Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText.
Kick-your-searchterm to multiple Engines kick-your-query now !>
A dictionary by aggregated review articles of nephrology, medicine and the life sciences
Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

suck abstract from ncbi


10.1371/journal.pone.0088036

http://scihub22266oqcxt.onion/10.1371/journal.pone.0088036
suck pdf from google scholar
24558374!3928118!24558374
unlimited free pdf from europmc24558374    free
PDF from PMC    free
html from PMC    free

Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24558374&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215

suck abstract from ncbi

pmid24558374      PLoS+One 2014 ; 9 (2): e88036
Nephropedia Template TP

gab.com Text

Twit Text FOAVip

Twit Text #

English Wikipedia


  • Mesenchymal stem cells ameliorate Th1-induced pre-eclampsia-like symptoms in mice via the suppression of TNF-alpha expression #MMPMID24558374
  • Liu L; Zhao G; Fan H; Zhao X; Li P; Wang Z; Hu Y; Hou Y
  • PLoS One 2014[]; 9 (2): e88036 PMID24558374show ga
  • Pre-eclampsia (PE) is thought to be a pregnancy-induced autoimmune disease. Despite several strategies carried out for targeting specific factors relevant to its pathogenesis, PE remains potentially fatal to some patients. Here, we reported a way to isolate mesenchymal stem cells (MSCs) from decidua. The MSCs not only exhibited differentiation and self-renewal capacities, they also possessed immunomodulatory functions and secreted some soluble mediators including IL-6, TGF-beta, IDO, VEGF and COX-2. Most importantly, the MSCs were specifically provided with the ability to suppress T cells proliferation by IDO in response to inflammatory cytokine IFN-gamma. Moreover, we developed a Th1 cell-induced PE mouse model which displayed a high level of pathogenesis factor TNF-alpha. Strikingly, MSCs-based therapy significantly ameliorated both clinical and histopathological severity of PE symptoms including decreasing the blood pressure and proteinuria, suppressing glomerulonephritis, protecting the feto-placental development. The therapy also reversed abnormal TNF-alpha expression in uterine and splenic lymphocytes. These data suggest that MSCs may ameliorate Th1-induced PE-like symptoms in mice via the suppression of TNF-alpha and MSCs-based therapy may provide a potential novel method for PE.
  • |Adipocytes/cytology[MESH]
  • |Animals[MESH]
  • |Blood Pressure[MESH]
  • |Cell Differentiation[MESH]
  • |Cell Proliferation[MESH]
  • |Disease Models, Animal[MESH]
  • |Female[MESH]
  • |Glomerulonephritis/metabolism[MESH]
  • |Lymphocytes/cytology[MESH]
  • |Male[MESH]
  • |Mesenchymal Stem Cells/*cytology[MESH]
  • |Mice[MESH]
  • |Mice, Inbred BALB C[MESH]
  • |Mice, Inbred C57BL[MESH]
  • |Osteogenesis[MESH]
  • |Pre-Eclampsia/*pathology[MESH]
  • |Pregnancy[MESH]
  • |Pregnancy, Animal[MESH]
  • |T-Lymphocytes/cytology[MESH]
  • |Th1 Cells/*cytology[MESH]
  • |Tumor Necrosis Factor-alpha/*metabolism[MESH]


  • DeepDyve
  • Pubget Overpricing
  • suck abstract from ncbi

    Linkout box