The effect of mesenchymal stromal cells on doxorubicin-induced nephropathy in rats

Ma, Hualin; Wu, Yaojiong; Zhang, Wanfan; Dai, Yong; Li, Furong; Xü, Ying; Wang, Yunshuai; Tu, Huiying; Li, Wuxian; Zhang, Xinzhou

doi:10.1016/j.jcyt.2013.02.002

Cited by 18 publications

(17 citation statements)

References 20 publications

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“…As above have mentioned, human mesenchymal stem cells produced IL-10 interacting with monocytes, and this cell-cell contact also lead monocytes to produce high levels of IL-10 [6]. WJ-MSC transplantation could cause increased expression of systemic IL-10 [7][8][9][10]. The present study showed that WJ-MSCs were able to immediately up-regulate the levels of IL-10 both in serum and brain, as fast as 24 h after their administration.…”

Section: Discussionsupporting

confidence: 66%

“…IL-10 is an important anti-inflammatory factor in many diseases including AD. Recently, there is increasing evidence to suggest that the immunomodulatory effects of MSCs on systemic IL-10 level are also a critical mechanism in the amelioration of inflammation-related disease, such as acute lung injury, neuropathic pain, acute respiratory distress syndrome, and renal injury [7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

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Wharton’s Jelly-derived mesenchymal stem cells alleviate memory deficits and reduce amyloid-β deposition in an APP/PS1 transgenic mouse model

et al. 2015

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Alzheimer's disease (AD) is the leading cause of dementia in the elderly and is characterized by amyloid plaques, neurofibrillary tangles, and neuronal loss. Cumulative evidence supports that neuroinflammation is an important factor for the pathogenesis of AD and contributes to amyloid beta (Aβ) generation. However, there has been no effective treatment for AD. Wharton's Jelly-derived mesenchymal stem cells (WJ-MSCs) have a potential therapeutic effect in the treatment for neurological diseases. In the present study, we evaluated the therapeutic effect of WJ-MSC transplantation on the neuropathology and memory deficits in amyloid precursor protein (APP) and presenilin-1 (PS1) double-transgenic mice and discussed the mechanism. WJ-MSCs were intravenously transplanted into the APP/PS1 mice. Four weeks after treatment, WJ-MSCs significantly improved the spatial learning and alleviated the memory decline in the APP/PS1 mice. Aβ deposition and soluble Aβ levels were significantly reduced after WJ-MSC treatment. Furthermore, WJ-MSCs significantly increased the expression of the anti-inflammatory cytokine, IL-10. Meanwhile, pro-inflammatory microglial activation and the expressions of pro-inflammatory cytokines, IL-1β and TNFα, were significantly down-regulated by WJ-MSC treatment. Thus, our findings suggest that WJ-MSCs might produce beneficial effects on the prevention and treatment for AD through modulation of neuroinflammation.

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Section: Discussionsupporting

confidence: 66%

Section: Introductionmentioning

confidence: 99%

Wharton’s Jelly-derived mesenchymal stem cells alleviate memory deficits and reduce amyloid-β deposition in an APP/PS1 transgenic mouse model

et al. 2015

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“…However, BH/DXR rats had milder glomerular and tubular damage compared to CD/DXR rats (Fig 3A–3F, Table 2). Glomerular and tubular damage were distributed unevenly in rats, similarly to human focal segmental glomerulosclerosis (FSGS) [18]. In parallel with milder proteinuria and urinary excretion of NGAL in BH rats, intact glomeruli (Score: 0) were significantly more common in DXR-injected BH than in CD rats (Table 2).…”

Section: Resultsmentioning

confidence: 99%

“…Although it is generally accepted that an initial injury to podocytes induces proteinuria, the exact pathomechanism of the DXR-induced nephropathy is poorly understood [13]. The role of sustained inflammation and oxidative stress has been demonstrated in many experimental models of renal fibrosis, including the remnant kidney [11,14,15] and DXR nephropathy models [12,16,17,18,19]. The myocardial and renal side effects of DXR are mainly attributed to the generation of free oxygen radicals [20].…”

Section: Introductionmentioning

confidence: 99%

Oxidative/Nitrative Stress and Inflammation Drive Progression of Doxorubicin-Induced Renal Fibrosis in Rats as Revealed by Comparing a Normal and a Fibrosis-Resistant Rat Strain

Szalay

Erdélyi²,

Kökény

et al. 2015

PLoS ONE

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Chronic renal fibrosis is the final common pathway of end stage renal disease caused by glomerular or tubular pathologies. Genetic background has a strong influence on the progression of chronic renal fibrosis. We recently found that Rowett black hooded rats were resistant to renal fibrosis. We aimed to investigate the role of sustained inflammation and oxidative/nitrative stress in renal fibrosis progression using this new model. Our previous data suggested the involvement of podocytes, thus we investigated renal fibrosis initiated by doxorubicin-induced (5 mg/kg) podocyte damage. Doxorubicin induced progressive glomerular sclerosis followed by increasing proteinuria and reduced bodyweight gain in fibrosis-sensitive, Charles Dawley rats during an 8-week long observation period. In comparison, the fibrosis-resistant, Rowett black hooded rats had longer survival, milder proteinuria and reduced tubular damage as assessed by neutrophil gelatinase-associated lipocalin (NGAL) excretion, reduced loss of the slit diaphragm protein, nephrin, less glomerulosclerosis, tubulointerstitial fibrosis and matrix deposition assessed by periodic acid–Schiff, Picro-Sirius-red staining and fibronectin immunostaining. Less fibrosis was associated with reduced profibrotic transforming growth factor-beta, (TGF-β1) connective tissue growth factor (CTGF), and collagen type I alpha 1 (COL-1a1) mRNA levels. Milder inflammation demonstrated by histology was confirmed by less monocyte chemotactic protein 1 (MCP-1) mRNA. As a consequence of less inflammation, less oxidative and nitrative stress was obvious by less neutrophil cytosolic factor 1 (p47phox) and NADPH oxidase-2 (p91phox) mRNA. Reduced oxidative enzyme expression was accompanied by less lipid peroxidation as demonstrated by 4-hydroxynonenal (HNE) and less protein nitrosylation demonstrated by nitrotyrosine (NT) immunohistochemistry and quantified by Western blot. Our results demonstrate that mediators of fibrosis, inflammation and oxidative/nitrative stress were suppressed in doxorubicin nephropathy in fibrosis-resistant Rowett black hooded rats underlying the importance of these pathomechanisms in the progression of renal fibrosis initiated by glomerular podocyte damage.

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“…Lastly, Ma et al (16) report that human MSCs reduce albuminuria that results from doxorubicin (adriamycin)-induced nephropathy in the rat. MSC treatment resulted in reduction in serum levels of pro-inflammatory cytokines tumor necrosis factor α, interleukin (IL)-6 and prostaglandin E2 with increases in the anti-inflammatory IL-10 in the serum.…”

mentioning

confidence: 99%

Multipotent mesenchymal stromal cells protect against kidney injury

Tögel

Bonventre²

2013

Cytotherapy

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The effect of mesenchymal stromal cells on doxorubicin-induced nephropathy in rats

Cited by 18 publications

References 20 publications

Wharton’s Jelly-derived mesenchymal stem cells alleviate memory deficits and reduce amyloid-β deposition in an APP/PS1 transgenic mouse model

Wharton’s Jelly-derived mesenchymal stem cells alleviate memory deficits and reduce amyloid-β deposition in an APP/PS1 transgenic mouse model

Oxidative/Nitrative Stress and Inflammation Drive Progression of Doxorubicin-Induced Renal Fibrosis in Rats as Revealed by Comparing a Normal and a Fibrosis-Resistant Rat Strain

Multipotent mesenchymal stromal cells protect against kidney injury

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