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Anne-kathrin Classen - One of the best experts on this subject based on the ideXlab platform.
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jak stat signalling mediates cell survival in response to Tissue Stress
Development, 2016Co-Authors: Marco La Fortezza, Andrea Cosolo, Madlin Schenk, Addie Kolybaba, Isabelle Grass, Anne-kathrin ClassenAbstract:Tissue homeostasis relies on the ability of Tissues to respond to Stress. Tissue regeneration and tumour models in Drosophila have shown that c-Jun amino-terminal kinase (JNK) acts as a prominent Stress-response pathway promoting injury-induced apoptosis and compensatory proliferation. A central question remaining unanswered is how both responses are balanced by activation of a single pathway. Signalling through the Janus kinase/Signal transducers and activators of transcription (JAK/STAT) pathway, which is a potential JNK target, is implicated in promoting compensatory proliferation. While we observe JAK/STAT activation in imaginal discs upon damage, our data demonstrate that JAK/STAT and its downstream effector Zfh2 promote the survival of JNK signalling cells. The JNK component fos and the pro-apoptotic gene hid are regulated in a JAK/STAT-dependent manner. This molecular pathway restrains JNK-induced apoptosis and spatial propagation of JNK signalling, thereby limiting the extent of Tissue damage, as well as facilitating systemic and proliferative responses to injury. We find that the pro-survival function of JAK/STAT also drives tumour growth under conditions of chronic Stress. Our study defines the function of JAK/STAT in Tissue Stress and illustrates how crosstalk between conserved signalling pathways establishes an intricate equilibrium between proliferation, apoptosis and survival to restore Tissue homeostasis.
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JAK/STAT signalling mediates cell survival in response to Tissue Stress.
Development (Cambridge England), 2016Co-Authors: Marco La Fortezza, Andrea Cosolo, Madlin Schenk, Addie Kolybaba, Isabelle Grass, Anne-kathrin ClassenAbstract:Tissue homeostasis relies on the ability of Tissues to respond to Stress. Tissue regeneration and tumour models in Drosophila have shown that c-Jun amino-terminal kinase (JNK) acts as a prominent Stress-response pathway promoting injury-induced apoptosis and compensatory proliferation. A central question remaining unanswered is how both responses are balanced by activation of a single pathway. Signalling through the Janus kinase/Signal transducers and activators of transcription (JAK/STAT) pathway, which is a potential JNK target, is implicated in promoting compensatory proliferation. While we observe JAK/STAT activation in imaginal discs upon damage, our data demonstrate that JAK/STAT and its downstream effector Zfh2 promote the survival of JNK signalling cells. The JNK component fos and the pro-apoptotic gene hid are regulated in a JAK/STAT-dependent manner. This molecular pathway restrains JNK-induced apoptosis and spatial propagation of JNK signalling, thereby limiting the extent of Tissue damage, as well as facilitating systemic and proliferative responses to injury. We find that the pro-survival function of JAK/STAT also drives tumour growth under conditions of chronic Stress. Our study defines the function of JAK/STAT in Tissue Stress and illustrates how crosstalk between conserved signalling pathways establishes an intricate equilibrium between proliferation, apoptosis and survival to restore Tissue homeostasis.
Jason H. T. Bates - One of the best experts on this subject based on the ideXlab platform.
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A Progressive Rupture Model of Soft Tissue Stress Relaxation
Annals of Biomedical Engineering, 2013Co-Authors: Jason H. T. Bates, Baoshun MaAbstract:A striking feature of Stress relaxation in biological soft Tissue is that it frequently follows a power law in time with an exponent that is independent of strain even when the elastic properties of the Tissue are highly nonlinear. This kind of behavior is an example of quasi-linear viscoelasticity, and is usually modeled in a purely empirical fashion. The goal of the present study was to account for quasi-linear viscoelasticity in mechanistic terms based on our previously developed hypothesis that it arises as a result of isolated micro-yield events occurring in sequence throughout the Tissue, each event passing the Stress it was sustaining on to other regions of the Tissue until they themselves yield. We modeled Stress relaxation computationally in a collection of Stress-bearing elements. Each element experiences a stochastic sequence of either increases in elastic equilibrium length or decreases in stiffness according to the Stress imposed upon it. This successfully predicts quasi-linear viscoelastic behavior, and in addition predicts power-law Stress relaxation that proceeds at the same slow rate as observed in real biological soft Tissue.
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A Progressive Rupture Model of Soft Tissue Stress Relaxation
Annals of biomedical engineering, 2013Co-Authors: Jason H. T. BatesAbstract:A striking feature of Stress relaxation in biological soft Tissue is that it frequently follows a power law in time with an exponent that is independent of strain even when the elastic properties of the Tissue are highly nonlinear. This kind of behavior is an example of quasi-linear viscoelasticity, and is usually modeled in a purely empirical fashion. The goal of the present study was to account for quasi-linear viscoelasticity in mechanistic terms based on our previously developed hypothesis that it arises as a result of isolated micro-yield events occurring in sequence throughout the Tissue, each event passing the Stress it was sustaining on to other regions of the Tissue until they themselves yield. We modeled Stress relaxation computationally in a collection of Stress-bearing elements. Each element experiences a stochastic sequence of either increases in elastic equilibrium length or decreases in stiffness according to the Stress imposed upon it. This successfully predicts quasi-linear viscoelastic behavior, and in addition predicts power-law Stress relaxation that proceeds at the same slow rate as observed in real biological soft Tissue.
Claudio Bonghi - One of the best experts on this subject based on the ideXlab platform.
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A deep survey of alternative splicing in grape reveals changes in the splicing machinery related to Tissue, Stress condition and genotype
BMC plant biology, 2014Co-Authors: Nicola Vitulo, Claudio Forcato, Elisa Corteggiani Carpinelli, Andrea Telatin, Davide Campagna, Michela D'angelo, Rosanna Zimbello, Massimiliano Corso, Alessandro Vannozzi, Claudio BonghiAbstract:Alternative splicing (AS) significantly enhances transcriptome complexity. It is differentially regulated in a wide variety of cell types and plays a role in several cellular processes. Here we describe a detailed survey of alternative splicing in grape based on 124 SOLiD RNAseq analyses from different Tissues, Stress conditions and genotypes. We used the RNAseq data to update the existing grape gene prediction with 2,258 new coding genes and 3,336 putative long non-coding RNAs. Several gene structures have been improved and alternative splicing was described for about 30% of the genes. A link between AS and miRNAs was shown in 139 genes where we found that AS affects the miRNA target site. A quantitative analysis of the isoforms indicated that most of the spliced genes have one major isoform and tend to simultaneously co-express a low number of isoforms, typically two, with intron retention being the most frequent alternative splicing event. As described in Arabidopsis, also grape displays a marked AS Tissue-specificity, while Stress conditions produce splicing changes to a minor extent. Surprisingly, some distinctive splicing features were also observed between genotypes. This was further supported by the observation that the panel of Serine/Arginine-rich splicing factors show a few, but very marked differences between genotypes. The finding that a part the splicing machinery can change in closely related organisms can lead to some interesting hypotheses for evolutionary adaptation, that could be particularly relevant in the response to sudden and strong selective pressures.
Jiaqi Lu - One of the best experts on this subject based on the ideXlab platform.
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Biaxial mechanical properties of bovine jugular venous valve leaflet Tissues
Biomechanics and Modeling in Mechanobiology, 2017Co-Authors: Hsiao-ying Shadow Huang, Jiaqi LuAbstract:Venous valve incompetence has been implicated in diseases ranging from chronic venous insufficiency (CVI) to intracranial venous hypertension. However, while the mechanical properties of venous valve leaflet Tissues are central to CVI biomechanics and mechanobiology, neither Stress–strain curves nor tangent moduli have been reported. Here, equibiaxial tensile mechanical tests were conducted to assess the tangent modulus, strength and anisotropy of venous valve leaflet Tissues from bovine jugular veins. Valvular Tissues were stretched to 60% strain in both the circumferential and radial directions, and leaflet Tissue Stress–strain curves were generated for proximal and distal valves (i.e., valves closest and furthest from the right heart, respectively). Toward linking mechanical properties to leaflet microstructure and composition, Masson’s trichrome and Verhoeff–Van Gieson staining and collagen assays were conducted. Results showed: (1) Proximal bovine jugular vein venous valves tended to be bicuspid (i.e., have two leaflets), while distal valves tended to be tricuspid; (2) leaflet Tissues from proximal valves exhibited approximately threefold higher peak tangent moduli in the circumferential direction than in the orthogonal radial direction (i.e., proximal valve leaflet Tissues were anisotropic; $$p
D J Winton - One of the best experts on this subject based on the ideXlab platform.
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Stem cells, quiescence and rectal carcinoma: an unexplored relationship and potential therapeutic target
British Journal of Cancer, 2011Co-Authors: S Buczacki, R J Davies, D J WintonAbstract:Stem cells are responsible for maintaining differentiated cell numbers during normal physiology and at times of Tissue Stress. They have the unique capabilities of proliferation, self-renewal, clonogenicity and multi-potentiality. It is a widely held belief that stem-like cells, known as cancer stem cells (CSCs), maintain tumours. The majority of currently identified intestinal stem cell populations appear to be rapidly cycling. However, quiescent stem cell populations have been suggested to exist in both normal intestinal crypts and tumours. Quiescent CSCs may have particular significance in the modern management of colorectal cancer making their identification and characterisation a priority. In this review, we discuss the current evidence surrounding the identification and microenvironmental control of stem cell populations in intestinal crypts and tumours as well as exploring the evidence supporting the existence of a quiescent stem and CSC population in the gut and other Tissues.
