| pubmed-article:21048024 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21048024 | lifeskim:mentions | umls-concept:C1257975 | lld:lifeskim |
| pubmed-article:21048024 | lifeskim:mentions | umls-concept:C0160420 | lld:lifeskim |
| pubmed-article:21048024 | lifeskim:mentions | umls-concept:C0538674 | lld:lifeskim |
| pubmed-article:21048024 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:21048024 | lifeskim:mentions | umls-concept:C0597170 | lld:lifeskim |
| pubmed-article:21048024 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:21048024 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:21048024 | pubmed:dateCreated | 2011-1-7 | lld:pubmed |
| pubmed-article:21048024 | pubmed:abstractText | Multipotent mesenchymal stem cells (MSC) have become a popular and promising therapeutic approach in many clinical conditions. MSC are beneficial in animal models of acute kidney injury (AKI), by mediating differentiation-independent paracrine properties, and have prompted ongoing clinical trials to evaluate the safety and efficacy of MSC. Heme oxygenase-1 (HO-1) is induced in response to stress including AKI and has important anti-apoptotic, anti-inflammatory, and proangiogenic properties in these settings. We therefore examined whether HO-1 plays a role in the beneficial effects of MSC in AKI. We isolated MSC from bone marrow of age-matched HO-1+/+ and HO-1-/- mice. Our studies indicate that while differentiation of MSC into osteo- and adipocytic lineages did not differ between cells isolated from HO-1+/+ and HO-1-/- mice, MSC from HO-1-/- mice had significantly lower angiogenic potential. Moreover, HO-1-/- MSC demonstrated reduced expression and secretion of several important growth and proangiogenic factors (stromal cell-derived factor-1, vascular endothelial growth factor-A, and hepatocyte growth factor) compared with MSC derived from HO-1+/+ mice. In addition, conditioned medium of HO-1+/+ MSC rescued functional and morphological changes associated with cisplatin-induced AKI, while the HO-1-/--conditioned medium was ineffectual. Our studies indicate that HO-1 plays an important role in MSC-mediated protection. The results expand understanding of the renoprotective effects of MSC and may provide novel strategies to better utilize MSC in various disease models. | lld:pubmed |
| pubmed-article:21048024 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21048024 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21048024 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21048024 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21048024 | pubmed:language | eng | lld:pubmed |
| pubmed-article:21048024 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21048024 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:21048024 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21048024 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21048024 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21048024 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21048024 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21048024 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21048024 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21048024 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21048024 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21048024 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:21048024 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:21048024 | pubmed:issn | 1522-1466 | lld:pubmed |
| pubmed-article:21048024 | pubmed:author | pubmed-author:AgarwalAnupam... | lld:pubmed |
| pubmed-article:21048024 | pubmed:author | pubmed-author:SandersPaul... | lld:pubmed |
| pubmed-article:21048024 | pubmed:author | pubmed-author:KimJunghyunJ | lld:pubmed |
| pubmed-article:21048024 | pubmed:author | pubmed-author:BallaJózsefJ | lld:pubmed |
| pubmed-article:21048024 | pubmed:author | pubmed-author:CurtisLisa... | lld:pubmed |
| pubmed-article:21048024 | pubmed:author | pubmed-author:ZarjouAbolfaz... | lld:pubmed |
| pubmed-article:21048024 | pubmed:author | pubmed-author:TraylorAmie... | lld:pubmed |
| pubmed-article:21048024 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:21048024 | pubmed:volume | 300 | lld:pubmed |
| pubmed-article:21048024 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:21048024 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:21048024 | pubmed:pagination | F254-62 | lld:pubmed |
| pubmed-article:21048024 | pubmed:dateRevised | 2011-5-9 | lld:pubmed |
| pubmed-article:21048024 | pubmed:meshHeading | pubmed-meshheading:21048024... | lld:pubmed |
| pubmed-article:21048024 | pubmed:meshHeading | pubmed-meshheading:21048024... | lld:pubmed |
| pubmed-article:21048024 | pubmed:meshHeading | pubmed-meshheading:21048024... | lld:pubmed |
| pubmed-article:21048024 | pubmed:meshHeading | pubmed-meshheading:21048024... | lld:pubmed |
| pubmed-article:21048024 | pubmed:meshHeading | pubmed-meshheading:21048024... | lld:pubmed |
| pubmed-article:21048024 | pubmed:meshHeading | pubmed-meshheading:21048024... | lld:pubmed |
| pubmed-article:21048024 | pubmed:meshHeading | pubmed-meshheading:21048024... | lld:pubmed |
| pubmed-article:21048024 | pubmed:meshHeading | pubmed-meshheading:21048024... | lld:pubmed |
| pubmed-article:21048024 | pubmed:meshHeading | pubmed-meshheading:21048024... | lld:pubmed |
| pubmed-article:21048024 | pubmed:meshHeading | pubmed-meshheading:21048024... | lld:pubmed |
| pubmed-article:21048024 | pubmed:meshHeading | pubmed-meshheading:21048024... | lld:pubmed |
| pubmed-article:21048024 | pubmed:meshHeading | pubmed-meshheading:21048024... | lld:pubmed |
| pubmed-article:21048024 | pubmed:meshHeading | pubmed-meshheading:21048024... | lld:pubmed |
| pubmed-article:21048024 | pubmed:meshHeading | pubmed-meshheading:21048024... | lld:pubmed |
| pubmed-article:21048024 | pubmed:meshHeading | pubmed-meshheading:21048024... | lld:pubmed |
| pubmed-article:21048024 | pubmed:year | 2011 | lld:pubmed |
| pubmed-article:21048024 | pubmed:articleTitle | Paracrine effects of mesenchymal stem cells in cisplatin-induced renal injury require heme oxygenase-1. | lld:pubmed |
| pubmed-article:21048024 | pubmed:affiliation | Department of Medicine, Nephrology Research Training Center, University of Alabama at Birmingham, 1900 Univ. Blvd., Birmingham, Alabama 35294, USA. | lld:pubmed |
| pubmed-article:21048024 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:21048024 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
| entrez-gene:15368 | entrezgene:pubmed | pubmed-article:21048024 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:21048024 | lld:entrezgene |
