Academic literature on the topic 'Coculture'

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Journal articles on the topic "Coculture"

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Miyoshi, Hirotoshi, Chiaki Sato, Yuichiro Shimizu, and Misa Morita. "Expansion of mouse hematopoietic stem/progenitor cells in three-dimensional cocultures on growth-suppressed stromal cell layer." International Journal of Artificial Organs 42, no. 7 (February 12, 2019): 374–79. http://dx.doi.org/10.1177/0391398819827596.

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With the aim of establishing an effective method to expand hematopoietic stem/progenitor cells for application in hematopoietic stem cell transplantation, we performed ex vivo expansion of hematopoietic stem/progenitor cells derived from mouse fetal liver cells in three-dimensional cocultures with stromal cells. In these cocultures, stromal cells were first cultured within three-dimensional scaffolds to form stromal layers and then fetal liver cells containing hematopoietic cells were seeded on these scaffolds to expand the hematopoietic cells over the 2 weeks of coculture in a serum-containing medium without the addition of cytokines. Prior to coculture, stromal cell growth was suppressed by treatment with the DNA synthesis inhibitor mitomycin C, and its effect on hematopoietic stem/progenitor cell expansion was compared with that in control cocultures in which fetal liver cells were cocultured with three-dimensional freeze-thawed stromal cells. After coculture with mitomycin C-treated stromal cells, we achieved a several-fold expansion of the primitive hematopoietic cells (c-kit+hematopoietic progenitor cells >7.8-fold, and CD34+hematopoietic stem/progenitor cells >3.5-fold). Compared with control cocultures, expansion of hematopoietic stem/progenitor cells tended to be lower, although that of hematopoietic progenitor cells was comparable. Thus, our results suggest that three-dimensional freeze-thawed stromal cells have higher potential to expand hematopoietic stem/progenitor cells compared with mitomycin C-treated stromal cells.
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Portnoy, Joshua, Tianli Pan, Charles A. Dinarello, John M. Shannon, Jay Y. Westcott, Lening Zhang, and Robert J. Mason. "Alveolar type II cells inhibit fibroblast proliferation: role of IL-1α." American Journal of Physiology-Lung Cellular and Molecular Physiology 290, no. 2 (February 2006): L307—L316. http://dx.doi.org/10.1152/ajplung.00102.2005.

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Alveolar type II (ATII) cells inhibit fibroblast proliferation in coculture by releasing or secreting a factor(s) that stimulates fibroblast production of prostaglandin E2(PGE2). In the present study, we sought to determine the factors released from ATII cells that stimulate PGE2production in fibroblasts. Exogenous addition of rat IL-1α to cultured lung fibroblasts induced PGE2secretion in a dose-response manner. When fibroblasts were cocultured with rat ATII cells, IL-1α protein was detectable in ATII cells and in the coculture medium between days 8 and 12 of culture, correlating with the highest levels of PGE2. Furthermore, under coculture conditions, IL-1α gene expression increased in ATII cells (but not fibroblasts) compared with either cell cultured alone. In both mixed species (human fibroblasts-rat ATII cells) and same species cocultures (rat fibroblasts and ATII cells), PGE2secretion was inhibited by the presence of IL-1 receptor antagonist (IL-1Ra) or selective neutralizing antibody directed against rat IL-1α (but not IL-1β). Conditioned media from cocultures inhibited fibroblast proliferation, and this effect was abrogated by the addition of IL-1Ra. Addition of keratinocyte growth factor (KGF) resulted in an earlier increase in PGE2secretion and fibroblast inhibition ( day 8 of coculture). This effect was inhibited by indomethacin but was not altered by IL-1Ra. We conclude that in this coculture system, IL-1α secretion by ATII cells is one factor that stimulates PGE2production by lung fibroblasts, thereby inhibiting fibroblast proliferation. In addition, these studies demonstrate that KGF enhances ATII cell PGE2production through an IL-1α-independent pathway.
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Gilead, L., O. Bibi, and E. Razin. "Fibroblasts induce heparin synthesis in chondroitin sulfate E containing human bone marrow-derived mast cells." Blood 76, no. 6 (September 15, 1990): 1188–95. http://dx.doi.org/10.1182/blood.v76.6.1188.1188.

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Abstract Human bone marrow-derived mast cells (hBMMCs), differentiated in vitro in suspension culture and under the influence of human peripheral blood mononuclear cells conditioned medium (hCM), were tested for their response to recombinant human interleukin-3 (rhIL-3) and for their behavior in different microenvironments. The hBMMCs were incubated in the presence of rhIL-3 and the changes in their proliferation rate were determined. Recombinant hIL-3 induced a more than sixfold increase in 3H-thymidine uptake into the hBMMC DNA in a dose-dependent manner. Human CM used as a control for proliferation response induced a more than eightfold maximal proliferation rate increase. Rabbit anti-rhIL-3 completely inhibited hBMMC 3H-thymidine uptake induced by rhIL-3 and decreased the hCM-induced proliferation by approximately 50%. These hBMMCs were cocultured with four different mytomicin C-treated cell monolayers and assayed for phenotypic changes. After only 2 days in coculture with either embryonic mouse skin-derived fibroblasts (MESFs) or human skin-derived fibroblasts (HSFs), a marked increase in granule number and density was noted on staining with toluidine blue. Mast cells that initially stained alcian blue+/safranin- at day 0 of coculture became alcian blue+/safranin+ during the coculture period. Human BMMC proteoglycan synthesis shifted from approximately 85% chondroitin sulfate E to approximately 60% heparin within 14 to 19 days of coculture with the MESF monolayer and to approximately 50% heparin within 19 days of coculture with the HSF monolayer. None of the above- mentioned changes were noted in cocultures of hBMMCs with 3T3 cell line fibroblast monolayers or in cocultures with bovine vascular endothelium (BVE) cell monolayers. These results demonstrate microenvironmental effects exerted by the MESF and HSF monolayers on IL-3-dependent hBMMCs similar to those reported in the conversion of murine mast cell phenotype.
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Gilead, L., O. Bibi, and E. Razin. "Fibroblasts induce heparin synthesis in chondroitin sulfate E containing human bone marrow-derived mast cells." Blood 76, no. 6 (September 15, 1990): 1188–95. http://dx.doi.org/10.1182/blood.v76.6.1188.bloodjournal7661188.

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Human bone marrow-derived mast cells (hBMMCs), differentiated in vitro in suspension culture and under the influence of human peripheral blood mononuclear cells conditioned medium (hCM), were tested for their response to recombinant human interleukin-3 (rhIL-3) and for their behavior in different microenvironments. The hBMMCs were incubated in the presence of rhIL-3 and the changes in their proliferation rate were determined. Recombinant hIL-3 induced a more than sixfold increase in 3H-thymidine uptake into the hBMMC DNA in a dose-dependent manner. Human CM used as a control for proliferation response induced a more than eightfold maximal proliferation rate increase. Rabbit anti-rhIL-3 completely inhibited hBMMC 3H-thymidine uptake induced by rhIL-3 and decreased the hCM-induced proliferation by approximately 50%. These hBMMCs were cocultured with four different mytomicin C-treated cell monolayers and assayed for phenotypic changes. After only 2 days in coculture with either embryonic mouse skin-derived fibroblasts (MESFs) or human skin-derived fibroblasts (HSFs), a marked increase in granule number and density was noted on staining with toluidine blue. Mast cells that initially stained alcian blue+/safranin- at day 0 of coculture became alcian blue+/safranin+ during the coculture period. Human BMMC proteoglycan synthesis shifted from approximately 85% chondroitin sulfate E to approximately 60% heparin within 14 to 19 days of coculture with the MESF monolayer and to approximately 50% heparin within 19 days of coculture with the HSF monolayer. None of the above- mentioned changes were noted in cocultures of hBMMCs with 3T3 cell line fibroblast monolayers or in cocultures with bovine vascular endothelium (BVE) cell monolayers. These results demonstrate microenvironmental effects exerted by the MESF and HSF monolayers on IL-3-dependent hBMMCs similar to those reported in the conversion of murine mast cell phenotype.
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Park, Jung Jae, Hong Joo Moon, Jin Hyun Park, Taek Hyun Kwon, Youn-Kwan Park, and Joo Han Kim. "Induction of proinflammatory cytokine production in intervertebral disc cells by macrophage-like THP-1 cells requires mitogen-activated protein kinase activity." Journal of Neurosurgery: Spine 24, no. 1 (January 2016): 167–75. http://dx.doi.org/10.3171/2015.3.spine14729.

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OBJECT To determine the role played by mitogen-activated protein kinase (MAPK) signaling in the interactions between macrophages and intervertebral disc (IVD) cells, it was hypothesized that MAPK inhibition would modulate the production of the proinflammatory cytokines associated with inflammatory reaction in IVD cells. METHODS Human annulus fibrosus (AF) and nucleus pulposus (NP) cells were cocultured with phorbol myristate acetate-stimulated macrophage-like THP-1 cells, with and without SB202190 (a p38-α and -β inhibitor), SP600125 (a c-Jun N-terminal kinase [JNK] inhibitor), and PD98059 (an extracellular signal-regulated kinase [ERK] 1/2 inhibitor). The cytokines in conditioned media from cocultured and macrophage-exposed (nemotic) cells were assayed using enzyme-linked immunosorbent assays (ELISAs). RESULTS Interleukin (IL)-6 and IL-8 were secreted in greater quantities by the cocultured cells compared with naive IVD cells and macrophages (MΦ) cultured alone. The tumor necrosis factor (TNF)- α and IL-6 levels produced by the NP cells cocultured with MΦs (NP-MΦ) were significantly lower than those produced by AF cells cocultured with MΦs (AF-MΦ). SB202190 dose-dependently suppressed IL-6 secretion by AF-MΦ and NP-MΦ cocultures, and 10 μM SB202190 significantly decreased IL-6 and IL-8 production in nemotic AF and NP pellets. SP600125 at 10 μM significantly suppressed the production of TNF α IL-6. and IL-8 in AF-MΦ and NP-MΦ cocultures and significantly suppressed IL-1β production in the NP-MΦ coculture. Administration of 10 μM PD98059 significantly decreased IL-6 levels in the AF-MΦ coculture, and decreased the levels of TNF α and IL-8 in both the AF-MΦ and NP-MΦ cocultures. CONCLUSIONS The present study shows that inhibitors of p38 MAPK effectively controlled IL-6 production during inflammatory reactions and that JNK and ERK1/2 inhibitors successfully suppressed the production of major proinflammatory cytokines during interactions between macrophages and IVD cells. Therefore, selective blockade of these signals may serve as a therapeutic approach to symptomatic IVD degeneration.
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Wang, Ying, Boping Yang, Pan Hu, Shentao Lu, Li Lei, and Lubin Liu. "The Role of Gap Junctions in the Generation of Smooth Muscle Cells from Bone Marrow Mesenchymal Stem Cells." Disease Markers 2022 (August 12, 2022): 1–9. http://dx.doi.org/10.1155/2022/1491327.

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Background. Studies have shown that stem cell transplantation can improve smooth muscle cell (SMC) regeneration and remodelling. Gap junctions can enhance the cytoprotective effects of neighbouring cells. We investigated the effect of gap junctions on the differentiation of bone marrow mesenchymal stem cells (BMSCs) into SMCs. Materials and Methods. Rat BMSCs and SMCs were obtained from the bone marrow and bladder of Sprague-Dawley rats, respectively. Flow cytometry and multilineage differentiation were performed to assess the characteristics of these cells. BMSCs and SMCs were incubated together in cocultures in the presence and absence of heptanol, an uncoupler of gap junctions. Cocultures were divided into three groups consisting of a contact coculture, noncontact coculture, and contact coculture plus heptanol groups. The expression of BMSC-specific markers and the effect of gap junctions on the differentiation of BMSCs were evaluated by performing real-time reverse transcription-polymerase chain reaction, immunofluorescence analysis, and western blotting after cocultures. Results. CD90 and CD44 were markedly expressed, and CD31 and CD45 were weakly or not expressed in BMSCs. The cells also showed good osteogenic and adipogenic differentiation ability. Compared with the noncontact coculture group, the SMC markers such as α-SMA, calponin, and connexin43 increased in the contact coculture group. The effect of contact in the coculture group was significantly weakened by heptanol. Conclusions. The results suggested that gap junctions play an important role in the generation of SMCs from BMSCs. The formation of SMCs can potentially be used to repair the sphincter muscle of patients with stress urinary incontinence.
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Wang, Qishan, Bingxin Xu, Kaijian Fan, Jing Wu, and Tingyu Wang. "CypB-CD147 Signaling Is Involved in Crosstalk between Cartilage and FLS in Collagen-Induced Arthritis." Mediators of Inflammation 2020 (August 29, 2020): 1–12. http://dx.doi.org/10.1155/2020/6473858.

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To investigate the crosstalk between cartilage and fibroblast-like synoviocytes (FLS) in rheumatoid arthritis (RA), we adopted an in vitro coculture system model of collagen-induced arthritis (CIA) cartilage and CIA FLS monolayer. CIA rat samples of the synovium and femur head were collected for isolation of FLS and coculture system. Cartilages were treated with vehicle (Ctrl group), 10 ng/mL interleukin- (IL-) 1α (IL-1α group), and 10 ng/mL IL-1α plus 10 μM dexamethasone (Dex group) for 3 days before coculture with FLS for further 2 days. After the coculture, FLS were collected to determine the influences of articular cartilage on synoviocytes. Whether the CypB-CD147 signaling pathway is involved in the interactions between cartilage and FLS is assayed. Results showed that IL-1α-stimulated CIA cartilage promoted the proliferation and reduced the apoptosis of FLS. Increased inflammatory cytokines and decreased p57 expression were found in cocultured FLS stimulated by IL-1α-challenged CIA cartilage. Upregulation of NF-κB and I-κB kinase β (IKK-β) and downregulation of the inhibitor of NF-κBα (I-κBα) protein were observed in cocultured FLS. After coculture, significant increases in the expression of cyclophilin B (CypB) and CD147 were observed in CIA cartilage and FLS, respectively. Furthermore, results of immunofluorescence staining showed that the anti-CD147 antibody significantly suppressed p65 nuclear translocation in cocultured FLS stimulated by IL-1α-challenged CIA cartilage. In conclusion, inflammatory effects in the cartilage-FLS coculture system are associated with the CypB-CD147 mediating NF-κB pathway which may further enhance the inflammation in RA.
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Gao, Chun-Hui, Hui Cao, Peng Cai, and Søren J. Sørensen. "The initial inoculation ratio regulates bacterial coculture interactions and metabolic capacity." ISME Journal 15, no. 1 (September 4, 2020): 29–40. http://dx.doi.org/10.1038/s41396-020-00751-7.

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AbstractCoculture is an important model system in microbial ecology studies. As a key experimental parameter, the initial inoculation ratio has a crucial impact on the results of the coculture system. However, such an effect has never been investigated under multiple niche conditions. In this study, we established a simple coculture system with two model bacteria in various carbon sources and investigated the influence of initial inoculum ratios of 1:1000 to 1000:1 on community structure, function, and bacterial interaction. We found that the final ratio of the cocultures with different initial inoculum ratios differed in approximately five-sixths of the carbon sources, suggesting that the final ratio is highly dependent on the initial inoculum ratio, while the carbon source preferences of bacteria could not predict the final ratio of cocultures. Furthermore, we found that the initial ratio could regulate the metabolic capacity of the coculture, as only cocultures with initial ratios of 1:1 and 1000:1 gained high capacity on 14 specific carbon sources. The underlying reason may be that the pattern of species interaction is changed by the initial ratio. In conclusion, we showed that the initial ratio can induce emergent properties in coculture. These findings suggest that the initial ratio not only impacts the reproducibility of coculture experiments but also can influence our understanding of generic microbial ecology.
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Hyakumura, Tomoko, Stuart McDougall, Sue Finch, Karina Needham, Mirella Dottori, and Bryony A. Nayagam. "Organotypic Cocultures of Human Pluripotent Stem Cell Derived-Neurons with Mammalian Inner Ear Hair Cells and Cochlear Nucleus Slices." Stem Cells International 2019 (November 20, 2019): 1–14. http://dx.doi.org/10.1155/2019/8419493.

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Stem cells have been touted as a source of potential replacement neurons for inner ear degeneration for almost two decades now; yet to date, there are few studies describing the use of human pluripotent stem cells (hPSCs) for this purpose. If stem cell therapies are to be used clinically, it is critical to validate the usefulness of hPSC lines in vitro and in vivo. Here, we present the first quantitative evidence that differentiated hPSC-derived neurons that innervate both the inner ear hair cells and cochlear nucleus neurons in coculture, with significantly more new synaptic contacts formed on target cell types. Nascent contacts between stem cells and hair cells were immunopositive for both synapsin I and VGLUT1, closely resembling expression of these puncta in endogenous postnatal auditory neurons and control cocultures. When hPSCs were cocultured with cochlear nucleus brainstem slice, significantly greater numbers of VGLUT1 puncta were observed in comparison to slice alone. New VGLUT1 puncta in cocultures with cochlear nucleus slice were not significantly different in size, only in quantity. This experimentation describes new coculture models for assessing auditory regeneration using well-characterised hPSC-derived neurons and highlights useful methods to quantify the extent of innervation on different cell types in the inner ear and brainstem.
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Mhyre, Andrew J., A. Mario Marcondes, Emily Y. Spaulding, and H. Joachim Deeg. "Stroma-dependent apoptosis in clonal hematopoietic precursors correlates with expression of PYCARD." Blood 113, no. 3 (January 15, 2009): 649–58. http://dx.doi.org/10.1182/blood-2008-04-152686.

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Abstract The role of the marrow microenvironment in the pathophysiology of myelodysplastic syndromes (MDSs) remains controversial. Using stromal/hematopoietic cell cocultures, we investigated the effects of stroma-derived signals on apoptosis sensitivity in hematopoietic precursors. The leukemia-derived cell line KG1a is resistant to proapoptotic ligands. However, when cocultured with the human stromal cell line HS5 (derived from normal marrow) and exposed to tumor necrosis factor-α (TNF-α), KG1a cells showed caspase-3 activation and induction of apoptosis. Apoptosis was contact dependent. Identical results were obtained in coculture with primary stroma. Gene-expression profiling of KG1a cells identified coculture-induced up-regulation of various genes involved in apoptosis, including PYCARD. Suppression of PYCARD expression in KG1a by miRNA interfered with apoptosis. Knockdown of the TNF receptor 1 (TNFR1) or TNFR2 in HS5 cells had no effect. However, knockdown of R1 in KG1a cells prevented TNF-α–induced apoptosis, while apoptosis was still induced by TNF-α–related apoptosis-inducing ligand. Primary CD34+ cells from MDS marrow, when cocultured with HS5 and TNF-α, also underwent apoptosis. In contrast, no apoptosis was observed in CD34+ cells from the marrow of healthy donors. These data indicate that stroma may convey not only protective effects on hematopoietic cells, but, dependent upon the milieu, may also facilitate apoptosis.
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Dissertations / Theses on the topic "Coculture"

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Jing, Duohui. "Mobilisation, Isolation and Coculture of Haematopoietic Stem Cells." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-39915.

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Since decades, hematopoietic stem cell transplantation (HSCT) has become a well established treatment modality for hematological malignancies and non-malignant disorders. Autologous and allogeneic hematopoietic stem cells (HSCs) mobilized into the peripheral blood (PB) have been used as a preferred source of transplantable stem cells1-3. And umbilical cord blood (UCB) has been introduced as a more attractive HSC source for HSCT, because fetal stem cells in UCB are speculated to be more primitive in comparison to adult stem cells. However the limited amount of HSCs is limiting their application for stem cell therapy in clinic. Therefore, people started to utilize extra-embryonic tissue to harvest more fetal stem cells, while people also tried to optimize the clinical protocol to mobilize more adult stem cells out of adult bone marrow. The innovative strategies and feasible procedures were discussed in this thesis. The axis of the chemokine receptor CXCR4 and its ligand SDF-1 is important for trafficking and homing of HSCs. It has already been demonstrated that the bicyclam AMD3100, a CXCR4 antagonist, in combination with G-CSF is able to induce a significant mobilization of CD34+ cells4. And human placenta is a potent hematopoietic niche containing hematopoietic stem and progenitor cells throughout development5. The homing of HSCs to the placenta is probably also mediated by the expression of SDF-1 as demonstrated for the bone marrow niche. In this study (part 1 of the chapter “Results and discussions”), we utilized AMD3100 to mobilize HSCs from placenta. And we can demonstrate that the CXCR4 antagonist AMD3100 mobilise placenta derived CD34+ cells ex utero already after 30 min of incubation and may further enhance the efficacy of harvesting placenta-derived HSC. The alpha4 integrin CD49d is involved in migration and homing of hematopoietic stem cells (HSC). Therapeutic application of natalizumab, an anti-CD49d antibody, in patients with multiple sclerosis (MS) has been associated with increased levels of circulating CD34+ progenitors. In our study (part 2 of the chapter “Results and discussions”), we compared circulating HSCs from MS patients after natalizumab treatment and HSCs mobilized by G-CSF in healthy volunteers, with regard to their migratory potential, clonogenicity and gene expression. CD34+ cells in the blood and marrow of natalizumab-treated patients expressed less of the stem cell marker CD133, were enriched for erythroid progenitors (CFU-E) and expressed lower levels of adhesion molecules. The level of surface CXCR-4 expression on CD34+ cells from patients treated with natalizumab was higher compared to that of CD34+ cells mobilized by granulocyte-colony stimulating factor (G-CSF) (median 43.9% vs. 15.1%). This was associated with a more than doubled migration capacity towards a chemokine stimulus. Furthermore, CD34+ cells mobilized by natalizumab contained more m-RNA for p21 and less MMP9 compared to G-CSF mobilised HSC. Our data indicate that G-CSF and CD49d blockade mobilize different HSC subsets and suggest that both strategies may be differentially applied in specific cell therapy approaches. In order to further improve the clinical outcome of HSC transplantation, many groups are focusing on ex vivo maintain or expand HSC. Unfortunately, the maintenance of HSC in vitro is difficult to achieve because of their differentiation. This is presumably caused by a lack of appropriate cues that are provided in vivo by the microenvironment. Indeed, HSCs located in the bone marrow are interacting with a specific microenvironment referred to as the stem cell niche, which regulates their fate in terms of quiescence, self-renewal and differentiation. An orchestra of signals mediated by soluble factors and/or cell-to-cell contact keeps the balance and homeostasis of self-renewal, proliferation and differentiation in vivo. To investigate the communication between HSCs and the niche, coculture assays with mesenchymal stromal cells (MSCs) were performed in vitro. Here, we can demonstrate that cell-to-cell contact has a significant impact on hematopoietic stem cells expansion, migratory potential and stemness. In this study (part 3 of the chapter “Results and discussions”), we investigated in more detail the spatial relationship between hematopoietic stem cells and mesenchymal stromal cells during ex-vivo expansion. And we defined three distinct localizations of HSCs relative to MSC layer: (i) those in supernatant (non-adherent cells); (ii) cells adhering on the surface of mesenchymal stromal cells (phase-bright cells) and (iii) cells beneath the mesenchymal stromal cells (phase-dim cells). Our data suggest that the mesenchymal stromal cell surface is the dominant location where hematopoietic stem cells proliferate, whereas the compartment beneath the mesenchymal stromal cell layer seems to be mimicking the stem cell niche for more immature cells. Our data provide novel insight into the construction and function of three-dimensional HSC–MSC microenvironments. In summary, we provided a new method to isolate fetal stem cells from extra-embryonic tissue (i.e. placenta) in the first part, then we discussed an innovative strategy with CD49d blockade to improve clinical modality for adult stem cell mobilization in the second part, and finally we investigated HSC maintenance and expansion in vitro and provided feasible way to mimic HSC niche in vitro in the last part. This thesis contributes to HSC-based stem cell therapy in two aspects, i.e. 1) fetal and adult stem cell isolation holding great therapeutic potential for blood diseases; 2) ex vivo stem cell manipulation providing a valuable platform to model HSC niche regulation.
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Apple, Allon Aliza. "Bilaminar coculture of stem cells and instructive cells for tissue regeneration." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2009. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3390115.

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Thesis (Ph.D.)--University of California, San Francisco with the University of California, Berkeley, 2009.
Source: Dissertation Abstracts International, Volume: 71-02, Section: B, page: . Adviser: Jeffrey C. Lotz.
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Hinkerohe, Daniel. "Effects of cytokines on microglial phenotypes and astroglial coupling in an inflammatory coculture model /." Bochum, 2006. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253108.

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Bernard, Yohann. "Stress oxydatif, inflammation vasculaire et métalloprotéinases : étude in vitro sur un modèle de coculture." Thesis, Nancy 1, 2008. http://www.theses.fr/2008NAN10067/document.

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Au cours de l’athérosclérose, l’invasion de la paroi vasculaire par les leucocytes conduit à l’inflammation de ce tissu et à l’établissement d’un stress oxydatif. Ce travail aborde les effets du stress oxydatif et les effets d’interactions potentielles entre un modèle de neutrophiles (?HL60) et des cellules endothéliales (HCAEC) ou musculaires lisses (HCSMC) de coronaires humaines sur les métalloprotéinases (MMPs) cellulaires et la mobilité des ?HL60. Au cours des passages, la lignée promyélocytaire HL60, différenciée en modèle de neutrophiles ?HL60, subit des variations d’expression et de production de MMP9 et de ses propriétés de mobilité. Les espèces réactives de l’oxygène (ERO) d’origine biochimique ou cellulaire ne modifient pas l’activité MMP2 ou MMP9 des HCAEC et HCSMC. Il n’y a pas modification des activités MMPs en coculture ?HL60/HCAEC mais stimulation de l’activité MMP9 en coculture ?HL60/HCSMC. Les HCSMC stimulent les capacités migratoires et favorisent la réponse invasive des ?HL60 au N-formyl-L-Méthionyl-L-Leucyl-L-Phénylalanine. Les enzymes antioxydantes ont peu d’effet sur la mobilité, stimulent expression et production de MMP9 des ?HL60 et semblent diminuer l’effet stimulant des HCSMC sur la production de MMP9 par ?HL60. Les HCSMC expriment et/ou sécrétent certains cytokines (IL8, IL6, IL1?, CCL2, CXCL12) impliquées dans l’athérosclérose. En conclusion, l’interaction ?HL60/HCSMC entraîne une augmentation de production de MMP9, modulée par les ERO, et une stimulation de mobilité des ?HL60. Les cytokines inflammatoires impliquées dans l’athérosclérose et exprimées par les HSCMC sont des acteurs potentiels dans la réponse sécrétoire et/ou migratoire des ?HL60
During atherosclerosis leucocytes invade the vascular wall, inducing inflammation and production of oxidative stress by reactive oxygen species (ROS). We tested the effects of an oxidative stress and/or potential interactions between a neutrophil model (?HL60) and human coronary endothelial (HCAEC) or smooth muscle (HCSMC) cells, on ?HL60 mobility and production and activity of cellular metalloproteinases. Cell passaging of the promyelocytic HL60 cell line, differentiated by DMSO in a neutrophil model (?HL60), induces variations in cell mobility and production of MMP9. ROS from biochemical or cellular sources did not modify MMP2 or MMP9 activity in HCAEC or HCSMC. There is no modification of MMPs activities in ?HL60/HCAEC cocultures, but stimulation of ?HL60 MMP9 activity in ?HL60/HCSMC cocultures. Basal migration capacities and N-formyl-L-Methionyl-L-Leucyl-L-Phenylalanine -stimulated invasion abilities of ?HL60 increase in presence of HCSMC. Antioxidant enzymes barely change ?HL60 mobility, increase expression and production of ?HL60 MMP9 and seem to reduce the stimulating effect of HCSMC on ?HL60 MMP9 production. HCSMC also express and/or secrete some cytokines (IL8, IL6, IL1?, CCL2, CXCL12) implicated in atherosclerosis. In conclusion, interactions between ?HL60 and HCSMC induce an increase in MMP9 secretion, which is modulated by ROS, and a stimulation of ?HL60 mobility. Expression by HCSMC of inflammatory cytokines implicated in atherosclerosis allows to identify potential candidates responsible for the secretory and/or migratory response of ?HL60
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L'Herondelle, Killian. "Etude sur neurones sensoriels et kératinocytes des mécanismes cellulaires et moléculaires impliqués dans le prurit de la ciguatéra." Thesis, Brest, 2016. http://www.theses.fr/2016BRES0115.

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La ciguatéra est une forme d’intoxication faisant suite à l’ingestion de poissons contaminés par des toxines appelées « ciguatoxines ». Cette intoxication endémique des régions tropicales est un problème économique et de santé non négligeable qui tend à prendre de plus en plus d’ampleur. L’essor du tourisme, le réchauffement climatique et la hausse des exportations internationales de poissons tropicaux favorisent l’expansion de la ciguatéra aux parties du globe au climat tempéré, jusqu’alors peu concernées par cette maladie. Les enjeux thérapeutiques et économiques de la ciguatéra sont de taille puisqu’il n’existe aucun moyen rapide et fiable de détecter un poisson contaminé et qu’aucun traitement efficace permettant sa prise en charge n’a actuellement été établi.Le prurit, terme médical désignant les démangeaisons est un symptôme notamment associé aux maladies de peau qui impacte grandement la qualité de vie des patients qui en souffrent.Ces dernières décennies, de nombreuses études scientifiques ont permis de mieux comprendre sa physiopathologie. Le prurit est un symptôme fréquemment observé chez les personnes atteintes de ciguatéra, d’où l’appellation « la Gratte », souvent employée pour faire référence à la pathologie.Dans le but d’étudier les mécanismes cellulaires à l’origine du prurit et des autres troubles sensoriels cutanés survenant lors de la ciguatéra, nous avons étudié l’effet des ciguatoxines sur un modèle in vitro de neurones sensoriels cocultivés avec des kératinocytes. Nous avons mis en évidence la libération dans le surnageant des neuropeptides de l'inflammation neurogène, SP et CGRP. L'effet d'antagonistes sélectionnés a été testé afin mettre en évidence les médiateurs impliqués dans la libération de neuropeptides. Par ailleurs, la signalisation cellulaire sous-jacente de cette sécrétion de neuropeptides a été étudiée par des expériences d’imagerie calcique réalisées sur neurones et kératinocytes.Les résultats obtenus valident notre coculture en tant que modèle de choix pour l’étude in vitro des mécanismes cellulaires, et plus généralement, dans les troubles neurocutanés impliqués dans le prurit ciguatérique. Parmi les antagonistes testés, une molécule s’est avérée particulièrement intéressante pour inhiber les effets constatés de la toxine. Ces résultats originaux, obtenus avec l’antagoniste d’un médiateur du prurit, présentent une perspective thérapeutique nouvelle et prometteuse, pour répondre à un enjeu de santé publique futur
Ciguatera fish poisoning (CFP) is a seafood poisoning occurring after contaminated fish fleshes ingestion containing toxins called « ciguatoxines » (CTXs). This illness, originating from tropical and subtropical areas, is an economic and health problems which becomes substantial in relation to international tropical fishes export and tourism development, as well as global warming rise. Those factors contribute to CFP sprouting in non-endemic temperate climate regions which were not until then concerned by CFP. Economic and health stakes of CFP are important since no reliable and ready-to-use detection system for CTXs in fishes have been developed, along with no relevant cure has been established to treat CFP.Pruritus, medical term refer to itch, is a clinical sign usually associated to skin diseases which strongly alter patients’ quality of life. Last decades, several studies allowed to better understand pruritus pathophysiology. Interestingly, people suffering from CFP frequently present pruritus, hence designation “La Gratte” or “La Gratel (le)” employed in endemic areas.The aim of these works was to study cellular and molecular mechanisms of CTXs at the root of neurological cutaneous troubles occurring in CFP. Here, we evaluated CTXs effects on in vitro model composed of sensory neurons cocultived with primary keratinocytes, quantifying neuropeptides known to be involved in pruritus. Compiling knowledges about CFP and pruritus pathophysiology, some antagonists were tested to neutralize CTXs-mediated neuropeptide release. To deal with signaling pathways in depth of neuropeptide exocytosis induced by CTXs, mechanism known to be accurately regulated by calcium homeostasis, calcium imaging experiments were performed.Results obtained in this project confirm the use of such a model to elucidate cellular mechanism of CFP pruritus, but also constitute an alternative in vitro tool to study chemicals inducing abnormal cutaneous senses. Among antagonists tested, one stands out from the crowd and was proved to be effective to inhibit CTXs-evoked effects studied. Those originals results, collected with antagonist of pruritus mediator, show new and promiscuous therapeutic prospects for future health concern
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Janny, Laurent. "Coculture embryonnaire en fecondation in vitro humaine : etude d'une serie prospective randomisee de 606 ponctions." Clermont-Ferrand 1, 1994. http://www.theses.fr/1994CLF1BOO1.

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Lease, Christopher William Minto, and Lease Chris@saugov sa gov au. "Biodegradation of High Molecular Weight Polycyclic Aromatic Hydrocarbons in Soils by Defined Bacterial and Fungal Cocultures." Flinders University. Biological Sciences, 2006. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20060803.114120.

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Despite microbial degradation being the primary route of degradation of PAHs in soils, high molecular weight polycyclic aromatic hydrocarbons (such as benzo[a]pyrene) have consistently proven to e resistant to microbial attack. However, recent research has demonstrated the potential for bacterial-fungal co-cultures to achieve biodegradation of high molecular weight PAHs. The aim of this research was to determine the efficacy of co-culture bioaugmentation for the remediation of high molecular weight PAHcontaminated soils. PAH degrading bacteria were enriched on multiple PAHs and isolated on pyrene from both contaminated (soil from a former manufactured gas plant) and uncontaminated (agricultural soil, termite mound matrix and kangaroo faeces) sources. The bacterial isolates were identified using 16SrRNA analysis as Mycobacterium sp. Strain BS5, Mycobacterium sp. Strain KA5 and Mycobacterium sp. Strain KF4 or fatty acid methyl ester (FAME) analysis as Ralstonia pickettii and Stenotrophomonas maltophilia. The initial phase of assessment of PAH degradation by fungal and bacterial coculture components was undertaken using liquid media. Two fungal isolates from a previous investigation into the coculture process (Penicillium janthinellum) and the American Type Culture Collection (Phanerochaete chrysosporium) were assessed for their ability to degrade benzo[a]pyrene in minimal media and MYPD. The fungal isolates were found to be able to degrade benzo[a]pyrene cometabolically in MYPD. The bacterial isolates and two others from previous investigations were assessed for their ability to degrade single PAHs (fluorene, phenanthrene, fluoranthene, pyrene and benzo[a]pyrene) in liquid culture. This process was used as an initial screen to select the best bacterial isolates for further investigation of PAH degradation by axenic cultures and cocultures with the fungal isolates using a PAH mixture. Based on the results of these experiments four bacterial isolates (VUN 10,010, Mycobacterium 1B, Mycobacterium sp. Strain BS5 and Mycobacterium sp. Strain KA5) and the two fungal isolates were selected to investigate further using a PAH mixture composed of the previously mentioned PAHs. It was found that the use of a fungal bacterial coculture increased the degradation of the PAH mixture beyond that of axenic bacterial cultures. Based on these experiments, the coculture composed of P. janthinellum and VUN 10,010 was selected for assessment of its ability to degrade the same PAH mixture in spiked soil microcosm experiments. Natural attenuation, axenic P. janthinellum, axenic VUN 10,010 and a coculture of these two organisms were assessed for PAH degradation in soil microcosms over a 100 day period. Inoculation of microcosms with the coculture resulted in the removal of benzo[a]pyrene by 11 mg/kg (± 1.21 mg/kg) (30%) over the 100 day incubation period. Substantial PAH degradation was also observed in the microcosms assesing natural attenuation. Using an alternative sequential inoculation method, initially inoculating with P. janthinellum then 50 days later with VUN 10,010 significantly enhanced the removal of benzo[a]pyrene. After 100 days incubation, benzo[a]pyrene was degraded below detection limits in two of three microcosms, compared to a 4.95 mg/kg (± 4.64 mg/kg) (14.7 %) reduction in soil microcosms inoculated using an alternative inoculation process of VUN 10,010 followed by P. janthinellum. Attempts were made to optimise the process using sequential inoculation and soil amendments intended to enhance the performance of the fungal component using distilled water and 1% glucose. The addition of distilled water was not observed to substantially influence the ability of the coculture to degrade PAHs, whereas the addition of 1% glucose was found to inhibit PAH degradation.
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Xu, Ruiling. "Investigating stroma-mediated resistance to gemcitabine, using a novel fluroescence-based coculture model of pancreatic cancer." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709342.

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Huppert, Cécile. "Développement d’un modèle de coculture cellules dendritiques lymphocytes T pour l’évaluation du danger des substances sensibilisantes." Thesis, Université de Lorraine, 2018. http://www.theses.fr/2018LORR0195/document.

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Les allergies représentent un problème majeur dans le domaine des maladies professionnelles et ont un impact sérieux sur la vie des travailleurs. Les allergies professionnelles sont principalement cutanées et respiratoires ; elles peuvent être causées par des produits chimiques de bas poids moléculaire. Dans le passé, les tests destinés à identifier les produits susceptibles d’entraîner des allergies étaient réalisés sur l’animal. Or, la législation européenne engage à limiter le recours à l’expérimentation animale pour évaluer le pouvoir sensibilisant des substances chimiques, incitant à développer des tests in vitro de substitution. C’est dans ce contexte que nous avons cherché à développer des modèles de cultures cellulaires destinés à identifier les substances sensibilisantes. Un premier modèle utilisant des cellules dendritiques dérivées de moelle osseuse (BMDC) de souris BALB/c a été développé et a donné des résultats prometteurs pour l’identification des produits sensibilisants et leur catégorisation selon leur puissance sensibilisante. De plus, la voie de signalisation Nrf2/Keap1 semble être impliquée dans la réponse de ce modèle cellulaire aux sensibilisants. Dans le but de compléter ce modèle et d’évaluer la capacité des BMDC à activer les lymphocytes T (LT), un modèle de coculture de BMDC et LT a été mis au point avec un sensibilisant de référence avant d’être testé sur un ensemble de produits de référence (sensibilisants cutanés et respiratoires, irritants et non sensibilisants). Les BMDC de notre modèle, exposées à des sensibilisants, se sont révélées capables d’activer les LT en coculture. Enfin, des essais préliminaires utilisant des cellules de souris de souche C57BL6/J dans notre modèle de coculture ont donné des résultats comparables à ceux obtenus avec des cellules issues de la souche BALB/c. Les modèles de cultures cellulaires BMDC et de coculture BMDC-LT sont prometteurs dans le cadre du développement de méthodes de substitution à l’expérimentation animale pour l’évaluation du pouvoir sensibilisant de substances chimiques
Allergies constitute an important issue in the field of occupational health and have a serious impact on the lives of workers. Occupational allergies are mainly contact and respiratory allergies and can be caused by low molecular weight chemicals. In the past, the tests that were used to identify the potential allergens were carried out on animals. However, European legislation has provided the impetus for reducing the use of animal testing to assess the sensitization potential of chemicals and promoted the development of alternative in vitro tests. In this context, we aimed to develop cell culture models to identify sensitizers. A first model using bone marrow derived dendritic cells (BMDC) from BALB/c mice was developed and showed promising results for identifying sensitizers and classify them according to their allergenic potency. Moreover, the Nrf2/Keap1 pathway seems to be involved in the response of this cell model to sensitizers. In order to supplement this model and to assess the functionality of BMDC, a BMDC-T cell (TC) coculture model was developed with a reference sensitizer before being tested on a range of reference sensitizers (cutaneous and respiratory sensitizers, irritants and non-sensitizers). The BMDC of our model, while exposed to sensitizers, were able to activate TC in coculture. Finally, preliminary tests using the cells of C57BL6/J mice in our coculture model showed that similar results to those obtained with cells from the BALB/c strain. The models of BMDC cultures and BMDC-TC coculture are promising for the development of alternative methods to animal experimentation assessing the sensitizing potential of chemicals
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Madiedo-Podvršan, Sabrina. "Development of a lung-liver in vitro coculture model for the risk assessment of inhaled xenobiotics." Electronic Thesis or Diss., Compiègne, 2022. http://www.theses.fr/2022COMP2703.

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L’urbanisation et la mondialisation sont des phénomènes de société qui multiplient et complexifient les sources de pollution. Parmi elles, la pollution atmosphérique impacte notablement la santé humaine à l’échelle mondiale de par son caractère transfrontière. L’appareil respiratoire est une voie d’absorption de nombreux xénobiotiques, sous forme de gaz, d’aérosols ou de nanoparticules. Une fois dans les voies respiratoires, les substances inhalées sont susceptibles d’interagir avec les cellules pulmonaires. Les mécanismes par lesquels des xénobiotiques inhalés induisent des dommages pulmonaires sont complexes, notamment en raison de l’hétérogénéité cellulaire des poumons. En raison de cette complexité, les modèles animaux constituent un outil de référence pour les études toxicologiques prédictives, cependant, dans le contexte européen de réduction de l’expérimentation animale (REACH, et les règles 3R), le développement de méthodes alternatives fiables est devenu une nécessité. Les modèles in vitro sont de bons candidats car plus simple et moins couteux à mettre en oeuvre que les modèles vivo et permettent de travailler avec des cellules ou des tissus d’origine humaine ce qui contribue à améliorer la pertinence des résultats. Cependant, l’extrapolation limitée du vitro au vivo est souvent liée à un manque de complexité des modèles, notamment en raison de l’absence de communication inter-organes. Les technologies des multi-organes sur puce cherchent à surmonter ces limitations en connectant plusieurs organoïdes métaboliquement actifs au sein d’un même circuit de culture afin de reproduire des interactions de type systémiques. Dans ce contexte, nous décrivons un modèle permettant de connecter in vitro, par le biais de la microfluidique, une barrière pulmonaire (voie d’entrée des xénobiotiques inhalés) à un organe détoxifiant tel que le foie, afin d’évaluer la toxicité liée à un stress inhalatoire de façon plus systémique. Cette approche permet de considérer la biotransformation des composés inhalés et l’interaction inter-organes comme possible modulateurs de la toxicité. Le projet étant dans les premières phase de développement, la robustesse expérimentale était au coeur du projet. L’objectif principal était de prouver qu’une substance modèle était capable de transiter dans le dispositif, au travers des deux compartiments tissulaires, afin de pouvoir étudier la dynamique inter-organes poumon/foie en condition de stress xénobiotique. Le projet a été articulé en trois phases expérimentales : - Caractérisation des réponses biologiques spécifiques aux tissus pulmonaire et hépatique en réponse à un stress. La viabilité, la fonctionnalité et les activités métaboliques des monocultures ont été évaluées après exposition à une substance modèle. - Adaptation et préparation des monocultures aux conditions de co-culture afin de préserver la viabilité et la fonctionnalité des tissus. - Les compartiments pulmonaire et hépatique ont été cultivés jointement dans un circuit de culture microfluidique fermé. La co-culture a été exposée à une substance modèle à travers la barrière pulmonaire afin d’imiter un mode d’exposition inhalatoire. Les paramètres de viabilité et de fonctionnalité des tissus ont été évalué post-culture afin de mettre en évidence quelconque phénomène d’interaction inter-organe. La caractérisation du modèle de co-culture a été réalisé grâce à l’exposition d’un agent hépatotoxique de référence, largement étudié dans la littérature : l’acétaminophène aussi connu sous le nom de paracétamol (APAP). L’exposition à la barrière pulmonaire n’est pas physiologique mais permet d’observer quantitativement le passage et la circulation du xénobiotique à travers le dispositif car l’APAP interfère avec la viabilité et les performances métaboliques hépatique, permettant ainsi de vérifier que le compartiment hépatique peut avoir accès à l’exposition effectuée à travers la barrière pulmonaire
Urbanization and globalization are prevailing social phenomena that multiply and complexify the sources of modern pollution. Amongst others, air pollution has been recognized as an omnipresent life-threatening hazard, comprising a wide range of toxic airborne xenobiotics that expose man to acute and chronic threats. The defense mechanisms involved in hazardous exposure responses are complex and comprise local and systemic biological pathways. Due to this complexity, animal models are considered prime study models. However, in light of animal experimentation reduction (3Rs), we developed and investigated an alternative in vitro method to study systemic-like responses to inhalationlike exposures. In this context, a coculture platform was established to emulate interorgan crosstalks between the pulmonary barrier, which constitutes the route of entry of inhaled compounds, and the liver, which plays a major role in xenobiotic metabolism. Both compartments respectively comprised a Calu-3 insert and a HepG2/C3A biochip which were jointly cultured in a dynamically-stimulated environment for 72 hours. The present model was characterized using acetaminophen (APAP), a well-documented hepatotoxicant, to visibly assess the passage and circulation of a xenobiotic through the device. Two kinds of models were developed: (1) the developmental model allowed for the technical setup of the coculture, and (2) the physiological-like model better approximates a vivo environment. Based on viability, and functionality parameters the developmental model showed that the Calu-3 bronchial barrier and the HepG2/C3A biochip can successfully be maintained viable and function in a dynamic coculture setting for 3 days. In a stress-induced environment, present results reported that the coculture model emulated active and functional in vitro crosstalk that seemingly was responsive to high (1.5 and 3 mM) and low (12 and 24 μM) xenobiotic exposure doses. Lung/liver crosstalk induced modulation of stress response dynamics, delaying cytotoxicity, proving that APAP fate, biological behaviors and cellular stress responses were modulated in a broader systemic-like environment
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Books on the topic "Coculture"

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Hinkerohe, Daniel. Effects of cytokines on microglial phenotypes and astroglial coupling in an inflammatory coculture model. 2006.

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Book chapters on the topic "Coculture"

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Pang, Yi, Kimberly Simpson, José Javier Miguel-Hidalgo, and Renate Savich. "Neuron/Oligodendrocyte Myelination Coculture." In Methods in Molecular Biology, 131–44. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7862-5_10.

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Swire, Matthew, and Charles ffrench-Constant. "Oligodendrocyte–Neuron Myelinating Coculture." In Oligodendrocytes, 111–28. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9072-6_7.

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Afshari, Fardad T., and James W. Fawcett. "Astrocyte–Schwann-Cell Coculture Systems." In Methods in Molecular Biology, 381–91. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-452-0_25.

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Godke, R. A., E. G. Blakewood, and J. K. Thibodeaux. "In Vitro Coculture of Mammalian Embryos." In Technology and Infertility, 135–64. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4613-9205-7_14.

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Richards, Mark, and Harry Mellor. "In Vitro Coculture Assays of Angiogenesis." In Methods in Molecular Biology, 159–66. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3628-1_10.

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Wei, Haoche, Ananthalakshmy Sundararaman, Sarah Line Bring Truelsen, David Gurevich, Jacob Thastrup, and Harry Mellor. "In Vitro Coculture Assays of Angiogenesis." In Methods in Molecular Biology, 39–46. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0916-3_4.

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Allen, Jennifer L., and Harry Mellor. "The Coculture Organotypic Assay of Angiogenesis." In Methods in Molecular Biology, 265–70. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1462-3_17.

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Park, Jaewon, Sunja Kim, Jianrong Li, and Arum Han. "Multi-compartment Neuron–Glia Coculture Microsystem." In Neuromethods, 149–59. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2510-0_9.

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Davies, P. F. "Coculture of Endothelial and Smooth Muscle Cells." In Cell Culture Techniques in Heart and Vessel Research, 290–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75262-9_19.

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do Nascimento Santos, Carlos Antônio, Radovan Borojevic, Luiz Eurico Nasciutti, and Christina M. Maedatakiya. "Characterization of Gastrospheres Using 3D Coculture System." In Somatic Stem Cells, 105–21. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8697-2_8.

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Conference papers on the topic "Coculture"

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Wei, Kun. "Microorganism Coculture-independent Synthesis of Berkeleypenostatin A." In The International Conference on Biomedical Engineering and Bioinformatics. SCITEPRESS - Science and Technology Publications, 2022. http://dx.doi.org/10.5220/0011296500003443.

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Lee, Jyong-Huei, Yi-Ting Lo, and Shih-Kang Fan. "Cell coculture within electrically patterned cells and hydrogel structures." In 2017 IEEE 30th International Conference on Micro Electro Mechanical Systems (MEMS). IEEE, 2017. http://dx.doi.org/10.1109/memsys.2017.7863478.

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Cevik, Ziysan Buse, Aylin Korkmaz, and Ozan Karaman. "Effects Of Laminin Derived Peptides On HBMSC-HUVEC Coculture." In 2021 Medical Technologies Congress (TIPTEKNO). IEEE, 2021. http://dx.doi.org/10.1109/tiptekno53239.2021.9632931.

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Saunders, Ruth, Davinder Kaur, Fay Hollins, Andrew Wardlaw, Peter Bradding, and Christopher Brightling. "Airway smooth muscle contractility is increased following coculture with fibrocytes." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa4654.

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Holle, Andrew W., Verena Kast, Ralf Kemkemer, and Joachim Spatz. "Abstract 5059: Cancer cell invasion dynamics in microchannels during stromal cell coculture." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-5059.

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Pullens, Rolf A. A., Maria Stekelenburg, Carlijn V. C. Bouten, Frank P. T. Baaijens, and Mark J. Post. "3D Coculture of Human Endothelial Cells and Myofibroblasts for Vascular Tissue Engineering." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176099.

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Cardiovascular disease is still the number one cause of death in the industrialized world. Diseased small diameter blood vessels are frequently replaced by native grafts. However, these vessels have a limited life time [1], for example the patency at 10 year after coronary artery bypass grafting of saphenous vein grafts is 57% [2]. Tissue engineering (TE) of small diameter blood vessels seems a promising approach to overcome these shortcomings or address the increasing need for substitutes during follow up surgery. Mechanical conditioning of myofibroblast (MFs) seeded constructs appears to be beneficial for functional tissue properties, such as cell proliferation, ECM production and mechanical strength [3,4]. Without a functional endothelial cell (ECs) layer however, patency may be compromised by thrombogenecity. Construction of an EC layer might on the other hand affect the tissue composition during culture, as was shown for bovine ECs, which influenced proliferation and ECM production of smooth muscle cells [5].
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Scott, Devon, Aaron Richman, Craig Lanning, Robin Shandas, and Wei Tan. "Devlopment of a Cell Coculture Microfluidic Shear Device for Mechano-Transmission Study." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176700.

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We have developed a microfluidic shear device that allows for the study of cell communication in a dynamically controlled biochemical and biomechanical environments simulating cells’ living environments in vivo. Such study may help to improve our understanding in the effects of hypertension-relevant and vascular development-relevant flow shear stress on cell behaviors. Endothelial cells may be a key factor for transmitting the blood flow conditions from the endothelial lining to interstitial layers and smooth muscle cells. The interstitial flow stress and the shear stress induced signaling factors may greatly alter vascular biology of these deep layers. Endothelial cells act as a mechano-transducer by converting shear stress into biochemical signaling factors. The biochemical factors diffuse to smooth muscle cells and further alter the biological structure of vascular tissues. Also, the flow shear stress will be transmitted to the interstitial tissue layer through the pores resulted from the pores in the fenestrated endothelial lining. Studies in both the mechano-transduction process and the mechano-transmission process will benefit from a biomimetic flow shear device with co-cultured cells. Our device will allow the co-culture of endothelial cells and smooth muscle cells to study these biomechanical processes. The pulmonary arterial cells are used as a model in the study. The microfluidic device developed here will be used to enhance the understanding of pulmonary vascular disease pathogenesis due to the variations in the flow shear stress.
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Benton, Gabriel J., Jay George, Gerald DeGray, Irina Arnaoutova, and Hynda K. Kleinman. "Abstract 2033: A comprehensive 3D triple coculture model for evaluating breast cancer progression." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2033.

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Harimoto, Tetsuhiro, Zakary Singer, Oscar Velazquez, Joanna Zhang, Samuel Castro, Taylor Hinchliffe, William Mather, and Tal Danino. "Abstract 6317: 3D multicellular coculture platform enables rapid engineering of tumor-homing bacteria." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-6317.

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Chen, Chi-Fan, Kuo-Wei Chang, Ting-Ru Yueh, Hong-Yuan Huang, and Chen-Shien Liu. "A microfluidic device for automatic embryo trapping and coculture with stromal cells in vitro." In 2014 9th IEEE International Conference on Nano/Micro Engineered and Molecular Systems (NEMS). IEEE, 2014. http://dx.doi.org/10.1109/nems.2014.6908808.

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Reports on the topic "Coculture"

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McKinlay, James B. Metabolism and Evolution of a Biofuel-Producing Microbial Coculture. Office of Scientific and Technical Information (OSTI), June 2018. http://dx.doi.org/10.2172/1459596.

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Orebaugh, Jack, and Pavlo Bohutskyi. Transcriptomic Network Analysis of Cyanobacterial-Methylotroph Interactions in Coculture and Axenic Conditions. Office of Scientific and Technical Information (OSTI), August 2023. http://dx.doi.org/10.2172/1999433.

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Karpeeva, E. A. Frequency of Occurrence of Pathogenicity Genes in Case of Coculture of Escherichia Coli With Protozoans Blastocystis Hominis. Prof. Dr Kuznetsov Alexandre Semenovich, March 2015. http://dx.doi.org/10.14526/25_2015_25.

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