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      Histological study on the protective effect of endogenous stem-cell mobilization in Adriamycin-induced chronic nephropathy in rats

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          Abstract

          Chronic kidney disease is a global health problem with increasing morbidity and mortality. Therefore, this study was planned to test the protective effect of hematopoietic-stem-cell mobilization by granulocyte colony-stimulating factor (G-CSF) on Adriamycin (ADR)-induced chronic renal disease in rats. Thirty albino rats were equally divided into three groups: control, ADR group [rats received a single intravenous injection of ADR (5 mg/kg)], and G-CSF group [rats received ADR by the same route and the same dose as the previous group, and then G-CSF (70 μg/kg/d) 2 hours after ADR injection then daily for five consecutive days]. At the time of sacrifice (after 6 weeks), blood samples were taken to estimate the blood urea nitrogen and serum creatinine. Kidney sections were stained with hematoxylin and eosin, toluidine blue, Masson's trichrome, periodic acid–Schiff stains, and immunohistochemical staining against CD34 and caspase-3. The G-CSF group exhibited protection against renal injury manifested by reducing blood urea nitrogen and serum-creatinine levels, improving histological architecture, and increasing the proliferative capacity of renal tubules.

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          Most cited references36

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          Renal interstitial fibrosis: mechanisms and evaluation.

          Tubulointerstitial injury in the kidney is complex, involving a number of independent and overlapping cellular and molecular pathways, with renal interstitial fibrosis and tubular atrophy (IFTA) as the final common pathway. Furthermore, there are multiple ways to assess IFTA. Cells involved include tubular epithelial cells, fibroblasts, fibrocytes, myofibroblasts, monocyte/macrophages, and mast cells with complex and still incompletely characterized cell-molecular interactions. Molecular mediators involved are numerous and involve pathways such as transforming growth factor (TGF)-β, bone morphogenic protein (BMP), platelet-derived growth factor (PDGF), and hepatocyte growth factor (HGF). Recent genomic approaches have shed insight into some of these cellular and molecular pathways. Pathologic evaluation of IFTA is central in assessing the severity of chronic disease; however, there are a variety of methods used to assess IFTA. Most assessment of IFTA relies on pathologist assessment of special stains such as trichrome, Sirius Red, and collagen III immunohistochemistry. Visual pathologist assessment can be prone to intra and interobserver variability, but some methods employ computerized morphometery, without a clear consensus as to the best method. IFTA results from on orchestration of cell types and molecular pathways. Opinions vary on the optimal qualitative and quantitative assessment of IFTA.
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            Administered mesenchymal stem cells enhance recovery from ischemia/reperfusion-induced acute renal failure in rats.

            Adult stem cells are promising for the development of novel therapies in regenerative medicine. Acute renal failure (ARF) remains a frequent clinical complication, associated with an unacceptably high mortality rate, in large part due to the ineffectiveness of currently available therapies. The aim of this study was, therefore, to evaluate the therapeutic effectiveness of bone marrow-derived mesenchymal stem cells in a rat model of ischemia/reperfusion (I/R) ARF. We used a common I/R model in rats to induce ARF by clamping both renal pedicles for 40 minutes. Mesenchymal stem cells were iron-dextran-labeled for in vivo tracking studies by magnetic resonance imaging (MRI) and kidneys were imaged for mesenchymal stem cells immediately after infusion and at day 3 after ARF. Renal injury was scored on day 3 and cells were additionally tracked by Prussian blue staining. We show in I/R-induced ARF in rats, modeling the most common form of clinical ARF, that infusion of mesenchymal stem cells enhances recovery of renal function. Mesenchymal stem cells were found to be located in the kidney cortex after injection, as demonstrated by MRI. Mesenchymal stem cells-treated animals had both significantly better renal function on days 2 and 3 and better injury scores at day 3 after ARF. Histologically, mesenchymal stem cells were predominantly located in glomerular capillaries, while tubules showed no iron labeling, indicating absent tubular transdifferentiation. We conclude that the highly renoprotective capacity of mesenchymal stem cells opens the possibility for a cell-based paradigm shift in the treatment of I/R ARF.
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              G-CSF prevents cardiac remodeling after myocardial infarction by activating the Jak-Stat pathway in cardiomyocytes.

              Granulocyte colony-stimulating factor (G-CSF) was reported to induce myocardial regeneration by promoting mobilization of bone marrow stem cells to the injured heart after myocardial infarction, but the precise mechanisms of the beneficial effects of G-CSF are not fully understood. Here we show that G-CSF acts directly on cardiomyocytes and promotes their survival after myocardial infarction. G-CSF receptor was expressed on cardiomyocytes and G-CSF activated the Jak/Stat pathway in cardiomyocytes. The G-CSF treatment did not affect initial infarct size at 3 d but improved cardiac function as early as 1 week after myocardial infarction. Moreover, the beneficial effects of G-CSF on cardiac function were reduced by delayed start of the treatment. G-CSF induced antiapoptotic proteins and inhibited apoptotic death of cardiomyocytes in the infarcted hearts. G-CSF also reduced apoptosis of endothelial cells and increased vascularization in the infarcted hearts, further protecting against ischemic injury. All these effects of G-CSF on infarcted hearts were abolished by overexpression of a dominant-negative mutant Stat3 protein in cardiomyocytes. These results suggest that G-CSF promotes survival of cardiac myocytes and prevents left ventricular remodeling after myocardial infarction through the functional communication between cardiomyocytes and noncardiomyocytes.
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                Author and article information

                Journal
                J Microsc Ultrastruct
                J Microsc Ultrastruct
                JMAU
                Journal of Microscopy and Ultrastructure
                Medknow Publications & Media Pvt Ltd (India )
                2213-879X
                2213-8803
                Jul-Sep 2016
                31 December 2015
                : 4
                : 3
                : 133-142
                Affiliations
                [1] Histology Department, Faculty of Medicine, Cairo University, Cairo, Egypt
                Author notes
                [* ] Corresponding author. Histology Department, Kasr Alainy Faculty of Medicine, Cairo University, 4, Alfalaky street, Kasr Alainy, Cairo, Egypt. E-mail address: drdaliaibrahim@ 123456hotmail.com (D.I. Ismail).
                Article
                JMAU-4-133
                10.1016/j.jmau.2015.12.003
                6014195
                30023219
                5d811abe-3c44-4add-a17c-8753da2d40ed
                Copyright: © 2015 Saudi Society of Microscopes

                This is an open access article under the CC BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 27 September 2015
                : 28 November 2015
                : 25 December 2015
                Categories
                Original Article

                adriamycin,caspase-3,cd34,chronic kidney disease,granulocyte colony-stimulating factor

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