The potential of statin and stromal cell-derived factor-1 to promote angiogenesis

Yu, Hong; Feng, Yingmei

doi:10.4161/cam.2.4.6818

Cited by 6 publications

(2 citation statements)

References 43 publications

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“…Cytokine SDF‐1 and its receptor CXCR4 are known to regulate cell migration and it has been reported that increased CXCR4 expression by HPC is responsible for the enhanced therapeutic properties of cardiac stem cells (CSCs) . In light of our results showing that the enhanced migration of MSCs requires leptin (Figs.…”

Section: Resultsmentioning

confidence: 51%

Leptin Signaling Is Required for Augmented Therapeutic Properties of Mesenchymal Stem Cells Conferred by Hypoxia Preconditioning

Jiang

et al. 2014

Stem Cells

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Hypoxia preconditioning enhances the therapeutic effect of mesenchymal stem cells (MSCs). However, the mechanism underlying hypoxia-induced augmentation of the protective effect of MSCs on myocardial infarction (MI) is poorly understood. We show that hypoxia-enhanced survival, mobility, and protection of cocultured cardiomyocytes were paralleled by increased expression of leptin and cell surface receptor CXCR4. The enhanced activities were abolished by either knockdown of leptin with a selective shRNA or by genetic deficiency of leptin or its receptor in MSCs derived, respectively, from ob/ob or db/db mice. To characterize the role of leptin in the regulation of MSC functions by hypoxia and its possible contribution to enhanced therapeutic efficacy, cell therapy using MSCs derived from wild-type, ob/ob, or db/db mice was implemented in mouse models of acute MI. Augmented protection by hypoxia pretreatment was only seen with MSCs from wild-type mice. Parameters that were differentially affected by hypoxia pretreatment included MSC engraftment, c-Kit+ cell recruitment to the infarct, vascular density, infarct size, and long-term contractile function. These data show that leptin signaling is an early and essential step for the enhanced survival, chemotaxis, and therapeutic properties of MSCs conferred by preculture under hypoxia. Leptin may play a physiological role in priming MSCs resident in the bone marrow endosteum for optimal response to systemic signaling molecules and subsequent tissue repair.

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Section: Resultsmentioning

confidence: 51%

Leptin Signaling Is Required for Augmented Therapeutic Properties of Mesenchymal Stem Cells Conferred by Hypoxia Preconditioning

Jiang

et al. 2014

Stem Cells

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“…Administration of erythropoietin or statins increases mobilization of EPCs and promotes vascular remodeling, as well as improving neurological outcome after brain ischemia and hemorrhagic brain injury (Lapergue et al, 2007;Wang et al, 2004;Yu and Feng, 2008). Hormonal status also modulates circulating EPCs (Bulut et al, 2007).…”

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confidence: 99%

Progesterone Increases Circulating Endothelial Progenitor Cells and Induces Neural Regeneration after Traumatic Brain Injury in Aged Rats

Wang

Kan

et al. 2012

Journal of Neurotrauma

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Vascular remodeling plays a key role in neural regeneration in the injured brain. Circulating endothelial progenitor cells (EPCs) are a mediator of the vascular remodeling process. Previous studies have found that progesterone treatment of traumatic brain injury (TBI) decreases cerebral edema and cellular apoptosis and inhibits inflammation, which in concert promote neuroprotective effects in young adult rats. However, whether progesterone treatment regulates circulating EPC level and fosters vascular remodeling after TBI have not been investigated. In this study, we hypothesize that progesterone treatment following TBI increases circulating EPC levels and promotes vascular remodeling in the injured brain in aged rats. Male Wistar 20-month-old rats were subjected to a moderate unilateral parietal cortical contusion injury and were treated with or without progesterone (n = 54/group). Progesterone was administered intraperitoneally at a dose of 16mg/kg at 1 h post-TBI and was subsequently injected subcutaneously daily for 14 days. Neurological functional tests and immnunostaining were performed. Circulating EPCs were measured by flow cytometry. Progesterone treatment significantly improved neurological outcome after TBI measured by the modified neurological severity score, Morris Water Maze and the long term potentiation in the hippocampus as well as increased the circulating EPC levels compared to TBI controls ( p < 0.05). Progesterone treatment also significantly increased CD34 and CD31 positive cell number and vessel density in the injured brain compared to TBI controls ( p < 0.05). These data indicate that progesterone treatment of TBI improves multiple neurological functional outcomes, increases the circulating EPC level, and facilitates vascular remodeling in the injured brain after TBI in aged rats.

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Endothelial Progenitor Cell Dysfunction in the Pathogenesis of Vascular Complications of Diabetes

Alexandru

Titorencu

Frunza

et al. 2017

Mechanisms of Vascular Defects in Diabetes Mellitus

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The potential of statin and stromal cell-derived factor-1 to promote angiogenesis

Cited by 6 publications

References 43 publications

Leptin Signaling Is Required for Augmented Therapeutic Properties of Mesenchymal Stem Cells Conferred by Hypoxia Preconditioning

Leptin Signaling Is Required for Augmented Therapeutic Properties of Mesenchymal Stem Cells Conferred by Hypoxia Preconditioning

Progesterone Increases Circulating Endothelial Progenitor Cells and Induces Neural Regeneration after Traumatic Brain Injury in Aged Rats

Endothelial Progenitor Cell Dysfunction in the Pathogenesis of Vascular Complications of Diabetes

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