Mesenchymal Stem Cells in Mesangial Repair in a Model of Immunoglobulin Light Chain-Mediated Mesangial InjuryGuillermo A Herrera1,2*, Jiamin Teng1, Xin Liu4, Yanping Zhang5 and Elba A Turbat-Herrera1-3
- *Corresponding Author:
- Guillermo A. Herrera, MD
1541 Kings Highway, Shreveport
Louisiana, 71103, USA
E-mail: [email protected]
Received date: May 19, 2014; Accepted date: July 14, 2014; Published date: July 16, 2014
Citation: Herrera GA, Teng J, Liu X, Zhang Y, Turbat-Herrera EA (2014) Mesenchymal Stem Cells in Mesangial Repair in a Model of Immunoglobulin Light Chain-Mediated Mesangial Injury. J Stem Cell Res Ther 4:215. doi:10.4172/2157-7633.1000215
Copyright: © 2014 Herrera GA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Mesangial injury produced by glomerulopathic monoclonal immunoglobulin light chains leads to two diametrically opposed results: matrix loss from mesangiolysis / replacement of mesangial matrix with amyloid (AL-amyloidosis) and increased matrix (light chain deposition disease), depending on the physicochemically abnormal light chains involved. In both situations; however, there is loss of mesangial cells resulting from apoptosis induced by the glomerulopathic light chains.
This unique experimental model of mesangial injury resulting in divergent manifestations allows examining the role of mesenchymal stem cells in mesangial glomerular repair in the two typical prototypes of alterations that occur in the mesangium when injured by a variety of injurious agents.
In vitro and ex vivo platforms are used to translate information from the in-vitro to the in-vivo arenas. Both platforms highlight the same sequence of events that take place: mesenchymal stem cells identify the site of damage, clear the damaged mesangium by eliminating debris from apoptotic cellular elements and deposited “foreign” (not belonging in the normal mesangium) material and eventually differentiate into mature mesangial cells laying down new matrix.
Each of the platforms employed exhibited certain advantages and limitations in visualizing and understanding the processes that occur. When the information generated was combined, a clear view of mechanisms involved and how mesenchymal stem cells participated in mesangial repair emerged.