To investigate the mechanism of liver regeneration induced by fusing the omentum to a small traumatic injury created in the liver. We studied three groups of rats. In one group the rats were omentectomized; in another group the omentum was left in situ and was not activated, and in the third group the omentum was activated by polydextran particles.
We pre-activated the omentum by injecting polydextran particles and then made a small wedge wound in the rat liver to allow the omentum to fuse to the wound. We monitored the regeneration of the liver by determining the ratio of liver weight/body weight, by histological evaluation (including immune staining for cytokeratin-19, an oval cell marker), and by testing for developmental gene activation using reverse transcription polymerase chain reaction (RT-PCR).
There was no liver regeneration in the omentectomized rats, nor was there significant regeneration when the omentum was not activated, even though in this instance the omentum had fused with the liver. In contrast, the liver in the rats with the activated omentum expanded to a size 50% greater than the original, and there was histologically an interlying tissue between the wounded liver and the activated omentum in which bile ducts, containing cytokeratin-19 positive oval cells, extended from the wound edge. In this interlying tissue, oval cells were abundant and appeared to proliferate to form new liver tissue. In rats pre-treated with drugs that inhibited hepatocyte growth, liver proliferation was ongoing, indicating that regeneration of the liver was the result of oval cell expansion.
Activated omentum facilitates liver regeneration following injury by a mechanism that depends largely on oval cell proliferation.
"Once activated, the flimsy sheet like organ enlarges in size and mass wherein the new cells are predominantly non-fat stromal cells , . These stromal cells are a rich source of growth factors like fibroblast growth factor (FGB) and vascular endothelial growth factor (VEGF) and express adult stem cell markers including SDF-1α, CXCR4, WT-1, as well as pluripotent embryonic stem cell markers, Nanog, Oct-4, and SSEA-1 , , . Further, they were engrafted in injured tissues showing that they function as stem cells in vivo
, . "
[Show abstract][Hide abstract] ABSTRACT: The omentum is a sheet-like tissue attached to the greater curvature of the stomach and contains secondary lymphoid organs called milky spots. The omentum has been used for its healing potential for over 100 years by transposing the omental pedicle to injured organs (omental transposition), but the mechanism by which omentum helps the healing process of damaged tissues is not well understood. Omental transposition promotes expansion of pancreatic islets, hepatocytes, embryonic kidney, and neurons. Omental cells (OCs) can be activated by foreign bodies in vivo. Once activated, they become a rich source for growth factors and express pluripotent stem cell markers. Moreover, OCs become engrafted in injured tissues suggesting that they might function as stem cells.
Omentum consists of a variety of phenotypically and functionally distinctive cells. To understand the mechanism of tissue repair support by the omentum in more detail, we analyzed the cell subsets derived from the omentum on immune and inflammatory responses. Our data demonstrate that the omentum contains at least two groups of cells that support tissue repair, immunomodulatory myeloid derived suppressor cells and omnipotent stem cells that are indistinguishable from mesenchymal stem cells. Based on these data, we propose that the omentum is a designated organ for tissue repair and healing in response to foreign invasion and tissue damage.
PLoS ONE 06/2012; 7(6):e38368. DOI:10.1371/journal.pone.0038368 · 3.23 Impact Factor
"Adipocytes derived from mesodermal stem cells were the first to differentiate from i.p. bone chips. This may reflect the recent observation that vascular omentum is a suitable stem cell niche8 and that the inflammatory milieu can facilitate liver regeneration.9 Adipocytes are known potent sources of nutrition and vascular endothelial growth factor and share a common progenitor with endothelial cells.10 "
[Show abstract][Hide abstract] ABSTRACT: Somatic tissue engraftment was studied in BXSB mice treated with mesenchymal stem cell transplantation. Hosts were conditioned with nonlethal radiation prior to introducing donor cells from major histocompatibility complex-matched green fluorescent protein transgenic mice. Transplant protocols differed for route of injection, ie, intravenous (i.v.) versus intraperitoneal (i.p.), and source of mesenchymal stem cells, ie, unfractionated bone marrow cells, ex vivo expanded mesenchymal stem cells, or bone chips. Tissue chimerism was determined after short (10-12 weeks) or long (62 weeks) posttransplant follow-up by immunohistochemistry for green fluorescent protein. Engraftment of endothelial cells was seen in several organs including liver sinusoidal cells in i.v. treated mice with ex vivo expanded mesenchymal stem cells or with unfractionated bone marrow cells. Periportal engraftment of liver hepatocytes, but not engraftment of endothelial cells, was found in mice injected i.p. with bone chips. Engraftment of adipocytes was a common denominator in both i.v. and i.p. routes and occurred during early phases post-transplant. Disease control was more robust in mice that received both i.v. bone marrow and i.p. bone chips compared to mice that received i.v. bone marrow alone. Thus, the data support potential use of mesenchymal stem cell transplant for treatment of severe lupus. Future studies are needed to optimize transplant conditions and tailor protocols that may in part be guided by fat and endothelial biomarkers. Furthermore, the role of liver chimerism in disease control and the nature of cellular communication among donor hematopoietic and mesenchymal stem cells in a chimeric host merit further investigation.
Stem Cells and Cloning: Advances and Applications 12/2011; 4(1):73-8. DOI:10.2147/SCCAA.S23014
[Show abstract][Hide abstract] ABSTRACT: The mobile world's rapid growth has spurred development of new protocols and new algorithms to meet changing operating requirements, such as mobile networking and quality-of-service support. Handoff is one of the most critical procedures in cellular systems. Network operators give emphasis to optimizing handover, since it is strongly related to dropped calls, network overload and, consequently, users' criticism. Handoff can be seen as a blind procedure, if it is only based on the comparison of measurements, without information of location. Since signal propagation and path-loss are complex in nature, we can expect unnecessary and wrong handoff executions. Both UMTS and second generation (GSM) systems require redefined handoff algorithms for active connections as smooth mobility support and continuous connection are essential issues for obtaining high performance and increasing user satisfaction. We present a set of intelligent algorithms using mobile terminal (MT) location information and area awareness to assist safe handoff decisions. The implemented algorithms are validated by means of cellular network simulators that clearly show the impact of these techniques to major system performance metrics.
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