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      Contribution of Vascular and Neural Segments to Baroreflex Sensitivity in Response to Postural Stress

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          Background/Aims: The baroreflex pathway has a vascular and a neural segment, both being modulated by variations in peripheral blood pressure (BP). Besides overall baroreceptor sensitivity (BRS), defined as the spectral relationship between changes in peripheral BP and R-R interval within the frequency band of 0.05–0.15 Hz, vascular and neural segment contributions to the overall BRS can be distinguished. We test the hypothesis that changes in overall BRS following a postural maneuver mainly originate from the vascular (peripheral pressure to carotid artery diameter) rather than the neural segment (carotid artery diameter to R-R interval). Methods: Peripheral pressure (Finapress), carotid artery diameter (ultrasound in B-/M-mode) and electrocardiogram values of 20 young subjects in supine and upright-seated postures were recorded simultaneously. Transfer gains were computed for the segmental and overall responses. Results:Postural change significantly increases peripheral BP and carotid artery diameter. The vascular segment has a uniform spectral distribution. Statistical analyses revealed that postural change decreased overall (p < 0.004) and vascular (p < 0.0001) transfer gains, but did not modify neural gain. Conclusions:Unlike the neural segment, the vascular segment is frequency non-specific. The decrease in overall BRS due to a postural change is mainly explained by the reduced transfer gain of the vascular segment.

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          Microvesicles Derived from Mesenchymal Stem Cells Enhance Survival in a Lethal Model of Acute Kidney Injury

          Several studies demonstrated that treatment with mesenchymal stem cells (MSCs) reduces cisplatin mortality in mice. Microvesicles (MVs) released from MSCs were previously shown to favor renal repair in non lethal toxic and ischemic acute renal injury (AKI). In the present study we investigated the effects of MSC-derived MVs in SCID mice survival in lethal cisplatin-induced AKI. Moreover, we evaluated in vitro the effect of MVs on cisplatin-induced apoptosis of human renal tubular epithelial cells and the molecular mechanisms involved. Two different regimens of MV injection were used. The single administration of MVs ameliorated renal function and morphology, and improved survival but did not prevent chronic tubular injury and persistent increase in BUN and creatinine. Multiple injections of MVs further decreased mortality and at day 21 surviving mice showed normal histology and renal function. The mechanism of protection was mainly ascribed to an anti-apoptotic effect of MVs. In vitro studies demonstrated that MVs up-regulated in cisplatin-treated human tubular epithelial cells anti-apoptotic genes, such as Bcl-xL, Bcl2 and BIRC8 and down-regulated genes that have a central role in the execution-phase of cell apoptosis such as Casp1, Casp8 and LTA. In conclusion, MVs released from MSCs were found to exert a pro-survival effect on renal cells in vitro and in vivo, suggesting that MVs may contribute to renal protection conferred by MSCs.
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            Stromal cells protect against acute tubular injury via an endocrine effect.

            Emerging evidence suggests that the intravenous injection of bone marrow-derived stromal cells (BMSC) improves renal function after acute tubular injury, but the mechanism of this effect is controversial. In this article, we confirm that intravenous infusion of male BMSC reduced the severity of cisplatin-induced acute renal failure in adult female mice. This effect was also seen when BMSC (or adipocyte-derived stromal cells (AdSC)), were given by intraperitoneal injection. Infusion of BMSC enhanced tubular cell proliferation after injury and decreased tubular cell apoptosis. Using the Y chromosome as a marker of donor stromal cells, examination of multiple kidney sections at one or four days after cell infusion failed to reveal any examples of stromal cells within the tubules, and only rare examples of stromal cells within the renal interstitium. Furthermore, conditioned media from cultured stromal cells induced migration and proliferation of kidney-derived epithelial cells and significantly diminished cisplatin-induced proximal tubule cell death in vitro. Intraperitoneal administration of this conditioned medium to mice injected with cisplatin diminished tubular cell apoptosis, increased survival, and limited renal injury. Thus, marrow stromal cells protect the kidney from toxic injury by secreting factors that limit apoptosis and enhance proliferation of the endogenous tubular cells, suggesting that transplantation of the cells themselves is not necessary. Identification of the stromal cell-derived protective factors may provide new therapeutic options to explore in humans with acute kidney injury.
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              Transfer of growth factor receptor mRNA via exosomes unravels the regenerative effect of mesenchymal stem cells.

              Bone marrow-mesenchymal stem cells (BM-MSC) ameliorate renal dysfunction and repair tubular damage of acute kidney injury by locally releasing growth factors, including the insulin-like growth factor-1 (IGF-1). The restricted homing of BM-MSC at the site of injury led us to investigate a possible gene-based communication mechanism between BM-MSC and tubular cells. Human BM-MSC (hBM-MSC) released microparticles and exosomes (Exo) enriched in mRNAs. A selected pattern of transcripts was detected in Exo versus parental cells. Exo expressed the IGF-1 receptor (IGF-1R), but not IGF-1 mRNA, while hBM-MSC contained both mRNAs. R- cells lacking IGF-1R exposed to hBM-MSC-derived Exo acquired the human IGF-1R transcript that was translated in the corresponding protein. Transfer of IGF-1R mRNA from Exo to cisplatin-damaged proximal tubular cells (proximal tubular epithelial cell [PTEC]) increased PTEC proliferation. Coincubation of damaged PTEC with Exo and soluble IGF-1 further enhanced cell proliferation. These findings suggest that horizontal transfer of the mRNA for IGF-1R to tubular cells through Exo potentiates tubular cell sensitivity to locally produced IGF-1 providing a new mechanism underlying the powerful renoprotection of few BM-MSC observed in vivo.

                Author and article information

                J Vasc Res
                Journal of Vascular Research
                S. Karger AG
                August 2009
                10 February 2009
                : 46
                : 5
                : 469-477
                Departments of Biophysics and Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands
                200962 J Vasc Res 2009;46:469–477
                © 2009 S. Karger AG, Basel

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                Page count
                Figures: 4, Tables: 2, References: 49, Pages: 9
                Research Paper


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