scholarly journals Hypoxia-Inducible Factor 1-α-AA-Modified Bone Marrow Stem Cells Protect PC12 Cells from Hypoxia-Induced Apoptosis, Partially Through VEGF/PI3K/Akt/FoxO1 Pathway

2012 ◽  
Vol 21 (14) ◽  
pp. 2703-2717 ◽  
Author(s):  
Qian Zhong ◽  
Yanfang Zhou ◽  
Weibiao Ye ◽  
Tuo Cai ◽  
Xiuquan Zhang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Pc12 Cells ◽  
Hypoxia Inducible Factor ◽  
Bone Marrow Stem Cells ◽  
Hypoxia Inducible Factor 1 ◽  
Induced Apoptosis

Stabilization of hypoxia-inducible factor-1 enhances proangiogenic potential of bone marrow–derived mesenchymal stem cells

2009 ◽  
Vol 209 (3) ◽  
pp. S88
Author(s):  
Sae Hee Ko ◽  
Denise A. Chan ◽  
Jason P. Glotzbach ◽  
Amato J. Giaccia ◽  
Geoffrey C. Gurtner ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1

Abstract 703: HIF-1α Dependent Expression of iNOS in Bone Marrow Stem Cells Mediates Protection of Cardiomyocytes against Ischemia

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Ying Dai ◽  
Muhammad Ashraf ◽  
Yigang Wang ◽  
Meifeng Xu
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Cellular Localization ◽  
Hypoxia Inducible Factor ◽  
Annexin V ◽  
Competitive Inhibitor ◽  
Bone Marrow Stem Cells ◽  
No Donor ◽  
Inos Inhibitor ◽  
Ldh Release

We hypothesized that inducible nitric oxide synthase (iNOS) upregulated in bone marrow stem cells (BMSCs) protect ischemic cardiomyocytes via hypoxia inducible factor-1α (HIF-1α) pathway. Methods: Isolated BMSCs were exposed to hypoxia for 24 hours. The level of HIF-1α protein and its activated form were measured by ELISA. The expression of iNOS and HIF-1α were analyzed by quantitative PCR and cellular localization was determined by immunohistochemistry. Cardiomyocytes in co-culture with BMSCs were subjected to hypoxia and H 2 O 2 (200 μmol). LDH release, DNA fragmentation and annexin-V positive cells were used as injury markers. Results : HIF-1α protein and its activated form were markedly increased (Fig. A, B ) and translocated to the nucleus or peri-nuclear area of BMSCs subjected to hypoxia, in parallel with increased expression of HIF-1α target gene iNOS, which was blocked by pretreating cells with neutralizing HIF-1α antibody (Fig. C ). Co-culture of cardiomyocytes with BMSCs not only prevented and reduced cardiomyocyte apoptosis induced by hypoxia and H 2 O 2 but also significantly reduced LDH release from cardiomyocytes (Fig. D–G ). The cardiac protection by BMSC was abolished by neutralizing HIF-1α antibodies, and by the selective iNOS inhibitor, 1400W (10 mg/L) as well as a potent competitive inhibitor of NOS, L-NAME (200 μmol/L). However, no effects of neutralizing HIF-1α antibody, L-NAME or 1400W on cardiomyocytes alone were seen. SNAP (300 μmol/L), a NO donor had no synergistic effect on the cardioprotective effect of BMSC. Conclusion: iNOS upregulated in bone marrow stem cells by hypoxia protects cardiomyocytes against ischemic injury via activating HIF-1α.

Bone marrow stem cells make hepatocytes with replicative potential

2001 ◽  
Vol 120 (5) ◽  
pp. A62-A62
Author(s):  
S FORBES ◽  
M ALISON ◽  
K HODIVALADILKE ◽  
R JEFFERY ◽  
R POULSOM ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Bone Marrow Stem Cells

Autologous 5-azacytidine-cultured bone-marrow stem cells in surgical treatment of heart failure

2008 ◽  
Vol 7 ◽  
pp. 114-115
Author(s):  
R AKCHURIN ◽  
T RAKHMATZADE ◽  
E SKRIDLEVSKAYA ◽  
L SAMOYLENKO ◽  
V SERGIENKO ◽  
...  
Keyword(s):  
Heart Failure ◽  
Stem Cells ◽  
Bone Marrow ◽  
Surgical Treatment ◽  
Bone Marrow Stem Cells
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