Bone blood flow and In vitro proliferation of bone marrow and trabecular bone osteoblast-like cells in ovariectomized rats

1992 ◽  
Vol 50 (4) ◽  
pp. 336-341 ◽  
Author(s):  
Dominique Egrise ◽  
Dominique Martin ◽  
Pierre Neve ◽  
Anne Vienne ◽  
Michel Verhas ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Blood Flow ◽  
Trabecular Bone ◽  
Ovariectomized Rats ◽  
Bone Blood Flow ◽  
In Vitro Proliferation

scholarly journals Mechanical, hormonal and metabolic influences on blood vessels, blood flow and bone

2017 ◽  
Vol 235 (3) ◽  
pp. R77-R100 ◽  
Author(s):  
Rhonda D Prisby
Keyword(s):  
Bone Marrow ◽  
Blood Flow ◽  
Trabecular Bone ◽  
Blood Vessels ◽  
Vascular Endothelium ◽  
Bone Cells ◽  
Vascular System ◽  
Bone Volume ◽  
Bone Blood Flow ◽  
Trabecular Bone Volume

Bone tissue is highly vascularized due to the various roles bone blood vessels play in bone and bone marrow function. For example, the vascular system is critical for bone development, maintenance and repair and provides O2, nutrients, waste elimination, systemic hormones and precursor cells for bone remodeling. Further, bone blood vessels serve as egress and ingress routes for blood and immune cells to and from the bone marrow. It is becoming increasingly clear that the vascular and skeletal systems are intimately linked in metabolic regulation and physiological and pathological processes. This review examines how agents such as mechanical loading, parathyroid hormone, estrogen, vitamin D and calcitonin, all considered anabolic for bone, have tremendous impacts on the bone vasculature. In fact, these agents influence bone blood vessels prior to influencing bone. Further, data reveal strong associations between vasodilator capacity of bone blood vessels and trabecular bone volume, and poor associations between estrogen status and uterine mass and trabecular bone volume. Additionally, this review highlights the importance of the bone microcirculation, particularly the vascular endothelium and NO-mediated signaling, in the regulation of bone blood flow, bone interstitial fluid flow and pressure and the paracrine signaling of bone cells. Finally, the vascular endothelium as a mediator of bone health and disease is considered.

scholarly journals HOXB4 confers a constant rate of in vitro proliferation to transduced bone marrow cells

Oncogene ◽  
2004 ◽  
Vol 24 (4) ◽  
pp. 561-572 ◽  
Author(s):  
Carolin Schmittwolf ◽  
Matthias Porsch ◽  
Axel Greiner ◽  
Andris Avots ◽  
Albrecht M Müller
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
In Vitro Proliferation ◽  
Constant Rate ◽  
Marrow Cells

scholarly journals Existence of a pool of T-lymphocyte colony-forming cells (T-CFC) in human bone marrow and their place in the differentiation of the T- lymphocyte lineage

Blood ◽  
1981 ◽  
Vol 58 (5) ◽  
pp. 911-915 ◽  
Author(s):  
F Triebel ◽  
WA Robinson ◽  
AR Hayward ◽  
PG Goube de Laforest
Keyword(s):  
Bone Marrow ◽  
T Cell ◽  
T Lymphocyte ◽  
Cell Lineage ◽  
Marrow Graft ◽  
In Vitro Proliferation ◽  
Complement Dependent Cytotoxicity ◽  
Self Tolerance ◽  
Proliferation And Differentiation

Abstract The existence and characteristics of bone marrow T-cell progenitors have not yet been established in man. Several pieces of evidence such as the reconstitution of certain immunodeficiencies by bone marrow graft suggest that T-cell precursors are present in the bone marrow. We report the growth of T-cell colonies from bone marrow populations using PHA-stimulated lymphocyte-conditioned medium containing T-cell growth factor (TCGF). Rosetting experiments and complement-dependent cytotoxicity assays with monoclonal antibodies indicate that the bone marrow T colony-forming cells (T-CFC) are E- OKT 3- and la+, i.e., immature progenitors. The colonies derived from these cells have the phenotype of mature T cells: E + OKT 3 + la- with either helper (OKT 4+) and suppressor (OKT 8 +) antigens. These results suggest that a thymic microenvironment may not be necessary for the in vitro proliferation and differentiation of the T-cell lineage in adult humans. These methodologies may permit direct investigation of early phenomena concerning the T-cell lineage, such as the acquisition of self-tolerance, the formation of a repertoire of specificities, and the HLA restriction phenomena that we believe takes place before the thymic maturation.

scholarly journals In vitro proliferation and differentiation of canine bone marrow derived mesenchymal stem cells over hydroxyl functionalized CNT substrates

2019 ◽  
Vol 24 ◽  
pp. e00387
Author(s):  
A.P. Madhusoodan ◽  
Kinsuk Das ◽  
Bhabesh Mili ◽  
Kuldeep Kumar ◽  
Ajay Kumar ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
In Vitro Proliferation ◽  
Proliferation And Differentiation

scholarly journals In vitro proliferation of primitive hemopoietic stem cells supported by stromal cells: evidence for the presence of a mechanism(s) other than that involving c-kit receptor and its ligand.

1992 ◽  
Vol 176 (2) ◽  
pp. 351-361 ◽  
Author(s):  
H Kodama ◽  
M Nose ◽  
Y Yamaguchi ◽  
J Tsunoda ◽  
T Suda ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Hemopoietic Stem Cells ◽  
In Vitro Proliferation ◽  
Kit Receptor ◽  
Colony Forming Units ◽  
Marrow Cells

The preadipose cell line, PA6, can support long-term hemopoiesis. Frequency of the hemopoietic stem cells capable of sustaining hemopoiesis in cocultures of bone marrow cells and PA6 cells for 6 wk was 1/5.3 x 10(4) bone marrow cells. In the group of dishes into which bone marrow cells had been inoculated at 2.5 x 10(4) cells/dish, 3 of 19 dishes (16%) contained stem cells capable of reconstituting erythropoiesis of WBB6F1-W/Wv mice, indicating that PA6 cells can support the proliferation of primitive hemopoietic stem cells. When the cocultures were treated with an antagonistic anti-c-kit monoclonal antibody, ACK2, only a small number of day 12 spleen colony-forming units survived; and hemopoiesis was severely reduced. However, when the cocultures were continued with antibody-free medium, hemopoiesis dramatically recovered. To examine the proliferative properties of the ACK2-resistant stem cells, we developed a colony assay system by modifying our coculture system. Sequential observations of the development of individual colonies and their disappearance demonstrated that the stem cells having higher proliferative capacity preferentially survive the ACK2 treatment. Furthermore, cells of subclones of the PA6 clone that were incapable of supporting long-term hemopoiesis expressed mRNA for the c-kit ligand. These results suggest that a mechanism(s) other than that involving c-kit receptor and its ligand plays an important role in the survival and proliferation of primitive hemopoietic stem cells.

scholarly journals In vitro Proliferation of Human Bone Marrow Mesenchymal Stem Cells Employing Donor Serum and Basic Fibroblast Growth Factor

2003 ◽  
Vol 43 (1-3) ◽  
pp. 89-96 ◽  
Author(s):  
Mutsumi Takagi ◽  
Tetsuya Nakamura ◽  
Chikayoski Matsuda ◽  
Takako Hattori ◽  
Shigeyuki Wakitani ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Fibroblast Growth ◽  
In Vitro Proliferation ◽  
Marrow Mesenchymal Stem Cells

Deletion Of Fanca Or Fancd2 Dysregulates Treg Activity and Exacerbates Gvhd In Mice

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 3239-3239
Author(s):  
Wei Du ◽  
Ozlem Erden ◽  
Andrew Wilson ◽  
Jared Sipple ◽  
Jonathan Schick ◽  
...  
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
Transcriptional Activity ◽  
Conflicts Of Interest ◽  
Bone Marrow Failure ◽  
Genetic Disorder ◽  
Allogeneic Bone Marrow Transplantation ◽  
Allogeneic Bone ◽  
In Vitro Proliferation

Abstract Fanconi anemia (FA) is a genetic disorder associated with bone marrow failure and leukemia. Recent studies demonstrate fundamental immune defects in FA. However, the mechanisms that are critical for FA immunodeficiency are not known. Here we report that deletion of Fanca or Fancd2 dysregulates the suppressive activity of regulatory T cells (Tregs) and exacerbates graft-versus-host disease (GVHD) in mice. Recipient mice of Fanca-/- or Fancd2-/- bone marrow chimeras exhibited severe acute GVHD after allogeneic bone marrow transplantation (BMT). Further study showed that T cells from Fanca-/- or Fancd2-/- mice induced higher GVHD lethality than those from WT littermates. Mechanistically, FA Tregs possessed lower proliferative suppression potential compared to WT Tregs, as demonstrated by in vitro proliferation assay and BMT. Analysis of CD25+Foxp3+ Tregs indicated that loss of Fanca or Fancd2 dysregulated Foxp3 transcriptional activity. Additionally, CD25+Foxp3+ Tregs of Fanca-/- or Fancd2-/- mice were less efficient in suppressing the production of GVHD-associated inflammatory cytokines. Consistently, incremental NF-kB transcriptional activity was observed in infiltrated T cells from FA GVHD mice. Conditional deletion of p65 in FA Tregs desreased GVHD mortality. Our study uncovers an essential role for the FA proteins in maintaining Treg homeostasis and suggests that targeted blocking NF-kB signaling within T cells represents an attractive therapeutic strategy to ameliorate GVHD in FA. Disclosures: No relevant conflicts of interest to declare.

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