is not treated with attempts at epigenetic manipulation of compromised brain neurochemistry using some manner of pro-dopamine regulation.
|
|
| 9. |
- Brinkmalm-Westman, Ann, 1966, et al.
(author)
-
Proteomics/peptidomics tools to find CSF biomarkers for neurodegenerative diseases.
- 2009
-
In: Frontiers in bioscience : a journal and virtual library. - : IMR Press. - 1093-4715. ; 14, s. 1793-806
-
Research review (peer-reviewed)abstract
- Neurodegenerative diseases are characterized by premature neuronal loss in specific brain regions. During the past decades our knowledge on molecular mechanisms underlying neurodegeneration has increased immensely and resulted in promising drug candidates that might slow down or even stop the neuronal loss. These advances have put a strong focus on the development of diagnostic tools for early or pre-clinical detection of the disorders. In this review we discuss our experience in the field of neuroproteomics/peptidomics, with special focus on biomarker discovery studies that have been performed on CSF samples from well-defined patient and control populations.
|
|
| 10. |
- Dilip Deb, Kaushik, et al.
(author)
-
Nanotechnology in stem cells research: advances and applications
- 2012
-
In: Frontiers in Bioscience. - : Frontiers in Bioscience. - 1093-9946 .- 1093-4715. ; 17, s. 1747-1760
-
Journal article (peer-reviewed)abstract
- Human beings suffer from a myriad of disorders caused by biochemical or biophysical alteration of physiological systems leading to organ failure. For a number of these conditions, stem cells and their enormous reparative potential may be the last hope for restoring function to these failing organ or tissue systems. To harness the potential of stem cells for biotherapeutic applications, we need to work at the size scale of molecules and processes that govern stem cells fate. Nanotechnology provides us with such capacity. Therefore, effective amalgamation of nanotechnology and stem cells - medical nanoscience or nanomedicine - offers immense benefits to the human race. The aim of this paper is to discuss the role and importance of nanotechnology in stem cell research by focusing on several important areas such as stem cell visualization and imaging, genetic modifications and reprogramming by gene delivery systems, creating stem cell niche, and similar therapeutic applications.
|
|
| 11. |
|
|
| 12. |
|
|
| 13. |
- Hansen-Schwartz, Jacob, et al.
(author)
-
Cerebral vasoconstriction after subarachnoid hemorrhage - Role of changes in vascular receptor phenotype
- 2008
-
In: Frontiers in Bioscience. - : IMR Press. - 1093-9946 .- 1093-4715. ; 13, s. 2160-2164
-
Journal article (peer-reviewed)abstract
- The pathological constriction of cerebral arteries known as cerebral vasospasm (CVS) is with a delay of 4 to 10 days linked to subarachnoid hemorrhage. Several agents have been suggested as being responsible; amongst these perhaps 5-hydroxytryptamine (5-HT) and endothelin-1 (ET-1) are the most prominent given their ability to elicit powerful constriction of cerebral arteries. Investigating both 5-HT and ET receptors we have observed that there are distinct changes in receptor phenotype after experimental SAH, namely upregulation of the ETB and 5-HT1B receptors, and that this upregulation is linked to a higher sensitivity to the endogenous agonists. It has also been shown that reduction in regional cerebral blood flow (CBF) is associated with receptor upregulation and interventional animal experiments have shown a benefit from inhibiting the PKC and MAP kinase pathways on receptor upregulation, CBF and neurological outcome.
|
|
| 14. |
|
|
| 15. |
|
|
| 16. |
|
|
| 17. |
|
|
| 18. |
- Kirby, T.J., et al.
(author)
-
The role of microRNAs in skeletal muscle health and disease
- 2015
-
In: Frontiers in Bioscience. - Irvine, USA : Frontiers in Bioscience. - 1093-9946 .- 1093-4715. ; 20, s. 37-77
-
Journal article (peer-reviewed)abstract
- Over the last decade non-coding RNAs have emerged as importance regulators of gene expression. In particular, microRNAs are a class of small RNAs of ∼ 22 nucleotides that repress gene expression through a post-transcriptional mechanism. MicroRNAs have been shown to be involved in a broader range of biological processes, both physiological and pathological, including myogenesis, adaptation to exercise and various myopathies. The purpose of this review is to provide a comprehensive summary of what is currently known about the role of microRNAs in skeletal muscle health and disease.
|
|
| 19. |
|
|
| 20. |
- Lee, Chunsik, et al.
(author)
-
Type 3 cystatins : fetuins, kininogen and histidine-rich glycoprotein
- 2009
-
In: Frontiers in Bioscience. - : IMR Press. - 1093-9946 .- 1093-4715. ; 14, s. 2911-2922
-
Journal article (peer-reviewed)abstract
- This review describes the properties of four structurally related, abundant plasma proteins denoted fetuin-A/alpha-2-Heremans Schmid-glycoprotein (AHSG), fetuin-B (FETUB), kininogen (KNG) and histidine-rich glycoprotein (HRG). These proteins form a subgroup (denoted type 3) within the cystatin superfamily of cysteine protease inhibitors. Apart from KNG, the type 3 proteins appear to lack cystatin activity. AHSG has its major function in regulation of bone mineralization; the physiological role of FETUB is poorly understood. KNG serves dual functions in the assembly of the protein complex initiating the surface-activated blood coagulation cascade and as a precursor for the kinin hormones. The heparin-binding HRG has also been implicated in regulation of coagulation. In addition, several members of the type 3 cystatins have been implicated in tumor growth and shown to regulate endothelial cell function and formation of new blood vessels, angiogenesis. Thus, these proteins may potentially be useful in treatment of diseases characterized by excess angiogenesis such as cancer.
|
|
| 21. |
- McLaughlin, Christopher R., et al.
(author)
-
Bioengineered corneas for transplantation and in vitro toxicology
- 2009
-
In: Frontiers in Bioscience. - : Frontiers in Bioscience. - 1093-9946 .- 1093-4715. ; 14, s. 3326-3337
-
Journal article (peer-reviewed)abstract
- Bioengineered corneas have been designed to replace partial or the full-thickness of defective corneas, as an alternative to using donor tissues. They range from prosthetic devices that solely address replacement of the corneas function, to tissue engineered hydrogels that permit regeneration of host tissues. In cases where corneal stem cells have been depleted by injury or disease, most frequently involving the superficial epithelium, tissue engineered lamellar implants reconstructed with stem cells have been transplanted. In situ methods using ultraviolet A (UVA) crosslinking have also been developed to strengthen weakened corneas. In addition to the clinical need, bioengineered corneas are also rapidly gaining importance in the area of in vitro toxicology, as alternatives to animal testing. More complex, fully innervated, physiologically active, three-dimensional organotypic models are also being tested.
|
|
| 22. |
- Meraviglia, Viviana, et al.
(author)
-
Higher cardiogenic potential of iPSCs derived from cardiac versus skin stromal cells
- 2016
-
In: Frontiers in Bioscience. - 1093-9946 .- 1093-4715. ; 21, s. 719-43
-
Journal article (peer-reviewed)abstract
- Prior studies have demonstrated that founder cell type could influence induced pluripotent stem cells (iPSCs) molecular and developmental properties at early passages after establishing their pluripotent state. Herein, we evaluated the persistence of a functional memory related to the tissue of origin in iPSCs from syngeneic cardiac (CStC) vs skin stromal cells (SStCs). We found that, at passages greater than 15, iPSCs from cardiac stromal cells (C-iPSCs) produced a higher number of beating embryoid bodies than iPSCs from skin stromal cells (S-iPSCs). Flow cytometry analysis revealed that dissected beating areas from C-iPSCs exhibited more Troponin-T positive cells compared to S-iPSCs. Beating areas derived from C-iPSCs displayed higher expression of cardiac markers, more hyperpolarized diastolic potentials, larger action potential amplitude and higher contractility than beaters from skin. Also, different microRNA subsets were differentially modulated in CStCs vs SStCs during the reprogramming process, potentially accounting for the higher cardiogenic potentials of C-iPSCs vs S-iPSCs. Therefore, the present work supports the existence of a founder organ memory in iPSCs obtained from the stromal component of the origin tissue.
|
|
| 23. |
- Månsson, Alf, et al.
(author)
-
In vitro assays of molecular motors - impact of motor-surface interactions
- 2008
-
In: Frontiers in Bioscience. - 1093-9946 .- 1093-4715. ; 13:May 1, s. 5732-5754
-
Research review (other academic/artistic)abstract
- In many types of biophysical studies of both single molecules and ensembles of molecular motors the motors are adsorbed to artificial surfaces. Some of the most important assay systems of this type (in vitro motility assays and related single molecule techniques) will be briefly described together with an account of breakthroughs in the understanding of actomyosin function that have resulted from their use. A poorly characterized, but potentially important, entity in these studies is the mechanism of motor adsorption to surfaces and the effects of motor surface interactions on experimental results. A better understanding of these phenomena is also important for the development of commercially viable nanotechnological applications powered by molecular motors. Here, we will consider several aspects of motor surface interactions with a particular focus on heavy meromyosin (HMM) from skeletal muscle. These aspects will be related to heavy meromyosin structure and relevant parts of the vast literature on protein-surface interactions for non-motor proteins. An overview of methods for studying motor-surface interactions will also be given. The information is used as a basis for further development of a model for HMM-surface interactions and is discussed in relation to experiments where nanopatterning has been employed for in vitro reconstruction of actomyosin order. The challenges and potentials of this approach in biophysical studies, compared to the use of self-assembly of biological components into supramolecular protein aggregates (e. g. myosin filaments) will be considered. Finally, this review will consider the implications for further developments of motor-powered lab-on-a-chip devices.
|
|
| 24. |
|
|
| 25. |
- Schwartz, Stefan
(author)
-
HPV-16 RNA processing
- 2008
-
In: Frontiers in Bioscience. - : IMR Press. - 1093-9946 .- 1093-4715. ; 13, s. 5880-5891
-
Journal article (peer-reviewed)abstract
- To understand human papillomavirus type 16 (HPV-16) gene regulation, it is necessary to understand HPV-16 RNA processing. HPV-16 encodes multiple 5'- and 3'-splice sites and two polyadenylation signals pAE and pAL (Figure 1). The major 3'-splice site on the HPV-16 genome (SA3358) is used for generation of E6, E7, E4, L1 and L2 mRNAs. It encodes a suboptimal splice signal but is under control of a strong enhancer that renders SA3358 one of the most efficiently used splice sites on the HPV-16 genome. Thereby SA3358 indirectly blocks HPV-16 late gene expression. The early polyA signal is also under control of the early UTR sequence and multiple RNA elements in the L2 coding region that interact with hnRNP H. The two splice sites SD3632 and SA5639 are used exclusively by late mRNAs and are under control of multiple splicing silencer elements. The silencers at SA5639 are located in the L1 coding region and interact with hnRNP A1. So far, only polypyrimidine tract binding protein (PTB) has been shown to induce late gene expression.
|
|
| 26. |
- Strauss, Johannes, et al.
(author)
-
Circadian clocks in crustaceans : identified neuronal and cellular systems
- 2010
-
In: Frontiers in Bioscience. - : IMR Press. - 1093-9946 .- 1093-4715. ; 15:1, s. 1040-1074
-
Journal article (peer-reviewed)abstract
- Circadian rhythms are known for locomotory and reproductive behaviours, and the functioning of sensory organs, nervous structures, metabolism and developmental processes. The mechanisms and cellular bases of control are mainly inferred from circadian phenomenologies, ablation experiments and pharmacological approaches. Cellular systems for regulation summarised here comprise the retina, the eyestalk neuroendocrine X-organ-sinus gland system, several neuropeptides such as red pigment concentrating, hyperglycaemic and pigment-dispersing hormones, and factors such as serotonin and melatonin. No master clock has been identified, but a model of distributed clockwork involves oscillators such as the retinular cells, neurosecretory systems in the optic lobes, putative brain pacemakers, and the caudal photoreceptor. Extraretinal brain photoreceptors mediate entrainment. Comparative analyses of clock neurons and proteins known from insects may allow the identification of candidate clock neurons in crustaceans as putative homologues in the two taxa. Evidence for the existence of "insect-like" intracellular clock proteins and (light sensitive) transcription factors is scarce, but clock-, period-, and cryptochrome-gene products have been localised in the CNS and other organs rendering further investigations into crustacean clockwork very promising.
|
|
| 27. |
|
|
| 28. |
|
|
| 29. |
|
|
| 30. |
- Tripathi, Rekha, PhD student, 1985-, et al.
(author)
-
SLC38A10 Transporter Plays a Role in Cell Survival Under Oxidative Stress and Glutamate Toxicity
- 2021
-
In: Frontiers in Bioscience. - : Frontiers Media S.A.. - 1093-9946 .- 1093-4715 .- 2296-889X. ; 8
-
Journal article (peer-reviewed)abstract
- Solute carrier (SLC) transporters regulate amino acids, glucose, ions, and metabolites that flow across cell membranes. In the brain, SLCs are the key regulators of neurotransmission, in particular, the glutamate/GABA-glutamine (GGG) cycle. Genetic mutations in SLCs are associated with various neurodevelopmental and neurodegenerative diseases. In this study, we have investigated the role of SLC38A10 under acute oxidative and glutamate stress in mouse primary cortical cells from SLC38A10 knockout (KO) mice. The ER/golgi localized transporter, SLC38A10, transports glutamate, glutamine, and alanine in brain cells, and the aim of this study was to determine the possible effects of removal of SLC38A10 in primary cortical cells under glutamate and oxidative challenges. Primary cortical neuronal cultures of wild-type (WT) cell and SLC38A10 KO mice were subjected to different concentrations of glutamate and hydrogen peroxide. There was no morphological change observed between KO and WT cortical neurons in culture. Interestingly, KO cells showed significantly lower cell viability and higher cell death compared to WT cells under both glutamate and hydrogen peroxide exposure. Further, we evaluated the possible role of p53 in neuronal cell apoptosis in KO cells. We found decreased intracellular p53 protein levels under glutamate and hydrogen peroxide treatment in KO cortical cells. In contrast, caspase 3/7 activity remains unaltered under all conditions. These results demonstrate an indirect relationship between the expression of SLC38A10 and p53 and a role in the cell defense mechanism against neurotoxicity.
|
|
| 31. |
|
|
| 32. |
- Wennmalm, Stefan, 1970-, et al.
(author)
-
Inverse-fluorescence correlation spectroscopy: more information and less labeling
- 2011
-
In: Frontiers in Bioscience. - : Frontiers in Bioscience. - 1093-9946 .- 1093-4715 .- 1945-0516 .- 1945-0524. ; s3, s. 385-392
-
Journal article (peer-reviewed)abstract
- Inverse-Fluorescence Correlation Spectroscopy(iFCS) is a recently developed modification of standardFCS that allows analysis of particles and biomoleculeswithout labeling. The particles generate no signal; insteadthe signal is generated by a surrounding medium. Particlesdiffusing through the FCS-detection volume displace afraction of the surrounding medium, causing transient dipsin the detected signal. These give information about themobility and concentration of the analyzed particles. Alsolabeled particles can be analyzed, whereby their signal iscross-correlated with that from the surrounding medium(iFCCS). This can give information about the volume of thelabeled particles, or alternatively about the size of thedetection volume. Also the interaction of unlabeledparticles with small, labeled ligands can be analyzed withiFCCS. This allows using cross-correlation as a sensitiveindication of binding, even though only one binding-partneris labeled. This review describes the principles of iFCS andiFCCS and measurements of microspheres dissolved in asurrounding medium containing alexa 488. We also discusspractical considerations, and future possibilities foranalyses of biomolecules.
|
|
| 33. |
- Brorsson, Ann-Christin, et al.
(author)
-
Methods and models in neurodegenerative and systemic protein aggregation diseases
- 2010
-
In: Frontiers in bioscience : a journal and virtual library. - : Frontiers in Bioscience Publications. - 1093-4715. ; 15, s. 373-396
-
Research review (peer-reviewed)abstract
- Protein misfolding and aggregation are implicated in a wide range of increasingly prevalent human diseases ranging from dementia to diabetes. In this review we discuss the current experimental strategies that are being employed in the investigation of the pathogenesis of three important protein misfolding disorders. The first, Alzheimers disease (AD), is the most prevalent neurodegenerative disease and is thought to be initiated by the aggregation of a natively unstructured peptide called amyloid beta (Abeta). We discuss methods for the characterization of the aggregation properties of Abeta in vitro and how the results of such experiments can be correlated with data from animal models of disease. We then consider another form of amyloidosis, where a systemic distribution of amyloid deposit is caused by aggregation and deposition of mutational variants of lysozyme. We describe how experiments in vitro, and more recently in vivo, have provided insights into the origins of this disease. Finally we outline the varied paradigms that have been employed in the study of the serpinopathies, and in particular, a dementia caused by neuroserpin polymerization.
|
|
| 34. |
|
|
| 35. |
- Liu, Kui
(author)
-
Stem cell factor (SCF)-kit mediated phosphatidylinositol 3 (PI3) kinase signaling during mammalian oocyte growth and early follicular development.
- 2006
-
In: Frontiers in bioscience : a journal and virtual library. - 1093-4715. ; 11, s. 126-35
-
Research review (other academic/artistic)abstract
- The bi-directional communication between mammalian oocytes and their surrounding granulosa cells has been shown to be crucial for ovarian follicular development. Studies on molecules derived from the oocytes, such as growth differentiation factor-9 (GDF-9) and bone morphogenetic protein-15 (BMP-15), have attracted great interest during the past decade, and it is common knowledge nowadays that these molecules participate in the bi-directional dialogue between the oocytes and their surrounding granulosa cells as well as follicular development. However, signaling molecules and pathways inside mammalian oocytes that control oocyte growth and early development of ovarian follicles, which may be monitored by factors produced by granulosa cells, have not been studied extensively. Based on our own data as well as ovarian phenotypes observed in several gene modified mice strains that were generated for studies of signal transduction, immunology and cancer, the current review focuses on the key features of the activation of oocyte phosphatidylinositol 3 kinase (PI3 kinase) pathway and its possible roles during mammalian oocyte growth and follicular development. We propose that the cascade from the granulosa cell-produced stem cell factor (SCF) to the oocyte surface SCF receptor Kit, and to the oocyte PI3 kinase pathway, may play an important role in the regulation of growth rate of mammalian oocytes, as well as in the activation and development of ovarian follicles.
|
|
| 36. |
- Medini, Paolo, et al.
(author)
-
Visual experience and plasticity of the visual cortex : a role for epigenetic mechanisms
- 2008
-
In: Frontiers in bioscience : a journal and virtual library. - 1093-4715. ; 13, s. 3000-3007
-
Journal article (peer-reviewed)abstract
- Plasticity of cortical circuits is maximal during critical periods of postnatal development. Ocular dominance plasticity is a classical model to understand the role of experience in development of the visual cortex. Recent studies are beginning to unravel the synaptic mechanisms underlying this form of plasticity and to elucidate the different plasticity of juvenile and adult animals at mechanistic and molecular level. These investigations indicate that this form of plasticity is regulated by factors located at extracellular and intracellular level. The molecular composition of the extracellular environment in which synaptic plasticity occurs changes during development becoming less permissive for plasticity. In addition, visual experience activates epigenetic mechanisms of regulation of gene transcription that becomes downregulated in adult animals.
|
|
| 37. |
|
|
