Improved Graft Mesenchymal Stem Cell Survival in Ischemic Heart With a Hypoxia-Regulated Heme Oxygenase-1 Vector

Tang, Yao; Tang, Yi; Zhang, Y. Clare; Qian, Keping; Shen, Leping; Phillips, M. Ian

doi:10.1016/j.jacc.2005.05.079

Cited by 370 publications

(313 citation statements)

References 37 publications

Supporting

Mentioning

297

Contrasting

Unclassified

Order By: Relevance

“…The present study found that a MOI of 100, which was established on a preliminary experiment (data not shown), was able to yield highly efficient transduction and amplified expression of HO-1 protein. A previous study related to HO-1 overexpression had shown that a hypoxia-regulated HO-1 vector improved grafted MSCs survival in ischemic heart and enhanced cardiac function (Tang et al 2005). In addition, Zeng et al (2008) found that HO-1 overexpression confers anti-inflammation and anti-fibrogenic properties on infarcted myocardium, and that the paracrine factors secreted from HO-1-modified MSCs dramatically limited infarct size and apoptosis in a rat MI model.…”

Section: Discussionmentioning

confidence: 99%

Transplantation of Adipose Tissue-Derived Stem Cells Overexpressing Heme Oxygenase-1 Improves Functions and Remodeling of Infarcted Myocardium in Rabbits

Yang

Liu

et al. 2012

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

Adipose tissue-derived stem cells (ADSCs) are a promising source of autologous stem cells that are used for regeneration and repair of infracted heart. However, the efficiency of their transplantation is under debate. One of the possible reasons for marginal improvement in ADSCs transplantation is the significant cell death rate of implanted cells after being grafted into injured heart. Therefore, overcoming the poor survival rate of implanted cells may improve stem cell therapy. Due to limited improvement concerning direct stem cell therapy, gene-transfer methods are used to enhance cellular cardiomyoplasty efficacy. Heme oxygenase-1 (HO-1) can provide various types of cells with protection against oxidative injury and apoptosis. However, exact effects of autologous ADSCs combined with HO-1 on cardiac performance remains unknown. In this study, rabbits were treated with ADSCs transduced with HO-1 (HO-1-ADSCs), treated with non-transduced ADSCs, or injected with phosphate buffered saline 14 days after experimental myocardial infarction was induced, when autologous ADSCs were obtained simultaneously. Four weeks after injection, echocardiography showed significant improvements for cardiac functions and left ventricular dimensions in HO-1-ADSCs-treated animals. Structural consequences of transplantation were determined by detailed histological analysis, which showed differentiation of HO-1-ADSCs to cardiomyocyte-like tissues and lumen-like structure organizations. Apart from improvement in angiogenesis and scar areas, more connexin 43-positive gap junction and greater tyrosine hydroxylase-positive cardiac sympathetic nerves sprouting were observed in the HO-1-ADSCs-treated group compared with ADSCs group. These data suggest that the transplantation of autologous ADSCs combined with HO-1 transduction is a feasible and efficacious method for improving infarcted myocardium.

show abstract

Section: Discussionmentioning

confidence: 99%

Transplantation of Adipose Tissue-Derived Stem Cells Overexpressing Heme Oxygenase-1 Improves Functions and Remodeling of Infarcted Myocardium in Rabbits

Yang

Liu

et al. 2012

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

show abstract

“…Therefore, knowledge of molecules able to enhance the viability of the transplanted cells is crucial. Various strategies have been carried out to potentiate cell viability after transplantation: (a) pretreatment of the cells with growth factors or cytokines, including bFGF, insulin-like growth factor and bone morphogenic protein-2 in myocardial precursors [172] or adiponectin [173] and nitric oxide in mesoangioblasts [174]; (b) genetic modification to induce over-expression of pro-survival molecules, including Akt [175,176], bFGF [177], haem oxygenase-1 [178], VEGF [179] and Bcl-2 [180]. Hence, strategies that improve cell viability during transplantation, allowing cells to evade anoikis when circulating in the bloodstream until they reach the target organ, appear essential for the success of cell-based therapy.…”

Section: Cell-based Therapies and Anoikismentioning

confidence: 99%

Anoikis: an emerging hallmark in health and diseases

Taddei

Giannoni

Fiaschi

et al. 2011

The Journal of Pathology

524

404

View full text Add to dashboard Cite

Anoikis is a programmed cell death occurring upon cell detachment from the correct extracellular matrix, thus disrupting integrin ligation. It is a critical mechanism in preventing dysplastic cell growth or attachment to an inappropriate matrix. Anoikis prevents detached epithelial cells from colonizing elsewhere and is thus essential for tissue homeostasis and development. As anchorage-independent growth and epithelial-mesenchymal transition, two features associated with anoikis resistance, are crucial steps during tumour progression and metastatic spreading of cancer cells, anoikis deregulation has now evoked particular attention from the scientific community. The aim of this review is to analyse the molecular mechanisms governing both anoikis and anoikis resistance, focusing on their regulation in physiological processes, as well as in several diseases, including metastatic cancers, cardiovascular diseases and diabetes.

show abstract

“…These modified MSCs exhibited advanced protection over MSCs alone. This gene delivery approach has also been used successfully to improve survival of MSCs when injected into infarcted hearts, where transduction with haem oxygenase (HO-1) leads to more efficient healing [52].…”

Section: Mesenchymal Stromal Cells (Mscs)mentioning

confidence: 99%

Stem cell options for kidney disease

Hopkins

Rae

et al. 2008

The Journal of Pathology

View full text Add to dashboard Cite

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...

show abstract

Improved Graft Mesenchymal Stem Cell Survival in Ischemic Heart With a Hypoxia-Regulated Heme Oxygenase-1 Vector

Cited by 370 publications

References 37 publications

Transplantation of Adipose Tissue-Derived Stem Cells Overexpressing Heme Oxygenase-1 Improves Functions and Remodeling of Infarcted Myocardium in Rabbits

Transplantation of Adipose Tissue-Derived Stem Cells Overexpressing Heme Oxygenase-1 Improves Functions and Remodeling of Infarcted Myocardium in Rabbits

Anoikis: an emerging hallmark in health and diseases

Stem cell options for kidney disease

Contact Info

Product

Resources

About