Determine exogenous humanDDAH2gene function in rabbit bone marrow-derived endothelial progenitor cells in vitro

2017 ◽  
Vol 35 (2) ◽  
pp. 69-76
Author(s):  
Sara Shoeibi ◽  
Shabnam Mohammadi ◽  
Hamid Reza Sadeghnia ◽  
Elahe Mahdipour ◽  
Majid Ghayour-Mobarhan
2020 ◽  
Vol 10 (5) ◽  
pp. 1270-1279
Author(s):  
Zhaohong Kong ◽  
Meixin Chen ◽  
Jian Jiang ◽  
Jiang Zhu ◽  
Yumin Liu

2010 ◽  
Vol 31 (3) ◽  
pp. 855-867 ◽  
Author(s):  
Akihiko Taguchi ◽  
Pengxiang Zhu ◽  
Fang Cao ◽  
Akie Kikuchi-Taura ◽  
Yukiko Kasahara ◽  
...  

Circulating bone marrow-derived immature cells, including endothelial progenitor cells, have been implicated in homeostasis of the microvasculature. Decreased levels of circulating endothelial progenitor cells, associated with aging and/or cardiovascular risk factors, correlate with poor clinical outcomes in a range of cardiovascular diseases. Herein, we transplanted bone marrow cells from young stroke-prone spontaneously hypertensive rats (SHR-SP) into aged SHR-SP, the latter not exposed to radiation or chemotherapy. Analysis of recipient peripheral blood 28 days after transplantation revealed that 5% of circulating blood cells were of donor origin. Cerebral infarction was induced on day 30 posttransplantation. Animals transplanted with bone marrow from young SHR-SP displayed an increase in density of the microvasculature in the periinfarction zone, reduced ischemic brain damage and improved neurologic function. In vitro analysis revealed enhanced activation of endothelial nitric oxide synthase and reduced activation p38 microtubule-associated protein (MAP) kinase, the latter associated with endothelial apoptosis, in cultures exposed to bone marrow-derived mononuclear cells from young animals versus cells from aged counterparts. Our findings indicate that partial rejuvenation of bone marrow from aged rats with cells from young animals enhances the response to ischemic injury, potentially at the level of endothelial/vascular activation, providing insight into a novel approach ameliorate chronic vascular diseases.


2012 ◽  
Vol 302 (6) ◽  
pp. C892-C901 ◽  
Author(s):  
Hidehito Saito ◽  
Yasuhiko Yamamoto ◽  
Hiroshi Yamamoto

Circulating endothelial progenitor cells (EPCs) derived from the bone marrow (BM) participate in maintaining endothelial integrity and vascular homeostasis. Reduced EPC number and function result in vascular complications in diabetes. EPCs are a population of cells existing in various differentiation stages, and their cell surface marker profiles change during the process of mobilization and maturation. Hence, a generally accepted marker combination and a standardized protocol for the quantification of EPCs remain to be established. To determine the EPC subsets that are affected by diabetes, we comprehensively analyzed 32 surface marker combinations of mouse peripheral blood (PB), BM, and spleen cells by multicolor flow cytometry. Ten subsets equivalent to previously reported mouse EPCs significantly declined in number in the PB of streptozotocin-induced diabetic mice, and this reduction was reversed by insulin treatment. The PI−Lin−c-Kit−Sca-1+Flk-1−CD34−CD31+ EPC cluster, which can differentiate into mature endothelial cells in vitro, was the highest population in the PB, BM, and spleen and occurred 61 times more in the spleen than in the PB. The cell number significantly decreased in the BM as well as in the PB but paradoxically increased in the spleen under diabetic conditions. Insulin treatment reversed the decrease of EPC subsets in the BM and PB and reversed their increase in spleen. A similar tendency was observed in some of the major cell populations in db/db mice. To the best of our knowledge, we are the first to report spatial population changes in mouse EPCs by diabetes in the blood and in the BM across the spleen. Diminished circulating EPC supply by diabetes may be ascribed to impaired EPC production in the BM and to decreased EPC mobilization from the spleen, which may contribute to vascular dysfunction in diabetic conditions.


2006 ◽  
Author(s):  
Yuming Zhang ◽  
Yasushi Adachi ◽  
Masayoshi Iwasaki ◽  
Keizo Minamino ◽  
Yasuhiro Suzuki ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-15 ◽  
Author(s):  
Sharath P. Sasi ◽  
Daniel Park ◽  
Sujatha Muralidharan ◽  
Justin Wage ◽  
Albert Kiladjian ◽  
...  

Bone-marrow- (BM-) derived endothelial progenitor cells (EPCs) are critical for endothelial cell maintenance and repair. During future space exploration missions astronauts will be exposed to space irradiation (IR) composed of a spectrum of low-fluence protons (1H) and high charge and energy (HZE) nuclei (e.g., iron-56Fe) for extended time. How the space-type IR affects BM-EPCs is limited. In media transfer experimentsin vitrowe studied nontargeted effects induced by1H- and56Fe-IR conditioned medium (CM), which showed significant increase in the number of p-H2AX foci in nonirradiated EPCs between 2 and 24 h. A 2–15-fold increase in the levels of various cytokines and chemokines was observed in both types of IR-CM at 24 h.Ex vivoanalysis of BM-EPCs from single, low-dose, full-body1H- and56Fe-IR mice demonstrated a cyclical (early 5–24 h and delayed 28 days) increase in apoptosis. This early increase in BM-EPC apoptosis may be the effect of direct IR exposure, whereas late increase in apoptosis could be a result of nontargeted effects (NTE) in the cells that were not traversed by IR directly. Identifying the role of specific cytokines responsible for IR-induced NTE and inhibiting such NTE may prevent long-term and cyclical loss of stem and progenitors cells in the BM milieu.


2010 ◽  
Vol 30 (9) ◽  
pp. 964-969
Author(s):  
Jian-guo WU ◽  
Tian-hang LUO ◽  
Xiao-jun SHEN ◽  
Hong ZHOU ◽  
Xu-chao XUE ◽  
...  

Cytokine ◽  
2009 ◽  
Vol 45 (3) ◽  
pp. 174-178 ◽  
Author(s):  
Qi Ru Wang ◽  
Feng Wang ◽  
Wen Biao Zhu ◽  
Jun Lei ◽  
Yan Hong Huang ◽  
...  

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