Arginine administration increases circulating endothelial progenitor cells and attenuates tissue injury in a mouse model of hind limb ischemia/reperfusion

Nutrition ◽  
2018 ◽  
Vol 55-56 ◽  
pp. 29-35 ◽  
Author(s):  
Kuan-Feng Hsieh ◽  
Juey-Ming Shih ◽  
Yao-Ming Shih ◽  
Man-Hui Pai ◽  
Sung-Ling Yeh
Keyword(s):  
Mouse Model ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Hind Limb ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Limb Ischemia ◽  
Endothelial Progenitor ◽  
Hind Limb Ischemia ◽  
Circulating Endothelial Progenitor Cells

Augmented neovascularization with magnetized endothelial progenitor cells in rats with hind-limb ischemia

2011 ◽  
Vol 51 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Hiroshi Koiwaya ◽  
Ken-ichiro Sasaki ◽  
Takafumi Ueno ◽  
Shinji Yokoyama ◽  
Yasuyuki Toyama ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Hind Limb ◽  
Limb Ischemia ◽  
Endothelial Progenitor ◽  
Hind Limb Ischemia

scholarly journals Circulating Endothelial Progenitor Cells Are Up-Regulated in a Mouse Model of Endometriosis

2011 ◽  
Vol 178 (4) ◽  
pp. 1782-1791 ◽  
Author(s):  
Christian M. Becker ◽  
Paul Beaudry ◽  
Tae Funakoshi ◽  
Ofra Benny ◽  
Alexander Zaslavsky ◽  
...  
Keyword(s):  
Mouse Model ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Progenitor ◽  
Circulating Endothelial Progenitor Cells

scholarly journals PARP Inhibition Modulates GAPDH Activity in a Diabetic Mouse Model of Hind Limb Ischemia–Reperfusion

2012 ◽  
Vol 56 (5) ◽  
pp. 1481-1482
Author(s):  
Valy Boulom ◽  
Chandler A. Long ◽  
Rahmi Oklu ◽  
Junaid Y. Malek ◽  
Hyung-Jin Yoo ◽  
...  
Keyword(s):  
Mouse Model ◽  
Hind Limb ◽  
Ischemia Reperfusion ◽  
Limb Ischemia ◽  
Diabetic Mouse ◽  
Parp Inhibition ◽  
Hind Limb Ischemia ◽  
Gapdh Activity

scholarly journals Dietary Supplemental Glutamine Enhances the Percentage of Circulating Endothelial Progenitor Cells in Mice with High-Fat Diet-Induced Obesity Subjected to Hind Limb Ischemia

2020 ◽  
Vol 2020 ◽  
pp. 1-9 ◽  
Author(s):  
Chi-Hsuan Ko ◽  
Sung-Ling Yeh ◽  
Chiu-Li Yeh
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
High Fat Diet ◽  
Limb Ischemia ◽  
Chow Diet ◽  
Obese Mice ◽  
High Fat ◽  
Endothelial Progenitor ◽  
Protein Nitrogen ◽  
Circulating Endothelial Progenitor Cells

This study investigated whether glutamine (GLN) pretreatment can enhance circulating endothelial progenitor cells (EPCs) and attenuate inflammatory reaction in high-fat diet-induced obese mice with limb ischemia. Mice were assigned to a normal control (NC), high-fat control (HC), limb ischemia (HI), and GLN limb ischemia (HG) groups. The NC group provided chow diet and treated as a negative control. Mice in the HC and HI groups were fed a high-fat diet which 60% energy provided by fat for 8 weeks. Mice in the HG group were fed the same diet for 4 weeks and then transferred to a high-fat diet with 25% of total protein nitrogen provided as GLN to replace part of the casein for the subsequent 4 weeks. After feeding 8 weeks, mice in the HC group were sham-operated, while the HI and HG groups underwent an operation to induce limb ischemia. All mice except the NC group were euthanized on either day 1 or 7 after the operation. The results showed that the 8 weeks’ high-fat diet feeding resulted in obesity. The HG group had higher circulating EPCs on day 1 while muscle vascular endothelial growth factor, matrix metalloproteinase-9, and hypoxia-inducible factor-1 gene expressions were higher on day 7 postischemia than those of the HI group. The superoxide dismutase activity and reduced glutathione content in affected muscles were higher, whereas mRNA expressions of interleukin-6 and tumor necrosis factor-α were lower in the HG than those in the HI group. These findings suggest that obese mice pretreated with GLN-supplemented high-fat diet increased circulating EPC percentage, enhanced the antioxidant capacity, and attenuated inflammatory reactions in response to limb ischemia.

scholarly journals MO334ERYTHROPOIETIN-STIMULATED HUMAN ENDOTHELIAL PROGENITOR CELLS AMELIORATE INFLAMMATION AND FIBROSIS VIA INFLAMMASOME IN ISCHEMIA/REPERFUSION-INDUCED ACUTE KIDNEY INJURY

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Ha Nee Jang ◽  
Jin Hyun Kim ◽  
Seunghye Lee ◽  
Sehyun Jung ◽  
Se-Ho Chang ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Tissue Injury ◽  
Apoptotic Cell ◽  
Human Peripheral Blood ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Endothelial Damage ◽  
Endothelial Progenitor ◽  
Erythroid Progenitor

Abstract Background and Aims Ischemia/reperfusion-induced AKI (IR-AKI) is a major cause of AKI and progress to chronic kidney disease. But an effective therapeutic intervention for IR-AKI is not established yet. Erythropoietin (EPO) is a potent stimulator of erythroid progenitor cells and is significantly upregulated during hypoxia. Endothelial progenitor cells (EPCs) are derived from the bone marrow or tissue-resident cells and play major roles in the maintenance of vascular integrity and the repair of endothelial damage. So, we investigated if EPO-stimulated human EPCs could have the renoprotective effects in an IR-AKI mouse model. Method EPCs originated from human peripheral blood were cultured with EPO (10 IU/mL). Mice were assigned to sham, IR only groups, IR with EPC, and IR with EPO-treated EPC. EPCs (5x105 cells, tail vein) were administered twice at 30 min prior to bilateral renal artery occlusion, and 5 min before reperfusion, with all mice sacrificed 24 h after IR-AKI. Results Both EPCs and EPO-treated EPCs significantly attenuated the renal dysfunction associated with IR-AKI, as well as tissue injury. Apoptotic cell death and oxidative stress were significantly reduced in EPC and EPO-treated EPC mice. Expression of PCNA, ICAM-1, MCP-1 and α-SMA were also significantly reduced in EPC and EPO-treated EPC mice. Furthermore, the expression of NLRP3 and caspase-1 via the activation of NF-κB signaling pathways were significantly reduced in EPC and EPO-treated EPC mice. These results show more effective in EPO-treated EPC than EPC alone and suggest EPO might be involved in the development of EPC. Conclusion This study provides that inflammasome-mediated inflammation and fibrosis might be a potential target of EPC as a treatment for IR-AKI.

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