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Добірка наукової літератури з теми "Bone marrow mesenchymal stromal cell"

Автор: Grafiati
Опубліковано: 11 березня 2023

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Статті в журналах з теми "Bone marrow mesenchymal stromal cell"

1

Srinivas, Ampati. "The Constantly Highly Expression of Limbal Stromal Cells Compared to the Bone Marrow Mesenchymal Stromal Cells, Adipose-Derived Mesenchymal Stromal Cells and Foreskin Fibroblasts." Stem Cells Research and Therapeutics International 1, no. 1 (April 16, 2019): 01–06. http://dx.doi.org/10.31579/2643-1912/005.

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2

Cilloni, Daniela, Carmelo Carlo-Stella, Franca Falzetti, Gabriella Sammarelli, Ester Regazzi, Simona Colla, Vittorio Rizzoli, Franco Aversa, Massimo F. Martelli, and Antonio Tabilio. "Limited engraftment capacity of bone marrow–derived mesenchymal cells following T-cell–depleted hematopoietic stem cell transplantation." Blood 96, no. 10 (November 15, 2000): 3637–43. http://dx.doi.org/10.1182/blood.v96.10.3637.h8003637_3637_3643.

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Анотація:
The engraftment capacity of bone marrow–derived mesenchymal cells was investigated in 41 patients who had received a sex-mismatched, T-cell–depleted allograft from human leukocyte antigen (HLA)–matched or –mismatched family donors. Polymerase chain reaction (PCR) analysis of the human androgen receptor (HUMARA) or the amelogenin genes was used to detect donor-derived mesenchymal cells. Only 14 marrow samples (34%) from 41 consenting patients generated a marrow stromal layer adequate for PCR analysis. Monocyte-macrophage contamination of marrow stromal layers was reduced below the levels of sensitivity of HUMARA and amelogenin assays (5% and 3%, respectively) by repeated trypsinizations and treatment with the leucyl-leucine (leu-leu) methyl ester. Patients who received allografts from 12 female donors were analyzed by means of the HUMARA assay, and in 5 of 12 cases a partial female origin of stromal cells was demonstrated. Two patients who received allografts from male donors were analyzed by amplifying the amelogenin gene, and in both cases a partial male origin of stromal cells was shown. Fluorescent in situ hybridization analysis using a Y probe confirmed the results of PCR analysis and demonstrated in 2 cases the existence of a mixed chimerism at the stromal cell level. There was no statistical difference detected between the dose of fibroblast progenitors (colony-forming unit–F [CFU-F]) infused to patients with donor- or host-derived stromal cells (1.18 ± 0.13 × 104/kg vs 1.19 ± 0.19 × 104/kg; P ≥ .97). In conclusion, marrow stromal progenitors reinfused in patients receiving a T-cell–depleted allograft have a limited capacity of reconstituting marrow mesenchymal cells.
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3

Borges, Fernanda T., Marcia Bastos Convento, and Nestor Schor. "Bone marrow-derived mesenchymal stromal cell: what next?" Stem Cells and Cloning: Advances and Applications Volume 11 (November 2018): 77–83. http://dx.doi.org/10.2147/sccaa.s147804.

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4

Cilloni, Daniela, Carmelo Carlo-Stella, Franca Falzetti, Gabriella Sammarelli, Ester Regazzi, Simona Colla, Vittorio Rizzoli, Franco Aversa, Massimo F. Martelli, and Antonio Tabilio. "Limited engraftment capacity of bone marrow–derived mesenchymal cells following T-cell–depleted hematopoietic stem cell transplantation." Blood 96, no. 10 (November 15, 2000): 3637–43. http://dx.doi.org/10.1182/blood.v96.10.3637.

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Анотація:
Abstract The engraftment capacity of bone marrow–derived mesenchymal cells was investigated in 41 patients who had received a sex-mismatched, T-cell–depleted allograft from human leukocyte antigen (HLA)–matched or –mismatched family donors. Polymerase chain reaction (PCR) analysis of the human androgen receptor (HUMARA) or the amelogenin genes was used to detect donor-derived mesenchymal cells. Only 14 marrow samples (34%) from 41 consenting patients generated a marrow stromal layer adequate for PCR analysis. Monocyte-macrophage contamination of marrow stromal layers was reduced below the levels of sensitivity of HUMARA and amelogenin assays (5% and 3%, respectively) by repeated trypsinizations and treatment with the leucyl-leucine (leu-leu) methyl ester. Patients who received allografts from 12 female donors were analyzed by means of the HUMARA assay, and in 5 of 12 cases a partial female origin of stromal cells was demonstrated. Two patients who received allografts from male donors were analyzed by amplifying the amelogenin gene, and in both cases a partial male origin of stromal cells was shown. Fluorescent in situ hybridization analysis using a Y probe confirmed the results of PCR analysis and demonstrated in 2 cases the existence of a mixed chimerism at the stromal cell level. There was no statistical difference detected between the dose of fibroblast progenitors (colony-forming unit–F [CFU-F]) infused to patients with donor- or host-derived stromal cells (1.18 ± 0.13 × 104/kg vs 1.19 ± 0.19 × 104/kg; P ≥ .97). In conclusion, marrow stromal progenitors reinfused in patients receiving a T-cell–depleted allograft have a limited capacity of reconstituting marrow mesenchymal cells.
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5

Reyes, Morayma, Sheng Li, Jessica Foraker, En Kimura, and Jeffrey S. Chamberlain. "Donor origin of multipotent adult progenitor cells in radiation chimeras." Blood 106, no. 10 (November 15, 2005): 3646–49. http://dx.doi.org/10.1182/blood-2004-12-4603.

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AbstractMultipotent adult progenitor cells (MAPCs) are bone marrow-derived stem cells that have extensive in vitro expansion capacity and can differentiate in vivo and in vitro into tissue cells of all 3 germinal layers: ectoderm, mesoderm, and endoderm. The origin of MAPCs within bone marrow is unknown. MAPCs are believed to be derived from the bone marrow stroma compartment as they are isolated within the adherent cell component. Numerous studies of bone marrow chimeras in the human and the mouse point to a host origin of bone marrow stromal cells. Mesenchymal stem cells (MSCs), which coexist with stromal cells, have also been proven to be of host origin after allogeneic bone marrow transplantation in numerous studies. We report here that following syngeneic bone marrow transplants into lethally irradiated C57BL6 mice, MAPCs are of donor origin.
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6

Krambs, Joseph R., Grazia Abou Ezzi, Juo-Chin Yao, Justin T. Li, and Daniel C. Link. "Canonical Signaling By TGF Family Members in Mesenchymal Stromal Cells Is Dispensable for Hematopoietic Niche Maintenance Under Basal and Stress Conditions." Blood 134, Supplement_1 (November 13, 2019): 1209. http://dx.doi.org/10.1182/blood-2019-128693.

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Анотація:
The bone marrow contains a complex population of stromal and hematopoietic cells that together generate a unique microenvironment, or niche, to support hematopoiesis. Mesenchymal stromal cells are an important component of the bone marrow hematopoietic niche and include CXCL12-abundant reticular (CAR) cells, adipocytes, osteolineage cells, and arteriolar pericytes, all of which have been implicated in hematopoietic stem/progenitor cell (HSPC) maintenance. There also is evidence that adaptive changes in bone marrow stromal cells contributes to recovery from myelosuppresive therapy and the development of certain hematopoietic malignancies. However, the signals that contribute to the development, maintenance, and stress response of bone marrow mesenchymal stromal cells are poorly understood. Here, we test the hypothesis that cytokines of the transforming growth factor superfamily, which include bone morphogenetic proteins (BMPs), growth differentiation factors (GDFs), and activins/inhibins, provide signals to mesenchymal stromal cells that contribute to basal and stress hematopoiesis responses. To test this hypothesis, we abrogated canonical TGF family signaling in mesenchymal stem/progenitor cells by deleting Smad4 using a doxycycline-repressible Osterix-Cre transgene (Osx-Cre), which targets all mesenchymal stromal cells in the bone marrow. We first performed lineage-tracing studies using Osx-Cre Smad4fl/fl Ai9 mice to show that activation of Osx-Cre at birth (by removal of doxycycline) results in the efficient targeting of bone marrow mesenchymal stromal cells. Moreover, we show that Smad4 mRNA expression is essentially undetectable in sorted mesenchymal stromal cells sorted from the bone marrow of these mice. Basal hematopoiesis and bone marrow stromal cells were analyzed in 6-8 week old Osx-Cre Smad4fl/fl mice. No alterations in the number or spatial organization of CAR cells, osteoblasts, or adipocytes was observed, and expression of key niche factors, including Scf, Cxcl12, and Spp1 was normal. Basal hematopoiesis, including the number of phenotypic HSCs in bone marrow and spleen, also was normal. Recent studies have shown that inhibition of activin signaling by treating with an activin receptor 2 alpha (ACVR2a) ligand trap stimulates erythropoiesis. Although ACVR2a signaling in erythroid progenitors contributes to this effect, two groups showed that inhibition of ACVR2a signaling in bone marrow stromal cells also stimulates erythropoiesis. Thus, we next characterized basal and stress erythropoiesis in Osx-Cre Smad4fl/fl mice. The frequency of phenotypic erythroid progenitors in bone marrow and spleen was similar to control mice. The stress erythropoiesis response was assessed after induction of acute hemolytic anemia by phenylhydrazine treatment. Both the magnitude of anemia and kinetics of erythroid recovery were similar to control mice. Myelosuppressive therapy induces marked alterations in the bone marrow microenvironment that includes an expansion of osteolineage cells and adipocytes, which have been linked to hematopoietic recovery. Thus, we next characterized stress hematopoiesis in Osx-Cre Smad4fl/fl mice in response to 5-fluorouracil (5-FU) treatment. Compared to control mice, the magnitude and duration of neutropenia following 5-FU were similar. Moreover, mouse survival after repeated weekly doses of 5-FU was comparable to control mice. HSPC mobilization by G-CSF is due, in large part, by downregulation of CXCL12 expression in bone marrow mesenchymal stromal cells. A prior study suggested that SMAD signaling negatively regulates CXCL12 expression in stromal cells. Consistent with this finding, we show that treatment of cultured bone marrow derived MSCs with TGF-b1 for 48 hours results in a significant (3.3-fold, P<0.0001) decrease in CXCL12 mRNA expression. Thus, in the final experiments, we characterized G-CSF induced HSPC mobilization in Osx-Cre, Smad4fl/fl or Osx-Cre, Tgfbr2fl/fl mice. HSPC mobilization, as quantified by CFU-C and Kit+ Sca+ lineage- (KSL) cell number in blood or spleen after 5 days of G-CSF treatment was comparable to control mice. Collectively, these data suggest the TGF family member signaling in mesenchymal stromal cells is dispensable for hematopoietic niche maintenance under basal and stress conditions. Disclosures No relevant conflicts of interest to declare.
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7

del Carmen Rodríguez, María, Antonio Bernad, and Miguel Aracil. "Interleukin-6 deficiency affects bone marrow stromal precursors, resulting in defective hematopoietic support." Blood 103, no. 9 (May 1, 2004): 3349–54. http://dx.doi.org/10.1182/blood-2003-10-3438.

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Abstract Interleukin-6 (IL-6) is a critical factor in the regulation of stromal function and hematopoiesis. In vivo bromodeoxyuridine incorporation analysis indicates that the percentage of Lin-Sca-1+ hematopoietic progenitors undergoing DNA synthesis is diminished in IL-6-deficient (IL-6-/-) bone marrow (BM) compared with wild-type BM. Reduced proliferation of IL-6-/- BM progenitors is also observed in IL-6-/- long-term BM cultures, which show defective hematopoietic support as measured by production of total cells, granulocyte macrophage-colony-forming units (CFU-GMs), and erythroid burst-forming units (BFU-Es). Seeding experiments of wild-type and IL-6-/- BM cells on irradiated wild-type or IL-6-deficient stroma indicate that the hematopoietic defect can be attributed to the stromal and not to the hematopoietic component. In IL-6-/- BM, stromal mesenchymal precursors, fibroblast CFUs (CFU-Fs), and stroma-initiating cells (SICs) are reduced to almost 50% of the wild-type BM value. Moreover, IL-6-/- stromata show increased CD34 and CD49e expression and reduced expression of the membrane antigens vascular cell adhesion molecule-1 (VCAM-1), Sca-1, CD49f, and Thy1. These data strongly suggest that IL-6 is an in vivo growth factor for mesenchymal precursors, which are in part implicated in the reduced longevity of the long-term repopulating stem cell compartment of IL-6-/- mice. (Blood. 2004;103:3349-3354)
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8

Widera, Darius. "Recent Advances in Translational Adipose-Derived Stem Cell Biology." Biomolecules 11, no. 11 (November 9, 2021): 1660. http://dx.doi.org/10.3390/biom11111660.

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9

Miura, Yasuo, Tatsuo Ichinohe, and Taira Maekawa. "Human Mesenchymal Stromal/Stem Cell-Mediated Bone Marrow Organization." Japanese Journal of Transfusion and Cell Therapy 61, no. 5 (2015): 489–90. http://dx.doi.org/10.3925/jjtc.61.489.

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10

Lim, Hong Kiat, Pravin Periasamy, and Helen C. O’Neill. "In Vitro Murine Hematopoiesis Supported by Signaling from a Splenic Stromal Cell Line." Stem Cells International 2018 (December 25, 2018): 1–9. http://dx.doi.org/10.1155/2018/9896142.

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Анотація:
There are very few model systems which demonstrate hematopoiesis in vitro. Previously, we described unique splenic stromal cell lines which support the in vitro development of hematopoietic cells and particularly myeloid cells. Here, the 5G3 spleen stromal cell line has been investigated for capacity to support the differentiation of hematopoietic cells from progenitors in vitro. Initially, 5G3 was shown to express markers of mesenchymal but not endothelial or hematopoietic cells and to resemble perivascular reticular cells in the bone marrow through gene expression. In particular, 5G3 resembles CXCL12-abundant reticular cells or perivascular reticular cells, which are important niche elements for hematopoiesis in the bone marrow. To analyse the hematopoietic support function of 5G3, specific signaling pathway inhibitors were tested for the ability to regulate cell production in vitro in cocultures of stroma overlaid with bone marrow-derived hematopoietic stem/progenitor cells. These studies identified an important role for Wnt and Notch pathways as well as tyrosine kinase receptors like c-KIT and PDGFR. Cell production in stromal cocultures constitutes hematopoiesis, since signaling pathways provided by splenic stroma reflect those which support hematopoiesis in the bone marrow.
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Більше джерел

Дисертації з теми "Bone marrow mesenchymal stromal cell"

1

François, Moïra. "Comprehensive study of the immunomodulatory properties of bone marrow-derived mesenchymal stromal cells." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103683.

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Анотація:
Over the course of the last decade, mesenchymal stromal cells (MSC) have made a remarkable entry in the field of cell-based immunotherapy. In vitro, MSC were shown to modulate the immune response, either by acting as an immunosuppressant on several immune cells, or upon IFN-γ stimulation, as an antigen presenting cell (APC) for the priming of CD4+ T cells. Although a vast array of in vivo experiments in animals and humans has undeniably proven the immunological properties of MSC, the exact mechanisms by which MSC mediate their effects remain unclear. In Chapter 1, I presented a succinct review of the literature in regards to the characteristics of MSC. In Chapter 2, I addressed the immunosuppressive mechanisms of human MSC toward T cell proliferation. Using an in vitro proliferation assay, I demonstrated that human MSC suppressed T cell proliferation through the expression indoleamine 2,3-dioxygenase (IDO) induced following IFN-γ priming. In addition, MSC derived from different donors were shown to suppress T cell proliferation at variable degrees, which corresponded to their individual expression level of IDO. The use of whole peripheral blood mononuclear cells (PBMC) as opposed to purified T cells revealed the role played by monocytes in the suppression of T cell proliferation by MSC. Factors secreted by MSC in addition to the enzymatic activity of IDO induced the differentiation of monocytes into immunosuppressive M2 macrophages. Stimulation by IFN-γ not only triggered the immunosuppressive mechanisms of MSC but also induced APC-like properties in MSC. In Chapter 3, I investigated the molecular mechanisms implicated in the modulation of IFN-γ-inducible expression of MHC class II molecules and mediated antigen presentation in MSC. I demonstrated that IFN-γ mediated the transcriptional activation of the class II transactivator gene (CIITA), which is responsible for the upregulation of MHC class II molecules on both mouse and human MSC, and that TGF-β counter-acted the effect of IFN-γ by inhibiting the transcription of CIITA. In addition, cell culture density also modulated MHC class II-mediated antigen presentation differentially in mouse and human MSC. In Chapter 4, I examined the capacity of mouse MSC to cross-present exogenously acquired antigens as part of their APC-like features. I demonstrated that cross-presentation by mouse MSC was induced by IFN-γ and dependent on MHC class I machinery molecules, TAP complex and proteasome. I also demonstrated using an in vivo immune reconstitution assay, that mouse MSC can prime CD8+ T cells against a specific antigen, a characteristic of professional APC. Finally, I investigated in Chapter 5 the immunological impact of TLR expression and signaling in human and mouse MSC. I demonstrated that TLR activation in MSC induced the expression of chemokines and cytokines, which created an attractive inflammatory milieu for immune cells. I concluded by demonstrating that MSC differ from classic APC in that they did not express IL-12p70, an essential cytokine involved in both innate and adaptive immunity, in response to TLR activation. The findings in this thesis illustrate the complexity of the mechanisms by which MSC modulate the immune system. Their response to environment clues such as inflammation and pathogens activate either their suppressive or stimulatory immune functions, depending on the situation. Overall, these findings help optimize the utilization of MSC in cell-based immunotherapy.
Au cours de la dernière décennie, les cellules stromales mésenchymateuses (MSC) ont fait une entrée remarquée dans le domaine de l'immunothérapie cellulaire. In vitro, les MSC ont démontrées des propriétés immunomodulatrices, soit par leur action inhibitrice sur les fonctions des cellules du système immunitaire ou par leur capacité à présenter des antigènes aux lymphocytes T CD4+, à la suite d'une stimulation par IFN-. Malgré l'existence de nombreuses recherches in vivo chez les animaux et l'homme prouvant leurs propriétés immunologiques, les mécanismes par lesquels les MSC modulent le système immunitaire n'ont pas encore été élucidés. Dans le Chapitre 1, j'ai présenté une revue succincte de la littérature traitant des caractéristiques des MSC. Dans le Chapitre 2, j'ai adressé les mécanismes immunosuppressifs des MSC humaines sur les lymphocytes T. À l'aide d'un test de prolifération in vitro, j'ai démontré que les MSC humaines suppriment la prolifération des lymphocytes T par grâce à l'expression indoleamine 2,3-dioxygenase (IDO) induite par l'exposition à l'IFN-. De plus, les MSC isolées de différents donneurs inhibent la prolifération des lymphocytes T à différents degrés qui correspondent au le niveau d'expression d'IDO par chaque donneur. L'utilisation de cellules mononucléaires sanguines (PBMC) complet comparativement à l'utilisation de lymphocytes T purifiés a révélé le rôle joué par les monocytes dans la suppression de la prolifération des lymphocytes T par les MSC. L'activité enzymatique d'IDO en combinaison avec d'autres facteurs sécrétés par les MSC induisent la différentiation des monocytes en macrophages immunosuppressifs de type M2. En plus de déclencher les mécanismes immunosuppressifs des MSC, l'IFN-a aussi eu pour effet d'induire des propriétés typiques des cellules présentatrices d'antigène (CPA) chez les MSC. Dans le Chapitre 3, j'ai étudié les mécanismes moléculaires impliqués dans la modulation de l'expression des molécules MHC de type II et la présentation d'antigène par celles-ci dans les MSC. J'ai démontré que l'IFN- active la transcription du transactivateur de classe II (CIITA), ce qui a eu pour résultat d'uprégulation les molécules MHC de type II dans les MSC murines et humaines, et que l'ajout de TGF- contrecarre l'effet de l'IFN- en inhibant la transcription de CIITA. De plus, la densité cellulaire des MSC en culture module la présentation d'antigène en affectant l'expression des molécules MHC de type II différemment chez les MSC murines et humaines. Dans le Chapitre 4, j'ai examiné la capacité des MSC de souris à cross-présenter des antigènes exogènes, une autre propriété typique des CPA. J'ai démontré que l'IFN- induit la cross-présentation dans les MSC murines et que celle-ci dépend des molécules TAP et du protéasome. J'ai aussi prouvé à l'aide d'un modèle de reconstitution immunitaire in vivo, que les MSC murines peuvent induire l'activation des lymphocytes T CD8+ contre un antigène spécifique. Finalement, j'ai enquêté dans le Chapitre 5, l'impact immunologique de l'expression et de la signalisation par les TLR chez les MSC humaines et murines. J'ai illustré que l'activation des TLR induisait l'expression de chemokines et de cytokines par les MSC créant ainsi un milieu inflammatoire propice au recrutement des cellules immunitaires. J'ai conclue en démontrant que les MSC différaient des CPA classiques par l'absence de production IL-12p70, une cytokine essentielle à la réponse immunitaire innée et acquise, en réponse à la stimulation des TLR. Les résultats inclus dans cette thèse illustrent la complexité des mécanismes immunomodulatoires des MSC. Leurs réponses face aux signaux de leur environnement, tel que l'inflammation ou l'infection activent soit leurs propriétés immunosuppressives ou –stimulatrices dépendamment de la situation. Mes découvertes pourront optimiser l'utilisation des MSC dans le domaine de l'immunothérapie cellulaire.
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2

Lenz, Daniel. "Dissecting the heterogeneity of murine mesenchymal bone marrow stromal cells." Doctoral thesis, Humboldt-Universität zu Berlin, 2020. http://dx.doi.org/10.18452/21017.

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Анотація:
Knochenmarks-Stromazellen sind in den letzten Jahren in den Fokus der Forschung gerückt. Es konnte gezeigt werden, dass sie durch Bereitstellung von Überlebenssignalen essenziell für die Erhaltung hämatopoetischer Nischen sind. Stromales Interleukin-7 (IL-7) konnte dabei für T Zellen als Überlebenssignal identifiziert werden. Gemeinsam ist allen Stromazellen die Expression des Oberflächenmarkers CD106/VCAM-1. Ein effizientes Protokoll erlaubte die qualitative wie quantitative Isolation von Stromazellen aus dem murinen Knochenmark mit anschließender ex vivo Microarray-Analyse. Die auf diese Weise ermittelten Kandidaten-Marker wurden auf Proteinebene via Histologie und (Hochdurchsatz-) Durchflusszytometrie validier. Dazu gehören z.B. die Marker CD1d, gas6 oder ANXA2R. CD1d wurde als guter Interimsmarker für VCAM-1+PECAM-1- Stromazellen identifiziert, wohingegen die IL-7-Produzenten in der Population von CD200int/BP 1+/CD73+/CD105- angereichert sind. Gleiches gilt für den Transkriptionsfaktor Prrx1. CD55, BP-1 and Cadherin-11 zeigten eine Expressionsmuster in Abhängigkeit des verwendeten IL-7-Reportermaus-Haplotyps. Für BP-1 und Cadherin 11 konnte die Abwesenheit von reifen Lymphozyten als Ursache des Feedbacks ausgeschlossen werden. Die Haplotypen der Reportermaus legten auch eine monoallele Expression des IL-7 nahe. Die Ergebnisse dieser Arbeit zeigen VCAM-1+ (IL-7+/-) Stromazellen als heterogene Population, wenn es nach der Vielzahl der möglichen exprimierten Marker geht. Zwischen vielen dieser Marker gibt es aber wiederum auf Zelloberflächenebene einen großen Überlapp. Die funktionelle Relevanz dieser Oberflächenmarker-Diversität wird in weiteren Arbeiten zu klären sein, gibt aber den Stromazellen ein breites Repertoire vor, um Interaktionen mit Lymphozyten zu initiieren, modulieren und inhibieren. Abschließend ist zu erwarten, dass diese Erkenntnisse in die klinische Behandlung der Stroma-Nischen in Autoimmun-Fragestellungen einfließen.
Bone marrow stromal cells receive increasing amounts of attention lately. They have been shown to support survival of hematopoietic stem cells as well as memory lymphocytes which is of great importance when targeting the perseverance of autoimmune diseases. CD4+ memory T lymphocytes reside in the proximity of VCAM-1 expressing stromal cells which provide them with survival signals such as Interleukin-7. Herein, a protocol was developed to quantitatively obtain VCAM-1+ and VCAM-1+ IL-7+/- stromal cells via enzymatic/mechanic digestion and cytoskeleton-inhibition. Ex vivo gene expression analysis was performed from sorted, pure cells with good recovery. Candidate genes/markers were validated in (high-throughput) flow cytometry and histological analysis including subsequent semi-automated colocalization was performed. CD1d was found to be good surrogate marker for VCAM-1+PECAM-1- non-endothelial stroma while the population of CD200int/BP-1+/CD73+/CD105- stromal cells is greatly enriched in IL-7 producers which was equally true for the stromal transcription factor Prrx1. CD55, BP-1 and Cadherin-11 were found to be differentially expressed in differing IL-7 reporter mice haplotypes. The reporter mice haplotypes revealed monoallelic expression features of IL-7. All methodologies suggest that VCAM-1+ as well as IL-7+/- stromal cells are heterogeneous by marker expression yet don’t cluster extensively in flow cytometry co-stains. The functional relevance of the marker diversity described in this thesis remains to be tested but insinuates a broad repertoire for bone marrow stroma cells for new interaction pathways with lymphocyte subsets. Ultimately, this knowledge will hopefully feedback to clinical questions of autoimmunity for targeted treatment of stromal niches.
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3

Tsui, Yat-ping, and 徐軼冰. "Derivation of oligodendrocyte precursor cells from adult bone marrow stromal cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/197485.

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Анотація:
Myelin is essential for neuronal survival and maintenance of normal functions of the nervous system. Demyelinating disorders are debilitating and are often associated with failure of resident oligodendrocyte precursor cells (OPCs) to differentiate into mature, myelinating oligodendrocytes. Derivation of OPCs, from a safe source that evades ethical issues offers a solution to remyelination therapy. We therefore hypothesized that bone marrow stromal cells (BMSCs) harbour neural progenitor cells at a pre-commitment stage and that in vitro conditions can be exploited to direct differentiation of these cells along the oligodendroglial lineage. For the current study, adult rat BMSCs used were >90% immunopositive for CD90, CD73, STRO-1 (stromal cell markers), 10% for nestin (neural progenitor marker) but negligible for CD45 (haematopoietic cell marker) as measured by flow cytometry. Transfer of the culture from a highly adhesive substratum to a moderately adhesive substratum resulted in increase in proportion of p75-positive cells but CD49b-positive cells remained at 97% and Sox 10-positive cells remained negligible. Transfer of the culture to a non-adherent substratum fostered the generation of neurospheres comprising cells that were positive for the neural stem/progenitor cell (NP) marker, nestin, and for the neural crest markers CD49b, p75 and Sox10. Prior to this stage, the BMSCs were not yet committed to the neural lineage even though transient upregulation of occasional marker may suggest a bias towards the neural crest cell lineage. The BM-NPs were then maintained in adherent culture supplemented with beta-Heregulin (β-Her), basic fibroblast growth factor (bFGF) and platelet-derived growth factor-AA (PDGF-AA) to direct differentiation along the oligodendroglial lineage. Within two weeks of glial induction, cells expressing the OPC markers - NG2, Olig2, PDGFRa and Sox10, were detectable and these could be expanded in culture for up to 3 months with no observable decline in marker expression. These BM-OPCs matured into myelinating oligodendrocytes after 2 weeks in co-culture with either dorsal root ganglion neurons or cortical neurons. In vivo myelination by BM-OPCs was demonstrated by exploitation of the non-myelinated axons of retinal ganglion cells of adult rats. By 8 weeks post-injection of BM-OPCs into the retina, myelin basic protein-positive processes were also observable along the retinal axons. The results not only suppport our hypothesis, but also provide pointers to the adult bone marrow as a safe and accessible source for the derivation of OPCs towards transplantation therapy in acute demyelinating disorders.
published_or_final_version
Biochemistry
Doctoral
Doctor of Philosophy
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4

Yoshioka, Satoshi. "CCAAT/Enhancer-Binding Proteinβ Expressed by Bone Marrow Mesenchymal Stromal Cells Regulates Early B-Cell Lymphopoiesis". Kyoto University, 2014. http://hdl.handle.net/2433/185198.

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5

Chandran, Priya. "Bone Marrow Microenvironment in Acute Myleoid Leukemia." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24301.

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Анотація:
Acute myeloid leukemia (AML) often remains refractory to current chemotherapy and transplantation approaches despite many advances in our understanding of mechanisms in leukemogenesis. The bone marrow “niche” or microenvironment, however, may be permissive to leukemia development and studying interactions between the microenvironment and leukemia cells may provide new insight for therapeutic advances. Mesenchymal stem cells (MSCs) are central to the development and maintenance of the bone marrow niche and have been shown to have important functional alterations derived from patients with different hematological disorders. The extent to which MSCs derived from AML patients are altered remains unclear. The aim of this study was to detect changes occurring in MSCs obtained from human bone marrow in patients with AML by comparing their function and gene expression pattern with normal age-matched controls. MSCs expanded from patients diagnosed with acute leukemia were observed to have heterogeneous morphological characteristics compared to the healthy controls. Immunohistochemistry and flow data confirmed the typical cell surface immunophenotype of CD90+ CD105+ CD73+ CD34- CD45-, although MSCs from two patients with AML revealed reduced surface expression of CD105 and CD90 antigens respectively. Differentiation assays demonstrated the potential of MSCs from AML patients and healthy donors to differentiate into bone, fat and cartilage. However, the ability of MSCs from AML samples to support hematopoietic function of CD34+ progenitors was found to be impaired while the key hematopoietic genes were found to be differentially expressed on AML-MSCs compared to nMSCs. These studies indicate that there exist differences in the biologic profile of MSCs from AML patients compared to MSCs derived from healthy donors. The results described in the thesis provide a formulation for additional studies that may allow us to identify new targets for improved treatment of AML.
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6

Lloyd, Brandon R. "Comparison of Bone Marrow Mesenchymal Stem Cells from Limb and Jaw Bones." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1458678153.

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7

Anastassiadis, Konstantinos, and Maria Rostovskaya. "Differential Expression of Surface Markers in Mouse Bone Marrow Mesenchymal Stromal Cell Subpopulations with Distinct Lineage Commitment." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-191602.

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Анотація:
Bone marrow mesenchymal stromal cells (BM MSCs) represent a heterogeneous population of progenitors with potential for generation of skeletal tissues. However the identity of BM MSC subpopulations is poorly defined mainly due to the absence of specific markers allowing in situ localization of those cells and isolation of pure cell types. Here, we aimed at characterization of surface markers in mouse BM MSCs and in their subsets with distinct differentiation potential. Using conditionally immortalized BM MSCs we performed a screening with 176 antibodies and high-throughput flow cytometry, and found 33 markers expressed in MSCs, and among them 3 were novel for MSCs and 13 have not been reported for MSCs from mice. Furthermore, we obtained clonally derived MSC subpopulations and identified bipotential progenitors capable for osteo- and adipogenic differentiation, as well as monopotential osteogenic and adipogenic clones, and thus confirmed heterogeneity of MSCs. We found that expression of CD200 was characteristic for the clones with osteogenic potential, whereas SSEA4 marked adipogenic progenitors lacking osteogenic capacity, and CD140a was expressed in adipogenic cells independently of their efficiency for osteogenesis. We confirmed our observations in cell sorting experiments and further investigated the expression of those markers during the course of differentiation. Thus, our findings provide to our knowledge the most comprehensive characterization of surface antigens expression in mouse BM MSCs to date, and suggest CD200, SSEA4 and CD140a as markers differentially expressed in distinct types of MSC progenitors.
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8

Anastassiadis, Konstantinos, and Maria Rostovskaya. "Differential Expression of Surface Markers in Mouse Bone Marrow Mesenchymal Stromal Cell Subpopulations with Distinct Lineage Commitment." Public Library of Science, 2012. https://tud.qucosa.de/id/qucosa%3A29135.

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Анотація:
Bone marrow mesenchymal stromal cells (BM MSCs) represent a heterogeneous population of progenitors with potential for generation of skeletal tissues. However the identity of BM MSC subpopulations is poorly defined mainly due to the absence of specific markers allowing in situ localization of those cells and isolation of pure cell types. Here, we aimed at characterization of surface markers in mouse BM MSCs and in their subsets with distinct differentiation potential. Using conditionally immortalized BM MSCs we performed a screening with 176 antibodies and high-throughput flow cytometry, and found 33 markers expressed in MSCs, and among them 3 were novel for MSCs and 13 have not been reported for MSCs from mice. Furthermore, we obtained clonally derived MSC subpopulations and identified bipotential progenitors capable for osteo- and adipogenic differentiation, as well as monopotential osteogenic and adipogenic clones, and thus confirmed heterogeneity of MSCs. We found that expression of CD200 was characteristic for the clones with osteogenic potential, whereas SSEA4 marked adipogenic progenitors lacking osteogenic capacity, and CD140a was expressed in adipogenic cells independently of their efficiency for osteogenesis. We confirmed our observations in cell sorting experiments and further investigated the expression of those markers during the course of differentiation. Thus, our findings provide to our knowledge the most comprehensive characterization of surface antigens expression in mouse BM MSCs to date, and suggest CD200, SSEA4 and CD140a as markers differentially expressed in distinct types of MSC progenitors.
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9

Espig, Sandy [Verfasser]. "Isolation and characterization of rat bone-marrow derived mesenchymal stromal cells / Sandy Espig." Ulm : Universität Ulm. Medizinische Fakultät, 2016. http://d-nb.info/1082294284/34.

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10

Clough, Sally. "IL7 as a marker of a subset of bone marrow mesenchymal stromal cells." Thesis, University of York, 2013. http://etheses.whiterose.ac.uk/4771/.

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The organisation of a multitude of cellular niche components, their communication via many signalling pathways and their response to physical factors, protects and regulates haematopoietic stem cell (HSC) fate in adult bone marrow. Whilst the contribution of osteoblasts, endothelial cells and perivascular cells have been examined, the role of a second stem cell population in the bone marrow; mesenchymal stem cells, is not well understood due to the lack of distinctive markers to identify them in vivo. There is therefore a requirement to determine a characteristic that allows their prospective isolation. Under certain conditions, stromal cells and osteoblasts in the bone marrow express IL-7. The use of a novel IL7-Cre BAC transgenic mouse line has allowed more accurate IL 7 protein detection in situ and demonstrated IL-7 reporter expression in mesenchymal lineage cells in endosteal and vascular HSC niche locations. These cells were further characterised in this study in order to determine if IL-7 or nestin, an intermediate filament associated with a wide range of stem cell populations, is expressed by and could identify bone marrow derived MSCs. YFP positive cells were analysed in sections of IL-7Cre Rosa26-eYFP mice. Interestingly, it was only a proportion of mesenchymal cells that expressed YFP, supporting the theory that subsets of MSCs exist and therefore, that they may have different roles in numerous bone marrow niches. IL-7 was not observed to have any effect on the proliferation or differentiation of human MSCs. Generation of MSC clones supported the suggestion that in vitro cultures of MSCs are a heterogeneous population and they displayed a wide range of IL-7 and nestin mRNA expression levels.
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Більше джерел

Книги з теми "Bone marrow mesenchymal stromal cell"

1

Liu, Chune. Cellular crosstalk between bone marrow-derived mesenchymal stromal cells (MSC) and pancreatic beta-cells. [S.l: s.n.], 2014.

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2

N, Beresford Jon, and Owen Maureen E, eds. Marrow stromal cell culture. Cambridge, [Eng.]: Cambridge University Press, 1998.

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3

Herbertson, Alexandra Lenore. The rat bone marrow stromal cell osteogenic system: Characterization of subpopulations, fractionation and effects of PDGF. [Toronto: University of Toronto, Faculty of Dentistry], 1998.

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4

Chen, Xiao, Chao Xie, Ce Dou, and Zhenhong Ni, eds. Differentiation and Regulation of Bone Marrow Mesenchymal Stromal Cells. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-756-4.

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5

Baksh, Dolores. Adhesion independent survival and expansion of an adult human bone marrow-derived mesenchymal progenitor cell population. 2004.

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6

Vergidis, Joanna. Culture conditions for generating human bone marrow stromal cells influence cell immunophenotype and in vivo biodistribution in immune deficient mice. 2006.

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Частини книг з теми "Bone marrow mesenchymal stromal cell"

1

Wuchter, Patrick, and Anthony D. Ho. "Human MSCs from Bone Marrow, Umbilical Cord Blood, and Adipose Tissue: All the Same?" In Mesenchymal Stromal Cells, 193–208. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5711-4_11.

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2

Nardi, Nance Beyer, and Melissa Camassola. "Isolation and Culture of Rodent Bone Marrow-Derived Multipotent Mesenchymal Stromal Cells." In Mesenchymal Stem Cell Assays and Applications, 151–60. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-999-4_12.

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3

Ghoneim, Nehal I., Alaa E. Hussein, and Nagwa El-Badri. "Isolation of Bone Marrow and Adipose-Derived Mesenchymal Stromal Cells." In Regenerative Medicine and Stem Cell Biology, 243–64. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-55359-3_8.

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4

Wolfe, Margaret, Radhika Pochampally, William Swaney, and Roxanne L. Reger. "Isolation and Culture of Bone Marrow-Derived Human Multipotent Stromal Cells (hMSCs)." In Mesenchymal Stem Cells, 3–25. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-169-1_1.

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5

Gronthos, Stan, and Andrew C. W. Zannettino. "A Method to Isolate and Purify Human Bone Marrow Stromal Stem Cells." In Mesenchymal Stem Cells, 45–57. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-169-1_3.

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6

Miller, Renuka P., and Patrick J. Hanley. "Isolation and Manufacture of Clinical-Grade Bone Marrow-Derived Human Mesenchymal Stromal Cells." In Mesenchymal Stem Cells, 301–12. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3584-0_18.

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7

Penfornis, Patrice, and Radhika Pochampally. "Isolation and Expansion of Mesenchymal Stem Cells/Multipotential Stromal Cells from Human Bone Marrow." In Mesenchymal Stem Cell Assays and Applications, 11–21. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-999-4_2.

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8

Stagg, J., and J. Galipeau. "Immune Plasticity of Bone Marrow-Derived Mesenchymal Stromal Cells." In Handbook of Experimental Pharmacology, 45–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-68976-8_3.

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9

Chen, Jieli, Poornima Venkat, and Michael Chopp. "Bone Marrow Mesenchymal Stromal Cell Transplantation: A Neurorestorative Therapy for Stroke." In Cellular Therapy for Stroke and CNS Injuries, 47–69. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-11481-1_4.

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10

Seshi, Beerelli. "Gene Expression Analysis at the Single Cell Level Using the Human Bone Marrow Stromal Cell as a Model: Sample Preparation Methods." In Mesenchymal Stem Cells, 117–32. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-169-1_9.

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Тези доповідей конференцій з теми "Bone marrow mesenchymal stromal cell"

1

Metzger, Thomas A., Stephen A. Schwaner, and Glen L. Niebur. "Pressure Gradients in the Trabecular Pore Space of Femurs During Physiologic Loading." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14433.

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Анотація:
Bone marrow is an important niche for mesenchymal stromal cells (MSCs), which are progenitors for connective tissue cells. MSCs respond to mechanical stimuli (1). For example, steady and oscillatory fluid flow both affect MSC differentiation to the osteogenic lineages (2), while hydrostatic pressure increases MSC osteogenic protein expression (3). Both pressure and fluid flow are induced in bone marrow during loading due to the poroelastic nature of trabecular bone, and these may affect the differentiation or proliferation of the resident stromal cells.
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2

Islam, Mohammad N., Li Sun, Jens Lindert, Shonit R. Das, and Jahar Bhattacharya. "Restoration Of Alveolar Bioenergetics By Bone Marrow-Derived Mesenchymal Stromal Cells." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1245.

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3

Coughlin, Thomas R., Matthew Haugh, Muriel Voisin, Evelyn Birmingham, Laoise M. McNamara, and Glen L. Niebur. "Primary Cilia Knockdown Reduces the Number of Stromal Cells in Three Dimensional Ex Vivo Culture." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14723.

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Mesenchymal stem cells (MSCs) are multipotent stromal cells that reside in the bone marrow and differentiate into connective cell lines, such as adipocytes and osteoblasts [1]. An appropriate balance of MSC differentiation toward adipocytes and osteoblasts is vital to bone homeostasis [6]. In vitro work demonstrates that differentiation of MSCs is influenced by mechanical stimuli [2, 3]. In a mouse model, the ratio of adipocytes to MSCs in the marrow was 19% lower compared to controls following treatment by low magnitude mechanical signals (LMMS) [4]. In mice, LMMS increased MSC number by 46% and the differentiation capacity of MSCs was biased towards osteoblastic compared to adipogenic differentiation [5]. Thus, mechanobiological stimuli may play an important role in maintaining balanced MSC differentiation.
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4

Nakata, Rie, Lucia Borriello, Muller Fabbri, Hiroyuki Shimada, and Yves A. Declerck. "Abstract 5076: Tumor cell-derived exosomes educate bone marrow mesenchymal stromal cells toward a protumorigenic function." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5076.

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5

Ilic, J., B. Schlierf, M. Rudert, R. Ebert, M. Herrmann, and D. Trivanovic. "Bone marrow mesenchymal stromal cells can support proliferative fraction of multiple myeloma cells with exhausted stem cell potential." In III. MuSkITYR Symposium. Georg Thieme Verlag, 2021. http://dx.doi.org/10.1055/s-0041-1736717.

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6

Khedoe, P. P. S. J., L. Jia, N. Li, P. S. Hiemstra, F. Koning, and J. Stolk. "Biomarker identification to assess effects of bone-marrow derived mesenchymal stromal cell-therapy in emphysema through immune profiling." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.lsc-0195.

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7

Khedoe, Padmini P. S. J., Li Jia, Na Li, Pieter S. Hiemstra, Frits Koning, and Jan Stolk. "Biomarker identification to assess effects of bone-marrow derived mesenchymal stromal cell-therapy in emphysema through immune profiling." In ERS Lung Science Conference 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/23120541.lsc-2022.195.

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8

Guiance-Varela, Carolina, Cristina Rodríguez-Pereira, Elena Fernandez-Burguera, Tamara Hermida Gómez, Noa Goyanes, Francisco J. Blanco, and joana magalhães. "FRI0516 CHONDROGENIC EFFECT OF KARTOGENIN ON AN IMMORTALIZED CELL LINE DERIVED FROM MESENCHYMAL STROMAL CELLS ISOLATED FROM HUMAN BONE MARROW." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.5526.

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9

Stöckl, Magdalena, Drenka Trivanovic, Maximilian Rudert, and Marietta Herrmann. "Platelet-released factors stimulate mobility and PI3K/AKT/mTOR pathway in bone marrow mesenchymal stromal cells." In Jahreskongress DVO OSTEOLOGIE 2022. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0042-1755921.

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10

Broekman, Winifred, Maria Zarcone, Annemarie Van Schadewijk, Helene Roelofs, Christian Taube, Jan Stolk, and Pieter Hiemstra. "Functional comparison of bone-marrow derived mesenchymal stromal cells obtained from COPD patients and non-COPD controls." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa5061.

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Звіти організацій з теми "Bone marrow mesenchymal stromal cell"

1

Jefcoate, Colin. Regulation of Tumor Cell Growth by the Mesenchymal Environment of the Bone Marrow is Enhanced by a High-Fat Diet. Fort Belvoir, VA: Defense Technical Information Center, April 2007. http://dx.doi.org/10.21236/ada470870.

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