scholarly journals Tapak liman (Elephantopus scaber L) extract–induced CD4+ and CD8+ differentiation from hematopoietic stem cells and progenitor cell proliferation in mice (Mus musculus L)

Author(s):  
Muhammad Sasmito Djati ◽  
Hindun Habibu ◽  
Nabilah A. Jatiatmaja ◽  
Muhaimin Rifa’i
2012 ◽  
Vol 21 (9) ◽  
pp. 1449-1454 ◽  
Author(s):  
Hal E. Broxmeyer ◽  
Ferdinand Kappes ◽  
Nirit Mor-Vaknin ◽  
Maureen Legendre ◽  
John Kinzfogl ◽  
...  

Blood ◽  
2012 ◽  
Vol 119 (3) ◽  
pp. 707-716 ◽  
Author(s):  
Julius G. Juarez ◽  
Nadia Harun ◽  
Marilyn Thien ◽  
Robert Welschinger ◽  
Rana Baraz ◽  
...  

Abstract CXCL12 and VCAM1 retain hematopoietic stem cells (HSCs) in the BM, but the factors mediating HSC egress from the BM to the blood are not known. The sphingosine-1-phosphate receptor 1 (S1P1) is expressed on HSCs, and S1P facilitates the egress of committed hematopoietic progenitors from the BM into the blood. In the present study, we show that both the S1P gradient between the BM and the blood and the expression of S1P1 are essential for optimal HSC mobilization by CXCR4 antagonists, including AMD3100, and for the trafficking of HSCs during steady-state hematopoiesis. We also demonstrate that the S1P1 agonist SEW2871 increases AMD3100-induced HSC and progenitor cell mobilization. These results suggest that the combination of a CXCR4 antagonist and a S1P1 agonist may prove to be sufficient for mobilizing HSCs in normal donors for transplantation purposes, potentially providing a single mobilization procedure and eliminating the need to expose normal donors to G-CSF with its associated side effects.


PLoS Biology ◽  
2013 ◽  
Vol 11 (6) ◽  
pp. e1001576 ◽  
Author(s):  
David G. Kent ◽  
Juan Li ◽  
Hinal Tanna ◽  
Juergen Fink ◽  
Kristina Kirschner ◽  
...  

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 1408-1408
Author(s):  
Yinshi Guo ◽  
Chao Niu ◽  
Peter Breslin ◽  
Shubin Zhang ◽  
Wei Wei ◽  
...  

Abstract It was shown that c-Myc is required for the proliferation and differentiation of hematopoietic stem cells and progenitors. Mice with c-Myc deletions develop severe anemia and cytopenia. However, hematopoietic stem cells (HSCs) accumulate in significant numbers in the bone marrow (BM) of mutant mice, probably due to an increase in adhesiveness of the mutant HSCs to BM osteoblastic niche cells. Previously, we demonstrated that PTEN might play a critical role in the process of adhesion of HSCs to BM niche cells. Deletion of PTEN results in the proliferation and peripheral mobilization of HSCs, followed by a decline in these cells. PTEN mutant mice proceed to develop myeloproliferative disorders. Here we report that c-Myc also has an essential role to play in regulating the lineage commitment of HSCs and progenitors (HSC/Ps). HSC/Ps in which c-Myc is deleted are biased toward megakaryocytic lineage differentiation at the expense of other lineages. c-Myc knockout mice develop significant thrombocytosis (3- to 5-fold increase in peripheral platelet numbers) due to an obviously increased megakaryopoiesis in BM and spleen. PTEN deletion causes down-regulation of expression of adhesive molecules, including integrins and N-cadherin, in HSCs, resulting not only in an increased mobilization of c-Myc-mutant HSCs from the BM niche but also mobilization of c-Myc-mutant megakaryocytic progenitors to the spleen. We found that HSCs and megakaryocytic progenitors are significantly reduced in BM but dramatically increased in the spleens of PTEN/c-MYC double-knockout mice, compared to c-Myc single-gene knockout mice. In addition, PTEN deletion further promotes megakaryocytic progenitor cell proliferation, as well as infiltration of these cells into the liver. PTEN/c-Myc double-gene knockout mice consistently develop megakaryocytic proliferative disorders. We conclude that the ability of c-Myc to regulate HSC-BM niche interactions is at least partially accomplished through inhibition of PTEN function by c-Myc. In addition, c-Myc controls the lineage commitment of HSC/Ps. Deletion of c-Myc converts the myeloproliferative disorder seen in PTEN knockout mice to a megakaryocytic proliferative disorder. Whether PTEN and c-Myc mutations are likewise etiologically involved in human megakaryocytic proliferative disorders and megakaryocytic leukemia is currently a topic of active investigation in our laboratory.


Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4045-4045
Author(s):  
Ferda Tekinturhan ◽  
Ludovic Zimmerlin ◽  
Vera S. Donnenberg ◽  
Melanie E. Pfeifer ◽  
Darlene A. Monlish ◽  
...  

Abstract Bone marrow (BM) contains hematopoietic stem cells (HSCs), which can give rise to all mature blood cells and marrow stromal cells as well. Recently, it has been shown that non-hematopoietic stem/progenitor cells which can differentiate into non-hematopoietic tissues also reside in the BM. Although culture expanded cells have been studied in great detail, little is known about the phenotype and quantity of these cells in freshly harvested adult human BM. The aim of this study is to isolate and characterize hematopoietic and non-hematopoietic stem/progenitor cells in adult human BM by comparing two different isolation techniques and their effects on the yield of hematopoietic, mesenchymal and endothelial stem/progenitor cell populations. BM samples were collected mechanically from isolated rib specimens obtained during lung resection (n=10), or from BM aspirates harvested from the humerus of orthopedic patients (n=17). BM mononuclear cells were purified on a Ficoll/Hypaque density gradient and stained simultaneously using CD105 FITC, CD73 PE, CD34 ECD, CD90 PE.Cy5, CD117 PE.Cy7, CD133 APC, CD45 APC.Cy7 and DAPI as a marker of nucleated cells. 2–15 million cells per sample were acquired on a Dako CyAn cytometer and the data were analyzed offline using prototype analytical software (Venturi, Applied Cytometry Systems). The significant difference in the percentage of the CD45 − singlets (non-hematopoietic cells) between BM aspirates and rib-derived samples indicates hemodilution in the bone marrow aspirates. Although we have observed a slight difference in the mean of hematopoietic stem cell content between samples, it was not statistically significant. According to our results, the quantity of mesenchymal stem cells was higher in rib-derived BM than BM aspirates (p value=0.028). The expression of some stem/progenitor cell markers, such as CD90 (Thy-1), CD117 (c-Kit) and CD133 remained similar for all cell types. Our results are shown in the table below. Surface Antigens RibBM (n=10)¥ BMA (n=17)¥ p Value % % Total Cells CD45- of nucleated cells 15.3 ± 7.9 5.7 ± 5.2 0.004 CD34+ Hematopoietic Stem Cells (HSCs)* CD34 of CD45+ 1.7 ± 1.48 2.6 ± 2.0 0.883 CD117 74.6 ± 31.3 53.3 ± 18.8 0.073 CD90 60.3 ± 44.5 35.9 ± 36.5 0.134 CD133 70.3 ± 31.8 62.3 ± 21.4 0.443 Endothelial Progenitor Cells (EPCs)* EPCs of nucleated cells 0.05 ± 0.03 0.12 ± 0.2 0.323 CD117 81.3 ± 29.8 78.1 ± 20.2 0.746 CD90 66.7 ± 39.7 53.7 ± 31.4 0.356 CD133 45.9 ± 32.7 33.9 ± 22.0 0.265 Mesenchymal Stem Cells (MSCs)* MSCs of nucleated cells 0.086 ± 0.14 0.008 ± 0.01 0.028 CD117 60.2 ± 36.8 49.8 ± 34.3 0.471 CD90 66.0 ± 27.7 65.7 ± 29.1 0.981 CD133 37.8 ± 27.4 39.9 ± 28.9 0.857 RibBM: Rib-derived BM, BMA: Bone Marrow Aspirate ¥Data are given as mean ± SD. *CD90, CD117 and CD133 expressions are shown for each stem/progenitor fraction: Hematopoietic stem cells (CD34 + CD45 + and light scatter properties according to the ISHAGE protocol), endothelial progenitor cells (CD34bright CD45 − CD105 +) and mesenchymal stem cells (CD34 − CD45 − CD73 + CD105 +).


Blood ◽  
2008 ◽  
Vol 112 (8) ◽  
pp. 3026-3035 ◽  
Author(s):  
Jean-Jacques Lataillade ◽  
Olivier Pierre-Louis ◽  
Hans Carl Hasselbalch ◽  
Georges Uzan ◽  
Claude Jasmin ◽  
...  

Abstract Primary myelofibrosis (PMF) is the rarest and the most severe Philadelphia-negative chronic myeloproliferative syndrome. By associating a clonal proliferation and a mobilization of hematopoietic stem cells from bone marrow to spleen with profound alterations of the stroma, PMF is a remarkable model in which deregulation of the stem cell niche is of utmost importance for the disease development. This paper reviews key data suggesting that an imbalance between endosteal and vascular niches participates in the development of clonal stem cell proliferation. Mechanisms by which bone marrow niches are altered with ensuing mobilization and homing of neoplastic hematopoietic stem cells in new or reinitialized niches in the spleen and liver are examined. Differences between signals delivered by both endosteal and vascular niches in the bone marrow and spleen of patients as well as the responsiveness of PMF stem cells to their specific signals are discussed. A proposal for integrating a potential role for the JAK2 mutation in their altered sensitivity is made. A better understanding of the cross talk between stem cells and their niche should imply new therapeutic strategies targeting not only intrinsic defects in stem cell signaling but also regulatory hematopoietic niche–derived signals and, consequently, stem cell proliferation.


2020 ◽  
Vol 27 (10-11) ◽  
pp. 830-833
Author(s):  
Mariana Tannús Ruckert ◽  
Annet Z. Brouwers-Vos ◽  
Luis Fernando P. Nagano ◽  
Jan Jacob Schuringa ◽  
Vanessa Silva Silveira

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