Transforming growth factor beta: is it a downregulator of stem cell inhibition by macrophage inflammatory protein 1 alpha?

Maltman, John; Pragnell, Ian B.; Graham, Gerard J.

doi:10.1084/jem.178.3.925

Cited by 24 publications

(7 citation statements)

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“…Members of this family have both proinflammatory as well as reparative activities. In addition, MIP‐1α may inhibit the progression of haematopoietic stem cells to the cell cycle ( Broxmeyer et al , 1991 ; Mancini et al , 1992 ; Eaves et al , 1993 ; Maltman et al , 1993 ; Verfaillie et al , 1994 ; Bonnet et al , 1995 ; Mayani et al , 1995 ). The effects of MIP‐1α, however, appeared to be highly variable, depending upon the maturational status of the target cells.…”

Section: Discussionmentioning

confidence: 99%

Human osteoblast‐like cells and osteosarcoma cell lines synthesize macrophage inhibitory protein 1α in response to interleukin 1β and tumour necrosis factor α stimulation in vitro

2000

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Recent investigations have demonstrated that macrophage inhibitory protein 1alpha (MIP-1alpha) plays a critical role in haematopoiesis. In part, MIP-1alpha limits the differentiation of early haematopoietic cells, thereby ensuring that sufficient quantities of blood precursors are available to meet haematopoietic demands. MIP-1alpha is produced by cells of the marrow microenvironment (marrow stromal cells) in response to a variety of stimuli, including interleukin 1beta (IL-1beta) and tumour necrosis factor alpha (TNF-alpha). Our recent investigations demonstrated that normal human osteoblast-like cells (HOBs) maintain the early phenotype of haematopoietic precursors, like other members of the bone marrow stroma. Although the precise molecular mechanisms for these observations have not been determined, the production of MIP-1alpha remains one such possibility. In the present study, we investigated whether cells of the osteoblast lineage under basal, IL-1beta and/or TNF-alpha stimulation produce MIP-1alpha. We observed that IL-1beta and TNF-alpha stimulated HOBs and human osteosarcoma cells to rapidly express MIP-1alpha mRNA and to secrete large quantities of the protein. MIP-1alpha mRNA and protein was not, however, detected under basal conditions. Perhaps more importantly, enriched human CD34+ bone marrow cells in co-culture may be capable of stimulating the expression of MIP-1alpha mRNA by HOBs in vitro. These findings suggest that human osteoblast-like cells may produce MIP-1alpha in vivo to support haematopoiesis at sites where osteoblasts and haematopoietic cells are closely associated.

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Section: Discussionmentioning

confidence: 99%

Human osteoblast‐like cells and osteosarcoma cell lines synthesize macrophage inhibitory protein 1α in response to interleukin 1β and tumour necrosis factor α stimulation in vitro

2000

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“…MIP-1␣ production may also be inhibited by other secondarily induced cytokines. Maltman et al (36) showed that TGF-␤ can inhibit MIP-1␣ gene expression by bone marrow macrophages. Our studies suggest that MIP-1␣ is not the primary chemoattractant for IL-2-induced lymphocytic infiltration.…”

Section: Discussionmentioning

confidence: 99%

The role of cytokines, adhesion molecules, and chemokines in interleukin-2-induced lymphocytic infiltration in C57BL/6 mice.

Anderson

Lentsch²,

Hadjiminas³

et al. 1996

J. Clin. Invest.

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“…In addition to its proinflammatory activities, MIP-1␣ is also known to inhibit proliferation of hematopoietic stem cells (20). However, studies have revealed that MIP-1␣-null mice have no overt abnormalities in peripheral blood or bone marrow cells (21,22), thus making it feasible to study the proinflammatory activities of MIP-1␣ following T-H using MIP-1␣ KO mice. , and MIP-1 ␣ (E).…”

Section: Discussionmentioning

confidence: 99%

The Role of MIP-1α in the Development of Systemic Inflammatory Response and Organ Injury following Trauma Hemorrhage

Hsieh

Frink

Hsieh

et al. 2008

The Journal of Immunology

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Although MIP-1α is an important chemokine in the recruitment of inflammatory cells, it remains unknown whether MIP-1α plays any role in the development of systemic inflammatory response following trauma-hemorrhage (T-H). C57BL/6J wild type (WT) and MIP-1α-deficient (KO) mice were used either as control, subjected to sham operation (cannulation or laparotomy only or cannulation plus laparotomy) or T-H (midline laparotomy, mean blood pressure 35 ± 5 mmHg for 90 min, followed by resuscitation) and sacrificed 2 h thereafter. A marked increase in serum α-glutathione transferase, TNF-α, IL-6, IL-10, MCP-1, and MIP-1α and Kupffer cell cytokine production was observed in WT T-H mice compared with shams or control. In addition lung and liver tissue edema and neutrophil infiltration (myeloperoxidase (MPO) content) was also increased following T-H in WT animals. These inflammatory markers were markedly attenuated in the MIP-1α KO mice following T-H. Furthermore, compared with 2 h, MPO activities at 24 and 48 h after T-H declined steadily in both WT and KO mice. However, normalization of MPO activities to sham levels within 24 h was seen in KO mice but not in WT mice. Thus, MIP-1α plays an important role in mediating the acute inflammatory response following T-H. In the absence of MIP-1α, acute inflammatory responses were attenuated; rapidly recovered and less remote organ injury was noted following T-H. Thus, interventions that reduce MIP-1α levels following T-H should be useful in decreasing the deleterious inflammatory consequence of trauma.

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Transforming growth factor beta: is it a downregulator of stem cell inhibition by macrophage inflammatory protein 1 alpha?

Cited by 24 publications

References 50 publications

Human osteoblast‐like cells and osteosarcoma cell lines synthesize macrophage inhibitory protein 1α in response to interleukin 1β and tumour necrosis factor α stimulation in vitro

Human osteoblast‐like cells and osteosarcoma cell lines synthesize macrophage inhibitory protein 1α in response to interleukin 1β and tumour necrosis factor α stimulation in vitro

The role of cytokines, adhesion molecules, and chemokines in interleukin-2-induced lymphocytic infiltration in C57BL/6 mice.

The Role of MIP-1α in the Development of Systemic Inflammatory Response and Organ Injury following Trauma Hemorrhage

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