scholarly journals Stromal cell-derived factor-1 promotes bone marrow-derived cells differentiation to cardiomyocyte phenotypes in vitro

2008 ◽  
Vol 41 (2) ◽  
pp. 336-347 ◽  
Author(s):  
M. Chen ◽  
H.-Q. Xie ◽  
L. Deng ◽  
X.-Q. Li ◽  
Y. Wang ◽  
...  
2020 ◽  
Vol 10 (2) ◽  
pp. 204589402091935 ◽  
Author(s):  
Taichi Kato ◽  
Yoshihide Mitani ◽  
Masahiro Masuya ◽  
Junko Maruyama ◽  
Hirofumi Sawada ◽  
...  

The aim of this study was to investigate whether a dual endothelin receptor antagonist bosentan modulates the kinetics of bone marrow-derived stem cells in inhibiting the development of pulmonary hypertension. Bone marrow chimeric mice, transplanted with enhanced green fluorescent protein (eGFP)-positive bone marrow mononuclear cells, were exposed to hypobaric hypoxia or kept in the ambient air, and were daily treated with bosentan sodium salt or saline for 21 days. After the treatment period, right ventricular pressure was measured and pulmonary vascular morphometry was conducted. Incorporation of bone marrow-derived cells was analyzed by immunohistochemistry. Gene expression and protein level in the lung tissue were evaluated by quantitative real-time PCR and western blotting, respectively. The results showed that, in hypoxic mice, right ventricular pressure and the percentage of muscularized vessel were increased and pulmonary vascular density was decreased, each of which was reversed by bosentan. Bone marrow-derived endothelial cells and macrophages in lungs were increased by hypoxia. Bosentan promoted bone marrow-derived endothelial cell incorporation but inhibited macrophage infiltration into lungs. Quantitative real-time PCR analysis revealed that interleukin 6, stromal cell-derived factor-1, and monocyte chemoattractant protein-1 were upregulated by hypoxia, in which interleukin 6 and monocyte chemoattractant protein-1 were downregulated and stromal cell-derived factor-1 was upregulated by bosentan. Protein level of endothelial nitric oxide synthase (eNOS) in the whole lung was significantly upregulated by hypoxia, which was further upregulated by bosentan. Bosentan modulated kinetics of bone marrow-derived ECs and macrophages and related gene expression in lungs in ameliorating pulmonary hypertension in mice. Altered kinetics of bone marrow-derived stem cells may be a novel mechanism of the endothelin receptor blockade in vivo and confer a new understanding of the therapeutic basis for pulmonary hypertension.


2007 ◽  
Vol 324 (2) ◽  
pp. 834-849 ◽  
Author(s):  
Woei-Cherng Shyu ◽  
Shinn-Zong Lin ◽  
Pao-Sheng Yen ◽  
Ching-Yuan Su ◽  
Der-Cherng Chen ◽  
...  

Blood ◽  
1998 ◽  
Vol 91 (1) ◽  
pp. 100-110 ◽  
Author(s):  
Chang H. Kim ◽  
Hal E. Broxmeyer

Abstract How multiple chemoattractants cooperate in directing the migration of hematopoietic progenitor cells (HPC) for homing and peripheral blood mobilization has not yet been established. We report here the behavior of HPC under the influence of two different chemoattractants, stromal cell-derived factor (SDF)-1 and steel factor (SLF), and the chemotactic nature of the bone marrow (BM) environment using a two-chamber in vitro migration system. Various formulae were adopted to quantitate these effects. Based on these quantitations, SDF-1 showed only chemotactic activity, while SLF showed both chemotactic and chemokinetic activities on factor-dependent MO7e cells. SLF, like SDF-1, attracted human HPC from a population of CD34+ cells and induced actin polymerization in MO7e cells. SLF and SDF-1 cooperated in attracting MO7e cells, as well as cord blood (CB) and BM CD34+cells. A negative concentration gradient of SLF and SDF-1, formed by the presence of chemoattractants in the upper chamber, showed potent inhibitory effects on MO7e cell migration induced by either of these chemoattractants in the lower chamber, and SDF-1 and SLF were synergistic in mobilizing cells to the lower chamber from this negative chemoattractant gradient. Plasma obtained from BM aspirates, but not CB or peripheral blood, showed strong chemotactic effects on BM and CB CD34+ cells, and an inhibitory effect in a negative gradient on SDF-1–dependent CD34+ cell migration. These in vitro migration experiments suggest that chemoattractants such as SDF-1 and SLF with other unidentified BM chemoattractants may be involved cooperatively in the migration of HPC to the BM and in preventing spontaneous mobilization of HPC out of the BM.


Blood ◽  
1998 ◽  
Vol 91 (1) ◽  
pp. 100-110 ◽  
Author(s):  
Chang H. Kim ◽  
Hal E. Broxmeyer

How multiple chemoattractants cooperate in directing the migration of hematopoietic progenitor cells (HPC) for homing and peripheral blood mobilization has not yet been established. We report here the behavior of HPC under the influence of two different chemoattractants, stromal cell-derived factor (SDF)-1 and steel factor (SLF), and the chemotactic nature of the bone marrow (BM) environment using a two-chamber in vitro migration system. Various formulae were adopted to quantitate these effects. Based on these quantitations, SDF-1 showed only chemotactic activity, while SLF showed both chemotactic and chemokinetic activities on factor-dependent MO7e cells. SLF, like SDF-1, attracted human HPC from a population of CD34+ cells and induced actin polymerization in MO7e cells. SLF and SDF-1 cooperated in attracting MO7e cells, as well as cord blood (CB) and BM CD34+cells. A negative concentration gradient of SLF and SDF-1, formed by the presence of chemoattractants in the upper chamber, showed potent inhibitory effects on MO7e cell migration induced by either of these chemoattractants in the lower chamber, and SDF-1 and SLF were synergistic in mobilizing cells to the lower chamber from this negative chemoattractant gradient. Plasma obtained from BM aspirates, but not CB or peripheral blood, showed strong chemotactic effects on BM and CB CD34+ cells, and an inhibitory effect in a negative gradient on SDF-1–dependent CD34+ cell migration. These in vitro migration experiments suggest that chemoattractants such as SDF-1 and SLF with other unidentified BM chemoattractants may be involved cooperatively in the migration of HPC to the BM and in preventing spontaneous mobilization of HPC out of the BM.


2013 ◽  
Vol 18 (6) ◽  
pp. 637-646 ◽  
Author(s):  
Kristine Misund ◽  
Katarzyna A. Baranowska ◽  
Toril Holien ◽  
Christoph Rampa ◽  
Dionne C. G. Klein ◽  
...  

The tumor microenvironment can profoundly affect tumor cell survival as well as alter antitumor drug activity. However, conventional anticancer drug screening typically is performed in the absence of stromal cells. Here, we analyzed survival of myeloma cells co-cultured with bone marrow stromal cells (BMSC) using an automated fluorescence microscope platform, ScanR. By staining the cell nuclei with DRAQ5, we could distinguish between BMSC and myeloma cells, based on their staining intensity and nuclear shape. Using the apoptotic marker YO-PRO-1, the effects of drug treatment on the viability of the myeloma cells in the presence of stromal cells could be measured. The method does not require cell staining before incubation with drugs, and less than 5000 cells are required per condition. The method can be used for large-scale screening of anticancer drugs on primary myeloma cells. This study shows the importance of stromal cell support for primary myeloma cell survival in vitro, as half of the cell samples had a marked increase in their viability when cultured in the presence of BMSC. Stromal cell–induced protection against common myeloma drugs is also observed with this method.


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