Effects of Ischemic Preconditioning in the Late Phase on Homing of Endothelial Progenitor Cells in Renal Ischemia/Reperfusion Injury

Bo, C.-J.; Chen, B.; Jia, Ru; Zhu, Jun; Cao, Pu; Liu, H.; Wu, Rongqian; Ge, Yu‐Zheng; Wu, Jianping

doi:10.1016/j.transproceed.2012.05.095

Cited by 19 publications

(15 citation statements)

References 25 publications

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“…Given that tubular cells are very susceptible to ROS (20)(21)(22), renal tubular apoptosis is a characteristic feature for the progression of IR insult (23).…”

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confidence: 99%

Aloperine Protects Mice against Ischemia-Reperfusion (IR)-Induced Renal Injury by Regulating PI3K/AKT/mTOR Signaling and AP-1 Activity

Zhang

et al. 2015

Mol Med

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Aloperine is a quinolizidine alkaloid extracted from the leaves of Sophora plants. It has been recognized with the potential to treat inflammatory and allergic diseases as well as tumors. In this report, we demonstrate that pretreatment with aloperine provided protection for mice against ischemia-reperfusion (IR)-induced acute renal injury as manifested by the attenuated inflammatory infiltration, reduced tubular apoptosis, and well-preserved renal function. Mechanistic studies revealed that aloperine selectively repressed IL-1β and IFN-γ expression by regulating PI3K/Akt/mTOR signaling and NF-κB transcriptional activity. However, aloperine did not show a perceptible impact on IL-6 and TGF-β expression and the related Jak2/Stat3 signaling. It was also noted that aloperine regulates AP-1 activity, through which it not only enhances SOD expression to increase reactive oxygen species (ROS) detoxification but also promotes the expression of antiapoptotic Bcl-2, thereby preventing tubular cells from IR-induced apoptosis. Collectively, our data suggest that administration of aloperine prior to IR insults, such as renal transplantation, could be a viable approach to prevent IR-induced injuries.

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“…Given that tubular cells are very susceptible to ROS (20)(21)(22), renal tubular apoptosis is a characteristic feature for the progression of IR insult (23).…”

mentioning

confidence: 99%

Aloperine Protects Mice against Ischemia-Reperfusion (IR)-Induced Renal Injury by Regulating PI3K/AKT/mTOR Signaling and AP-1 Activity

Zhang

et al. 2015

Mol Med

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“…We also found that iNO upregulated VEGF, vascular endothelial growth factor receptor 2 (VEGFR2), and eNOS expression in the lungs of animal with acute lung injury and promoted EPCs mobilization from bone marrow (23), and VEGF plays an important role in EPCs homing (24). In the present study, we established a BPD model with a prolonged hyperoxia exposure, mimicking the clinical late phase of BPD.…”

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confidence: 75%

Combined iNO and endothelial progenitor cells improve lung alveolar and vascular structure in neonatal rats exposed to prolonged hyperoxia

Sun

Qian

2015

Pediatr Res

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Background: Stem cells or inhaled nitric oxide (iNO) are reported to improve lung structures in bronchopulmonary dysplasia (BPD) models. We hypothesized that combined iNO and transplanted endothelial progenitor cells (EPCs) might restore lung structure in rats after neonatal hyperoxia. Methods: Litters were separated into eight groups: room air, hyperoxia, hyperoxia + iNO, hyperoxia + iNO + L-NAME, hyperoxia + EPCs, hyperoxia + EPCs + L-NAME, hyperoxia + EPCs + iNO, and hyperoxia + EPCs + iNO + L-NAME. Litters were exposed to hyperoxia from the 21st day, then, sacrificed. EPCs were injected on the 21st day. L-NAME was injected daily for 7 d from the 21st day. Serum vascular endothelial growth factor (VEGF), radial alveolar count (RAC), VIII factor, EPCs engraftment, lung VEGF, VEGFR2, endothelial nitric oxide (eNOS) and SDF-1 expression, and NO production were examined. results: Hyperoxia exposure led to air space enlargement, loss of lung capillaries, and low expression of VEGF and eNOS. Transplanted EPCs, when combined with iNO, had significantly increased engraftment in lungs, compared to EPCs alone, upon hyperoxia exposure. There was improvement in alveolarization, microvessel density, and upregulation of VEGF and eNOS proteins in the hyperoxia-exposed EPCs with iNO group, compared to hyperoxia alone. conclusion: Combined EPCs and iNO improved lung structures after neonatal hyperoxia. This was associated with the upregulation of VEGF and eNOS expression.B ronchopulmonary dysplasia (BPD) is a chronic lung disease associated with significant mortality and morbidity in premature infants. New BPD is characterized by arrested alveolar and vascular growth (vascular hypothesis of BPD) (1,2). Alveolar formation is a highly coordinated process between the development of airways and pulmonary vasculature (3). Exposure to inflammation caused by excessive O 2 supplementation is hypothesized to interfere with the coordinated process of normal human lung development. Neonatal hyperoxia exposure is known to disrupt alveolar formation and growth, providing a useful model for studying BPD (4).Cell-based therapy is a novel approach that offers much promise in the prevention and treatment of BPD, including embryonic stem cells, mesenchymal stem cells, placental stem cells, umbilical cord stem cells, amniotic fluid and amnionderived cells, and lung progenitor cells. Endothelial progenitor cells (EPCs) are precursors of endothelial cells, which have the capacity of self-renewal and proliferation. EPCs is one of the key cells mediating vascular growth, which can mobilize from bone marrow and home to the site of vascular injuries, promoting neovascularization (5). There is data showing that reduced numbers or dysfunction of EPCs at birth is associated with the development of BPD (6,7). In addition, a reduction in the number of EPCs in the bone marrow, circulation and lungs has also emerged in animal models of BPD (8). Evidences that angiogenic cells treatment can restore lung structure have been demonstrated. Balasubramaniam et al...

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“…Moreover, several strategies aiming to circumvent the poor homing efficiency of cell-based therapies for stroke have already been explored, including arterial infusion (20), C-X-C chemokine receptor type 4 or vascular endothelial growth factor overexpression, or pharmacologic cotreatment (6,21).…”

Section: Discussionmentioning

confidence: 99%

Erythropoietin Pretreatment of Transplanted Endothelial Colony-Forming Cells Enhances Recovery in a Cerebral Ischemia Model by Increasing Their Homing Ability: A SPECT/CT Study

et al. 2016

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Endothelial colony-forming cells (ECFCs) are promising candidates for cell therapy of ischemic diseases, as less than 10% of patients with an ischemic stroke are eligible for thrombolysis. We previously reported that erythropoietin priming of ECFCs increased their in vitro and in vivo angiogenic properties in mice with hindlimb ischemia. The present study used SPECT/CT to evaluate whether priming of ECFCs with erythropoietin could enhance their homing to the ischemic site after transient middle cerebral artery occlusion (MCAO) followed by reperfusion in rats and potentiate their protective or regenerative effect on blood-brain barrier (BBB) disruption, cerebral apoptosis, and cerebral blood flow (CBF). Methods: Rats underwent a 1-h MCAO followed by reperfusion and then 1 d after MCAO received an intravenous injection of either PBS (control, n 5 10), PBS-primed ECFCs (ECFC PBS , n 5 13), or erythropoietinprimed ECFCs (ECFC EPO , n 5 10). ECFC homing and the effect on BBB disruption, cerebral apoptosis, and CBF were evaluated by SPECT/CT up to 14 d after MCAO. The results were expressed as median 6 interquartile range for ipsilateral-to-contralateral ratio of the activity in middle cerebral artery-vascularized territories in each hemisphere. Histologic evaluation of neuronal survival and astrocytic proliferation was performed on day 14. Results: Erythropoietin priming increased homing of ECFCs to the ischemic hemisphere (ECFC PBS , 111.0% 6 16.0%; ECFC EPO , 146.5% 6 13.3%). BBB disruption was significantly reduced (control, 387% 6 153%; ECFC PBS , 151% 6 46% [P , 0.05]; ECFC EPO , 112% 6 9% [P , 0.001]) and correlated negatively with ECFC homing (Pearson r 5 20.6930, P 5 0.0002). Cerebral apoptosis was significantly reduced (control, 161% 6 10%; ECFC PBS , 141% 6 9% [P , 0.05]; ECFC EPO ,118% 6 5% [P , 0.001]) and correlated negatively with ECFC homing (r 5 20.7251, P , 0.0001). CBF was significantly restored with ECFCs and almost totally so with erythropoietin priming (control, 72% 6 2%; ECFC PBS , 90% 6 4% [P , 0.01]; ECFC EPO , 99% 6 4% [P , 0.001]) and correlated positively with ECFC homing (r 5 0.7348, P , 0.0001). Immunoblocking against the CD146 receptor on ECFCs highlighted its notable role in ECFC homing with erythropoietin priming (ECFC EPO , 147% 6 14%, n 5 4; ECFC EPO with antibody against CD146, 101% 6 12%, n 5 4 [P , 0.05]). Conclusion: Priming with erythropoietin before cell transplantation is an efficient strategy to amplify the migratory and engraftment capacities of ECFCs and their beneficial impact on BBB disruption, apoptosis, and CBF.

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Effects of Ischemic Preconditioning in the Late Phase on Homing of Endothelial Progenitor Cells in Renal Ischemia/Reperfusion Injury

Cited by 19 publications

References 25 publications

Aloperine Protects Mice against Ischemia-Reperfusion (IR)-Induced Renal Injury by Regulating PI3K/AKT/mTOR Signaling and AP-1 Activity

Aloperine Protects Mice against Ischemia-Reperfusion (IR)-Induced Renal Injury by Regulating PI3K/AKT/mTOR Signaling and AP-1 Activity

Combined iNO and endothelial progenitor cells improve lung alveolar and vascular structure in neonatal rats exposed to prolonged hyperoxia

Erythropoietin Pretreatment of Transplanted Endothelial Colony-Forming Cells Enhances Recovery in a Cerebral Ischemia Model by Increasing Their Homing Ability: A SPECT/CT Study

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