Differentiation of human mesenchymal stem cells into mesangial cells in post-glomerular injury murine model

Wong, Chee-Yin; Cheong, Soon-Keng; Mok, Pooi Ling; Leong, Chooi Fun

doi:10.1080/00313020701716367

Cited by 77 publications

(54 citation statements)

References 19 publications

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“…Indirect support for the putative contribution of donor MSC to the management of individuals with DN includes: (i) recipient MSCs play a key role in normal turnover and remodeling of renal structures including renal vessels, interstitial myofibroblast cells, glomerular mesang ium, podocytes and tubular epithelium (Cornacchia et al, 2001;Grimm et al, 2001;Poulsom et al 2001;Gupta et al, 2002); (ii) in mice models of Alport syndrome and glomerulonephropathy, MSC administr ation results in clinical improvements (Sugimoto et al, 2006;Wong et al, 2008); (iii) in rodent models of acute tubular epithelial injury and experimental glomerulonephritis, donor MSCs contribute to the functional and structural recovery of b oth glomerular and tubular compartments (Morigi et al, 2004;Krause and Cantley, 2005;Qian et al, 2008); (iv) in rat remnant kidney models, MSC transplantation attenuates renal fi brosis and pro duces a reduced glomerulosclerosis index (Semedo et al, 2009a). This was correlated with a reduction in the expression of pro-fi brotic molecules such as collagen type I, collagen type III, fi bronectin, vimentin, ASMA, FSP-1 and TGF-beta.…”

Section: Indirect Supportmentioning

confidence: 99%

MSC transplantation: a promising therapeutic strategy to manage the onset and progression of diabetic nephropathy

Ezquer

Arango-Rodríguez

et al. 2012

Biol. Res.

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Currently, one of the main threats to public health is diabetes mellitus. Its most detrimental complication is diabetic nephropathy (DN), a clinical syndrome associated with kidney damage and an increased risk of cardiovascular disease. Irrespective of the type of diabetes, DN follows a well-known temporal course. The earliest detectable signs are microalbuminuria and histopathological changes including extracellular matrix deposition, glomerular basement membrane thickening, glomerular and mesangial expansion. Later on macroalbuminuria appears, followed by a progressive decline in glomerular fi ltration rate and the loss of glomerular podocytes, tubulointerstitial fi brosis, glomerulosclerosis and arteriolar hyalinosis. Tight glycemic and hypertension controls remain the key factors for preventing or arresting the progression of DN. Nevertheless, despite considerable educational eff ort to control the disease, a signifi cant number of patients not only develop DN, but also progress to chronic kidney disease. Therefore, the availability of a strategy aimed to prevent, delay or revert DN would be highly desirable. In this article, we review the pathophysiological features of DN and the therapeutic mechanisms of multipotent mesenchymal stromal cells, also referred to as mesenchymal stem cells (MSCs). The perfect match between them, together with encouraging pre-clinical data available, allow us to support the notion that MSC transplantation is a promising therapeutic strategy to manage DN onset and progression, not only because of the safety of this procedure, but mainly because of the renoprotective potential of MSCs.

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Section: Indirect Supportmentioning

confidence: 99%

MSC transplantation: a promising therapeutic strategy to manage the onset and progression of diabetic nephropathy

Ezquer

Arango-Rodríguez

et al. 2012

Biol. Res.

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“…Some studies have shown improvement after MSC delivery in a model of glomerulonephropathy [54] and no evidence of a long-term fibrotic response 3 months after delivery of MSCs to animals with severe AKI [44]. Other studies have suggested that the beneficial effects linked to MSC injection can be marred by a long-term partial maldifferentiation of intraglomerular MSCs into adipocytes accompanied by glomerular sclerosis in a model of chronic glomerulonephritis [55].…”

Section: Mesenchymal Stromal Cells (Mscs)mentioning

confidence: 99%

Stem cell options for kidney disease

Hopkins

Rae

et al. 2008

The Journal of Pathology

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Chronic kidney disease (CKD) is increasing at the rate of 6-8% per annum in the US alone. At present, dialysis and transplantation remain the only treatment options. However, there is hope that stem cells and regenerative medicine may provide additional regenerative options for kidney disease. Such new treatments might involve induction of repair using endogenous or exogenous stem cells or the reprogramming of the organ to reinitiate development. This review addresses the current state of understanding with respect to the ability of non-renal stem cell sources to influence renal repair, the existence of endogenous renal stem cells and the biology of normal renal repair in response to damage. Understanding repair options via an understanding of renal developmentThe prevalence and incidence of chronic kidney disease (CKD) is increasing at 6-8% per annum in the USA alone, largely as a result of increased prevalence of diabetes and obesity [1]. To understand what might be possible with respect to cellular therapies or regenerative medicine for the kidney, one first needs to consider what is understood about normal renal development and response to injury. The kidney has been classically regarded as an organ with minimal cellular turnover and no capacity for regeneration. The subsequent identification of stem cells in a number of such organs, including the brain, has challenged this view. However, the dogma remains that the kidney reaches a maximal complement of nephrons and then loses these over time [2]. This dogma is drawn from our understanding of the development of this organ. The progenitor population during developmentThe kidney is mesodermal in origin and develops from two populations derived from intermediate mesoderm, the ureteric bud (UB) and the metanephric mesenchyme (MM). While an even broader potential had been proposed [3], genetic and lineage analyses have confirmed that the MM gives rise to all portions of the nephron other than the collecting ducts and also gives rise to elements of the renal interstitium [4][5][6]. The UB gives rise to the ureter and collecting ducts only. The MM is apparently not homogeneous but forms condensed mesenchyme around the tips of the branching UB. This cap mesenchyme (CM) contains self-renewing progenitors capable of generating all cells of the nephron other than the collecting ducts via an initial mesenchyme-epithelial transition (MET) event throughout the prenatal developmental period [6]. The continued expression of the transcription factor Six2 in CM is required for maintenance of this stem cell population during kidney development [5]. As the UB branches and extends through the MM, individual MET events occur at the underside of each tip to form a new nephron [2]. This nephron endowment therefore proceeds from the centre of the kidney out to the periphery, with the CM stem cell field remaining on the outer edge of the expanding organ. Endowment of new nephrons is restricted to prenatal development in humans, while in rodents it persists only until the imm...

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“…Once cleaning has taken place, the mesenchymal stem cells which are typically primitive and poorly differentiated with minimal amounts of cytoplasm with few organelles, differentiate into mature mesangial cells acquiring more cytoplasm in the form of cell process, and contractile elements such as myofilaments and attachment plaques [39,45,46]. This sequence of events was clearly depicted using the 6D liver cell imaging system ( Figure 20) and confirmed in the ex-vivo platform.…”

Section: Exogenous Mesenchymal Stem Cells In the Repair Of The Damagementioning

confidence: 69%

“…Injection of exogenous mesenchymal stem cells will provide not only cells that can be engaged in the process of repair but also important paracrine effects that will make the repair process much more efficient [38,[44][45][46].…”

Section: Exogenous Mesenchymal Stem Cells In the Repair Of The Damagementioning

confidence: 99%

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Differentiation of human mesenchymal stem cells into mesangial cells in post-glomerular injury murine model

Cited by 77 publications

References 19 publications

MSC transplantation: a promising therapeutic strategy to manage the onset and progression of diabetic nephropathy

MSC transplantation: a promising therapeutic strategy to manage the onset and progression of diabetic nephropathy

Stem cell options for kidney disease

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