<i>In vivo</i>
            and
            <i>in vitro</i>
            Effects of TGF‐β1 on Normal and Neoplastic Haemopoiesis

Ruscetti, Francis W.; Dubois, Claire M.; Falk, Lydia A.; Jacobsen, Sten Eirik W.; Sing, Garwin K.; Longo, Dan L.; Wiltrout, Robert H.; Keller, Jonathan R.

doi:10.1002/9780470514061.ch14

Cited by 12 publications

(2 citation statements)

References 29 publications

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“…In the bone marrow microenvironment, TGF-b1 plays a central role as a negative controller of hematopoiesis, which prevents progenitor cells from entering the cell cycle by interfering with expression and intracellular signaling of the receptors for growth stimulatory molecules (47). TGF-b1 also modulates negatively the synthesis of proinflammatory cytokines and cytokine receptors (48), and, therefore, its deficiency may indirectly contribute to the changes outlined in the previous paragraph.…”

Section: Rsv Effects On Bmscsmentioning

confidence: 99%

Respiratory Syncytial Virus Infection in Human Bone Marrow Stromal Cells

Rezaee¹,

Gibson²,

Piktel³

et al. 2011

Am J Respir Cell Mol Biol

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Respiratory syncytial virus (RSV) is the most common respiratory pathogen in infants and young children. The pathophysiology of this infection in the respiratory system has been studied extensively, but little is known about its consequences in other systems. We studied whether RSV infects human bone marrow stromal cells (BMSCs) in vitro and in vivo, and investigated whether and how this infection affects BMSC structure and hematopoietic support function. Primary human BMSCs were infected in vitro with recombinant RSV expressing green fluorescent protein. In addition, RNA from naive BMSCs was amplified by PCR, and the products were sequenced to confirm homology with the RSV genome. The BMSC cytoskeleton was visualized by immunostaining for actin. Finally, we analyzed infected BMSCs for the expression of multiple cytokines and chemokines, evaluated their hematopoietic support capacity, and measured their chemotactic activity for both lymphoid and myeloid cells. We found that BMSCs support RSV replication in vitro with efficiency that varies among cell lines derived from different donors; furthermore, RNA sequences homologous to the RSV genome were found in naive primary human BMSCs. RSV infection disrupted cytoskeletal actin microfilaments, altered cytokine/chemokine expression patterns, decreased the ability of BMSCs to support B cell maturation, and modulated local chemotaxis. Our data indicate that RSV infects human BMSCs in vitro, and this infection has important structural and functional consequences that might affect hematopoietic and immune functions. Furthermore, we have amplified viral RNA from naive primary BMSCs, suggesting that in vivo these cells provide RSV with an extrapulmonary target.

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Section: Rsv Effects On Bmscsmentioning

confidence: 99%

Respiratory Syncytial Virus Infection in Human Bone Marrow Stromal Cells

Rezaee¹,

Gibson²,

Piktel³

et al. 2011

Am J Respir Cell Mol Biol

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“…The amino acid sequences of all the three isoforms are 70-80% homologous. TGF-beta1 is a 25-kDa nonglycosylated homodimer with nine disulfide bonds and is expressed in endothelial (20), hematopoietic (21)(22)(23), and connective tissue cells (24). TGF-beta2 is expressed in epithelial and neuronal cells and TGF-beta3 primarily in mesenchymal cells (25).…”

Section: Tgf-beta Ligands and Receptorsmentioning

confidence: 99%

Transforming growth factor -beta receptor signaling in cancer

Narayan¹

2005

Front Biosci

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Transforming growth factor-beta (TGF-beta) is an ubiquitous cytokine that affects various biological processes, such as regulation of cell proliferation, immune responses, growth, differentiation, angiogenesis, and apoptosis of various cell types. The TGF-beta ligand initiates signaling by binding to and joining type I and II receptors of serine/threonine kinases. This review discusses the TGF-beta ligands and receptors, its positive and negative regulators in signaling, as well as its important roles with respect to tumor suppression and progression.

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