scholarly journals Impaired Ability of Bone Marrow Stromal Cells to Support B-Lymphopoiesis With Age

Blood ◽  
1998 ◽  
Vol 91 (1) ◽  
pp. 75-88 ◽  
Author(s):  
Robert P. Stephan ◽  
Colette R. Reilly ◽  
Pamela L. Witte
Keyword(s):  
Bone Marrow ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Lymphoid Cells ◽  
Marrow Stromal Cells ◽  
Cell Contact ◽  
B Lymphopoiesis ◽  
Interleukin 7 ◽  
Age Related ◽  
B Lymphoid

B-lymphopoiesis decreases with age. We studied how aging affects bone marrow stromal cells, because they provide the growth factors and cell contacts required for B-lymphopoiesis. No differences were noted in the cell-surface phenotype of young and old primary-cultured stromal cells. Fluorescence-activated cell sorter-purified stromal cells from old mice were deficient in the ability to support the proliferation of interleukin-7 (IL-7)–specific B-lymphoid cell lines. The kinetics of this response indicated that IL-7 was not immediately available from stromal cells of either age and was further delayed on aged stromal cells. The levels of IL-7 protein within stromal cells were equivalent between young and old animals, suggesting that the production of IL-7 was not altered by aging. Negligible amounts of IL-7 were found either freely secreted or in the extracellular matrix of cultures of young and old marrow. Contact between the lymphoid cells and the primary stromal cells was required for detectable proliferation, suggesting that cell contact was required for the release of IL-7. We propose that stromal cells regulate B-lymphopoiesis by limiting the amount of IL-7 available to the developing precursors. Therefore, we conclude that the age-related decrease in the function of bone marrow stromal cells is related to the impaired release of IL-7.

scholarly journals Impaired Ability of Bone Marrow Stromal Cells to Support B-Lymphopoiesis With Age

Blood ◽  
1998 ◽  
Vol 91 (1) ◽  
pp. 75-88 ◽  
Author(s):  
Robert P. Stephan ◽  
Colette R. Reilly ◽  
Pamela L. Witte
Keyword(s):  
Bone Marrow ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Lymphoid Cells ◽  
Marrow Stromal Cells ◽  
Cell Contact ◽  
B Lymphopoiesis ◽  
Interleukin 7 ◽  
Age Related ◽  
B Lymphoid

Abstract B-lymphopoiesis decreases with age. We studied how aging affects bone marrow stromal cells, because they provide the growth factors and cell contacts required for B-lymphopoiesis. No differences were noted in the cell-surface phenotype of young and old primary-cultured stromal cells. Fluorescence-activated cell sorter-purified stromal cells from old mice were deficient in the ability to support the proliferation of interleukin-7 (IL-7)–specific B-lymphoid cell lines. The kinetics of this response indicated that IL-7 was not immediately available from stromal cells of either age and was further delayed on aged stromal cells. The levels of IL-7 protein within stromal cells were equivalent between young and old animals, suggesting that the production of IL-7 was not altered by aging. Negligible amounts of IL-7 were found either freely secreted or in the extracellular matrix of cultures of young and old marrow. Contact between the lymphoid cells and the primary stromal cells was required for detectable proliferation, suggesting that cell contact was required for the release of IL-7. We propose that stromal cells regulate B-lymphopoiesis by limiting the amount of IL-7 available to the developing precursors. Therefore, we conclude that the age-related decrease in the function of bone marrow stromal cells is related to the impaired release of IL-7.

Abstract P120: Increased [ca 2+ ] e Enhances Adipocyte Development In Bone Marrow Stroma

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Ryota Hashimoto ◽  
Youichi Katoh ◽  
Seigo Itoh ◽  
Takafumi Iesaki ◽  
Hiroyuki Daida ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Marrow Stromal Cells ◽  
Bone Marrow Stroma ◽  
Age Related ◽  
Marrow Stroma ◽  
High Concentrations ◽  
Adipocyte Development ◽  
Oil Red O

Background: Bone marrow stroma contains adipocytes, osteoblasts, and lymphohematopoietic donor cells. With age, fatty marrow gradually predominates in bone marrow stroma and is a factor underlying age-related fracture and anemia. Thus, it is important to understand the mechanism of adipocyte development in bone marrow stroma. Bone marrow Ca 2+ levels can reach high concentrations of 8 to 40 mM, while circulating plasma Ca 2+ levels normally range from 2.3 to 2.6 mM. However, the effects of a high extracellular calcium concentration ([Ca 2+ ] e ) on adipocyte development in bone marrow stroma remain largely unknown. Methods and Results: We studied the effects of high [Ca 2+ ] e on adipocyte development in bone marrow stroma. First, we used the fura-2 method to examine whether a change in [Ca 2+ ] e alters [Ca 2+ ] i levels in bone marrow stromal cells. Changes of [Ca 2+ ] e from 1.8 mM to 5.4 mM and 10.8 mM significantly increased [Ca 2+ ] i by 1.1 and 1.3 times, respectively. Next, bone marrow stromal cells were cultured for 14 days in high [Ca 2+ ] e (5.4 mM and 10.8 mM) and normal [Ca 2+ ] e (1.8 mM) conditions. Adipocyte development was monitored by Oil Red O staining of cytoplasmic lipids and by the activity of glycerol-3-phosphate dehydrogenase (GPDH). In 5.4 mM and 10.8 mM [Ca 2+ ] e , Oil Red O-stained cells increased significantly by 1.4 and 2.3 times, respectively, and GPDH activity increased significantly by 1.7 and 2.3 times, respectively, compared with the respective values in 1.8 mM [Ca 2+ ] e . Conclusions: These results indicate that high [Ca 2+ ] e induces an increase of [Ca 2+ ] i , which enhances adipocyte development in bone marrow stroma. Further studies are required to determine the influx pathway of Ca 2+ , since prevention of Ca 2+ influx into bone marrow stromal cells might suppress development of fatty marrow and reduce age-related fracture and anemia.

LFA-1-Mediated Adhesion Of Human Hematopoietic Progenitors To Bone Marrow Stromal Cells Enhances B-Lineage Differentiation Toward CD19+ ProB Cells, While The Generation Of CD7+CD56-CD45RA+ Multipotent Lymphoid and CD10+CD19- B-Biased Progenitors Is Supported By Soluble Factors Produced From Stromal Cells

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 3697-3697
Author(s):  
Hirohito Minami ◽  
Kohshi Ohishi ◽  
Yoshiki Nakamori ◽  
Masahiro Masuya ◽  
Naoyuki Katayama
Keyword(s):  
Bone Marrow ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Culture Conditions ◽  
Marrow Stromal Cells ◽  
Cell Contact ◽  
Hematopoietic Progenitors ◽  
Monocytic Cells ◽  
Lineage Differentiation ◽  
B Lineage

Abstract The regulatory mechanism of human lymphoid differentiation remains less defined. Here we examined how bone marrow stromal cells regulate human early lymphoid differentiation, using human telomerized bone marrow stromal cells that support the generation of CD7+CD56- early T and CD10+CD19+ proB cells from human hematopoietic progenitors. To examine the role of direct contact between hematopoietic progenitors and stromal cells in lymphopoiesis, cultures were performed by inhibiting the cell-cell contact with microporous insert or by incubating hematopoietic progenitors with conditioned medium collected from stromal cell cultures. The separation suppressed B-lineage differentiation to CD10+CD19+ cells, while the generation of CD7+ cells was not significantly influenced. The CD7+ cells generated with or without direct contact with stromal cells similarly had multipotent differentiation capacity for T, B, NK, granulocytic, and monocytic cells but not for erythroid cells in various culture conditions. On the other hand, even CD10+CD19- immature cells had more limited differentiation capacity for T, B, and monocytic cells in various culture conditions, and mostly differentiated toward CD10+CD19+ proB cells on the stromal cells. By time course analysis after coculture on the stromal cells, CD7+CD10- followed by CD10+CD19- and then CD10+CD19+ cells were developed. Some portion of CD7+CD10- and most of CD7-CD10+CD19- cells, upon recultured on stromal cells, differentiated toward CD10+CD19+ cells, but such B-lineage differentiation on the stromal cells was diminished by reculture with conditioned medium. ICAM-1 was expressed on the telomerized stromal cells. Coculture on stromal cells in the presence of LFA-1 neutralizing antibody that blocks the binding to ICAM-1 inhibited the differentiation to CD19+ proB cells. Our findings show that stromal cells support the generation of CD7+ multipotent lymphoid and CD10+ B-biased progenitors by producing soluble factors, but enhances B-lineage differentiation toward CD19+ proB cells in part via LFA-1-mediated direct cell-cell contact. Disclosures: No relevant conflicts of interest to declare.

Kynurenine induces an age-related phenotype in bone marrow stromal cells

2021 ◽  
Vol 195 ◽  
pp. 111464
Author(s):  
Dhara Patel ◽  
Matthew Potter ◽  
Jordan Marcano Anaya ◽  
Meghan E. McGee-Lawrence ◽  
Mark W. Hamrick ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Marrow Stromal Cells ◽  
Age Related ◽  
Related Phenotype

scholarly journals Gfi1 expressed in bone marrow stromal cells is a novel osteoblast suppressor in patients with multiple myeloma bone disease

Blood ◽  
2011 ◽  
Vol 118 (26) ◽  
pp. 6871-6880 ◽  
Author(s):  
Sonia D'Souza ◽  
Davide del Prete ◽  
Shunqian Jin ◽  
Quanhong Sun ◽  
Alissa J. Huston ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Bone Disease ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Trichostatin A ◽  
Transcriptional Repressor ◽  
Marrow Stromal Cells ◽  
Cell Contact ◽  
Differentiation Markers

Abstract Protracted inhibition of osteoblast (OB) differentiation characterizes multiple myeloma (MM) bone disease and persists even when patients are in long-term remission. However, the underlying pathophysiology for this prolonged OB suppression is unknown. Therefore, we developed a mouse MM model in which the bone marrow stromal cells (BMSCs) remained unresponsive to OB differentiation signals after removal of MM cells. We found that BMSCs from both MM-bearing mice and MM patients had increased levels of the transcriptional repressor Gfi1 compared with controls and that Gfi1 was a novel transcriptional repressor of the critical OB transcription factor Runx2. Trichostatin-A blocked the effects of Gfi1, suggesting that it induces epigenetic changes in the Runx2 promoter. MM-BMSC cell-cell contact was not required for MM cells to increase Gfi1 and repress Runx2 levels in MC-4 before OBs or naive primary BMSCs, and Gfi1 induction was blocked by anti–TNF-α and anti–IL-7 antibodies. Importantly, BMSCs isolated from Gfi1−/− mice were significantly resistant to MM-induced OB suppression. Strikingly, siRNA knockdown of Gfi1 in BMSCs from MM patients significantly restored expression of Runx2 and OB differentiation markers. Thus, Gfi1 may have an important role in prolonged MM-induced OB suppression and provide a new therapeutic target for MM bone disease.

Bone marrow stromal cells and interleukin-7 induce coordinate expression of the BP-1/6C3 antigen and pre-B cell growth

1990 ◽  
Vol 2 (8) ◽  
pp. 697-705 ◽  
Author(s):  
Pamela A. Welch ◽  
Peter D. Burrows ◽  
Anthony Namen ◽  
Steven Gillis ◽  
Max D. Cooper
Keyword(s):  
Bone Marrow ◽  
Cell Growth ◽  
B Cell ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Marrow Stromal Cells ◽  
Coordinate Expression ◽  
Interleukin 7

scholarly journals Age-related increase of kynurenine enhances miR29b-1-5p to decrease both CXCL12 signaling and the epigenetic enzyme Hdac3 in bone marrow stromal cells

Bone Reports ◽  
2020 ◽  
Vol 12 ◽  
pp. 100270 ◽  
Author(s):  
Ahmed M. Elmansi ◽  
Khaled A. Hussein ◽  
Sergio Mas Herrero ◽  
Sudharsan Periyasamy-Thandavan ◽  
Alexandra Aguilar-Pérez ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Marrow Stromal Cells ◽  
Age Related ◽  
Related Increase
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