File Download
  Links for fulltext
     (May Require Subscription)
  • Find via Find It@HKUL
Supplementary

Conference Paper: Human bone marrow derived mesenchymal stromal/stem cells attenuate tubular inflammation upon albumin challenge

TitleHuman bone marrow derived mesenchymal stromal/stem cells attenuate tubular inflammation upon albumin challenge
Authors
Issue Date2011
PublisherAmerican Society of Nephrology. The Journal's web site is located at https://www.asn-online.org/abstracts/
Citation
The 2011 Kidney Week, Philadelphia, PA., 8-13 November 2011. In Journal of the American Society of Nephrology, 2011, v. 22, p. 135A, abstract no. TH-PO107 How to Cite?
AbstractBACKGROUND: Emerging evidence indicates that bone marrow derived mesenchymal stem cells (BM-MSC) protect against many forms of chronic renal diseases (CKD). The mechanism underlying this effect is not completely understood. We have previously shown the tubular expression of proinflammatory mediators induced by proteinuria play a vital role in the pathogenesis of CKD. This study aims to explore whether BM-MSC exerted anti-inflammatory effects in renal proximal tubular cells (PTEC) under milieu mimicking proteinuric nephropathy. METHODS: PTEC were treated with human albumin serum (HSA) and co-cultured with BM-MSC for 6 hours and 24 hours. Transcription and secretion of proinflammatory mediators were measured by real-time qPCR and ELISA, respectively. NF-κB signaling was assessed by western blot. RESULTS: Real-time qPCR revealed that co-culture with BM-MSC significantly reduced the up-regulated mRNA transcripts including IL6, CCL2, CCL5, IL8, TNF-alpha, IL1-beta, and ICAM-1 in PTEC exposed to HSA. The suppression of proinflammtory genes translated into reduced secretion of IL-6, CCL2, CCL5, IL8 and TNF-alpha proteins as detected by ELISA. In addition, the reduction of these proinflammtory cytokines and chemokines by BM-MSC was associated with attenuation of HSA induced I-κB phosphorylation in PTEC. To dissect the potential mechanism, we detected that the anti-inflammatory genes, HGF and IL1RN (IL1 receptor antagonist), were significantly induced in BM-MSC during co-culture with PTEC under protein overload condition. CONCLUSIONS: Our in vitro data suggest an anti-inflammatory role of BM-MSC in HSA-elicited PTEC inflammation, probably through paracrine effects of HGF and IL1RN via NF-κB signaling.
DescriptionThursday Poster Presentation - Basic/Experimental Inflammation: no. TH-PO107
Persistent Identifierhttp://hdl.handle.net/10722/160325
ISSN
2015 Impact Factor: 8.491
2015 SCImago Journal Rankings: 4.699

 

DC FieldValueLanguage
dc.contributor.authorWu, Hen_US
dc.contributor.authorYiu, WHen_US
dc.contributor.authorLeung, JCKen_US
dc.contributor.authorChan, LYYen_US
dc.contributor.authorLian, Qen_US
dc.contributor.authorLin, Men_US
dc.contributor.authorTse, HFen_US
dc.contributor.authorLai, KNen_US
dc.contributor.authorTang, SCWen_US
dc.date.accessioned2012-08-16T06:08:02Z-
dc.date.available2012-08-16T06:08:02Z-
dc.date.issued2011en_US
dc.identifier.citationThe 2011 Kidney Week, Philadelphia, PA., 8-13 November 2011. In Journal of the American Society of Nephrology, 2011, v. 22, p. 135A, abstract no. TH-PO107en_US
dc.identifier.issn1046-6673-
dc.identifier.urihttp://hdl.handle.net/10722/160325-
dc.descriptionThursday Poster Presentation - Basic/Experimental Inflammation: no. TH-PO107-
dc.description.abstractBACKGROUND: Emerging evidence indicates that bone marrow derived mesenchymal stem cells (BM-MSC) protect against many forms of chronic renal diseases (CKD). The mechanism underlying this effect is not completely understood. We have previously shown the tubular expression of proinflammatory mediators induced by proteinuria play a vital role in the pathogenesis of CKD. This study aims to explore whether BM-MSC exerted anti-inflammatory effects in renal proximal tubular cells (PTEC) under milieu mimicking proteinuric nephropathy. METHODS: PTEC were treated with human albumin serum (HSA) and co-cultured with BM-MSC for 6 hours and 24 hours. Transcription and secretion of proinflammatory mediators were measured by real-time qPCR and ELISA, respectively. NF-κB signaling was assessed by western blot. RESULTS: Real-time qPCR revealed that co-culture with BM-MSC significantly reduced the up-regulated mRNA transcripts including IL6, CCL2, CCL5, IL8, TNF-alpha, IL1-beta, and ICAM-1 in PTEC exposed to HSA. The suppression of proinflammtory genes translated into reduced secretion of IL-6, CCL2, CCL5, IL8 and TNF-alpha proteins as detected by ELISA. In addition, the reduction of these proinflammtory cytokines and chemokines by BM-MSC was associated with attenuation of HSA induced I-κB phosphorylation in PTEC. To dissect the potential mechanism, we detected that the anti-inflammatory genes, HGF and IL1RN (IL1 receptor antagonist), were significantly induced in BM-MSC during co-culture with PTEC under protein overload condition. CONCLUSIONS: Our in vitro data suggest an anti-inflammatory role of BM-MSC in HSA-elicited PTEC inflammation, probably through paracrine effects of HGF and IL1RN via NF-κB signaling.-
dc.languageengen_US
dc.publisherAmerican Society of Nephrology. The Journal's web site is located at https://www.asn-online.org/abstracts/-
dc.relation.ispartofJASN Abstract Supplementen_US
dc.titleHuman bone marrow derived mesenchymal stromal/stem cells attenuate tubular inflammation upon albumin challengeen_US
dc.typeConference_Paperen_US
dc.identifier.emailYiu, WH: whyiu@hku.hken_US
dc.identifier.emailLeung, JCK: jckleung@hku.hken_US
dc.identifier.emailChan, LYY: yychanb@hkucc.hku.hken_US
dc.identifier.emailLian, Q: qzlian@hkucc.hku.hken_US
dc.identifier.emailTse, HF: hftse@hkucc.hku.hken_US
dc.identifier.emailLai, KN: knlai@hku.hken_US
dc.identifier.emailTang, SCW: scwtang@hku.hken_US
dc.identifier.authorityLeung, JCK=rp00448en_US
dc.identifier.authorityLian, Q=rp00267en_US
dc.identifier.authorityTse, HF=rp00428en_US
dc.identifier.authorityLai, KN=rp00324en_US
dc.identifier.authorityTang, SCW=rp00480en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros204001en_US
dc.identifier.volume22en_US
dc.identifier.spage135A, abstract no. TH-PO107-
dc.identifier.epage135A, abstract no. TH-PO107-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats