Effects of autologous SCF- and G-CSF-mobilized bone marrow stem cells on hypoxia-inducible factor-1 in rats with ischemia-reperfusion renal injury

Bi, Lingyun; Zhao, Dean; Da-sheng, Yang; Guo, J.G.; Liang, Bin; Zhang, R.X.; Zhao, Jingjie; Bai, Hao; Li, S.J.

doi:10.4238/2015.april.27.25

Cited by 13 publications

(9 citation statements)

References 13 publications

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“…Analysis of the expression of other HIF target genes could help explain how the effects of HUCB‐MNCs on detrusor smooth muscle are mediated through the HIF pathway. Thus, we suggest that upregulation of HIF‐1α in the diabetic bladder contributes to an increase in VEGF protein, as similarly shown in a previous study …”

Section: Discussionsupporting

confidence: 89%

“…Thus, we suggest that upregulation of HIF-1α in the diabetic bladder contributes to an increase in VEGF protein, as similarly shown in a previous study. 70 In the present study, intracavernous injection of HUCB-MNCs enhanced the smooth muscle content and levels of α-SMA (a specific marker of SMCs) in the bladder of diabetic rats. Similarly, Dong et al 47 previously reported that treatment with 2 × 10 6 urine-derived stem cells effectively improved impaired detrusor contractility by ameliorating bladder fibrosis and decreasing α-SMA protein levels and SMC apoptosis in the diabetic bladder.…”

Section: Hucb-mncs May Exert Beneficial Effects On Contractions Inducsupporting

confidence: 52%

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Administration of human umbilical cord blood mononuclear cells restores bladder dysfunction in streptozotocin‐induced diabetic rats

Kaya‐Sezginer

Yilmaz‐Oral

Gür

2019

LUTS

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Objective This study evaluated the effect of human umbilical cord blood mononuclear cells (HUCB‐MNCs) on bladder dysfunction in streptozotocin (STZ; 35 mg/kg, i.v.)‐induced diabetic rats. Methods Adult male Sprague–Dawley rats (n = 30) were equally divided into three groups: control group, STZ‐diabetic group, and HUCB‐MNC‐treated group (1 × 106 cells). HUCB‐MNCs were isolated by density gradient centrifugation from eight healthy donors and injected into the corpus cavenosum in STZ‐diabetic rats 4 weeks after the induction of diabetes. Studies were performed 4 weeks after HUCB‐MNC or vehicle injection. In vitro organ bath studies were performed on bladder strips, whereas protein expression of hypoxia‐inducible factor (HIF)‐1α, vascular endothelial growth factor (VEGF), and α‐smooth muscle actin (SMA) in the bladder and the ratio of smooth muscle cells (SMCs) to collagen were determined using western blotting and Masson trichrome staining. Results Neurogenic contractions of detrusor smooth muscle strips were 55% smaller in the diabetic group than control group (P < 0.05); these contractions were normalized by HUCB‐MNC treatment. In addition, HUCB‐MNC treatment restored the impaired maximal carbachol‐induced contractile response in detrusor strips in the diabetic group (29%; P < 0.05). HUCB‐MNC treatment improved the KCl‐induced contractile response in the diabetic bladder (68%; P < 0.05), but had no effect on ATP‐induced contractile responses. Increased expression of HIF‐1α and VEGF protein and decreased expression of α‐SMA protein and the SMC/collagen ratio in diabetic rats were reversed by HUCB‐MNC. Conclusion Administration of HUCB‐MNCs facilitates bladder function recovery, which is likely related to downregulation of HIF‐1α expression and attenuation of fibrosis in STZ‐diabetic rats.

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Section: Discussionsupporting

confidence: 89%

Section: Hucb-mncs May Exert Beneficial Effects On Contractions Inducsupporting

confidence: 52%

Administration of human umbilical cord blood mononuclear cells restores bladder dysfunction in streptozotocin‐induced diabetic rats

Kaya‐Sezginer

Yilmaz‐Oral

Gür

2019

LUTS

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“…Jamadarkhana et al found that administrating PHD inhibitor TRC160334 at 2 h, 6 h, and 10 h post the onset of kidney ischemia activated the expression of HIF-1 and attenuated kidney injury by inducing heat shock protein 70 (HSP70) [102]. Also, administrating granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF) 6 h after IRI also activated the expression of HIF-1 and reduced the degree of kidney tissue injury by upregulating the expression of VEGF and EPO [103]. But, other studies demonstrated that administrating PHD inhibitors after renal ischemia had no effects in attenuating AKI and renal fibrosis [99,100].…”

Section: Hif In Aki and Mechanisms Of Hif Signaling In Akimentioning

confidence: 99%

Hypoxia and Hypoxia-Inducible Factors in Kidney Injury and Repair

Shu

Wang

Zheng

et al. 2019

Cells

204

200

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Acute kidney injury (AKI) is a major kidney disease characterized by an abrupt loss of renal function. Accumulating evidence indicates that incomplete or maladaptive repair after AKI can result in kidney fibrosis and the development and progression of chronic kidney disease (CKD). Hypoxia, a condition of insufficient supply of oxygen to cells and tissues, occurs in both acute and chronic kidney diseases under a variety of clinical and experimental conditions. Hypoxia-inducible factors (HIFs) are the “master” transcription factors responsible for gene expression in hypoxia. Recent researches demonstrate that HIFs play an important role in kidney injury and repair by regulating HIF target genes, including microRNAs. However, there are controversies regarding the pathological roles of HIFs in kidney injury and repair. In this review, we describe the regulation, expression, and functions of HIFs, and their target genes and related functions. We also discuss the involvement of HIFs in AKI and kidney repair, presenting HIFs as effective therapeutic targets.

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“…Because G-CSF can mobilize progenitors from bone marrow, which home to sites of injury to mount anti-inflammatory and repair responses 32 , we wanted to test whether H/R mobilizes progenitors that home to lung tissue. Therefore, we investigated pulmonary and circulating CD133 + progenitors, which are pluripotential cells that can be mobilized by G-CSF 33 .…”

Section: Resultsmentioning

confidence: 99%

Hydrogen protects lung from hypoxia/re-oxygenation injury by reducing hydroxyl radical production and inhibiting inflammatory responses

Chen

Zhang

Chen

et al. 2018

Sci Rep

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Here we investigated whether hydrogen can protect the lung from chronic injury induced by hypoxia/re-oxygenation (H/R). We developed a mouse model in which H/R exposure triggered clinically typical lung injury, involving increased alveolar wall thickening, infiltration by neutrophils, consolidation, alveolar hemorrhage, increased levels of inflammatory factors and recruitment of M1 macrophages. All these processes were attenuated in the presence of H2. We found that H/R-induced injury in our mouse model was associated with production of hydroxyl radicals as well as increased levels of colony-stimulating factors and circulating leukocytes. H2 attenuated H/R-induced production of hydroxyl radicals, up-regulation of colony-stimulating factors, and recruitment of neutrophils and M1 macrophages to lung tissues. However, H2 did not substantially affect the H/R-induced increase in erythropoietin or pulmonary artery remodeling. Our results suggest that H2 ameliorates H/R-induced lung injury by inhibiting hydroxyl radical production and inflammation in lungs. It may also prevent colony-stimulating factors from mobilizing progenitors in response to H/R-induced injury.

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Effects of autologous SCF- and G-CSF-mobilized bone marrow stem cells on hypoxia-inducible factor-1 in rats with ischemia-reperfusion renal injury

Cited by 13 publications

References 13 publications

Administration of human umbilical cord blood mononuclear cells restores bladder dysfunction in streptozotocin‐induced diabetic rats

Administration of human umbilical cord blood mononuclear cells restores bladder dysfunction in streptozotocin‐induced diabetic rats

Hypoxia and Hypoxia-Inducible Factors in Kidney Injury and Repair

Hydrogen protects lung from hypoxia/re-oxygenation injury by reducing hydroxyl radical production and inhibiting inflammatory responses

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