File Download
There are no files associated with this item.
Links for fulltext
(May Require Subscription)
- Publisher Website: 10.1152/ajprenal.00423.2007
- Scopus: eid_2-s2.0-44949252210
- WOS: WOS:000254623200031
- Find via
Supplementary
- Citations:
- Appears in Collections:
Article: Activation of podocytes by mesangial-derived TNF-α: Glomerulo-podocytic communication in IgA nephropathy
Title | Activation of podocytes by mesangial-derived TNF-α: Glomerulo-podocytic communication in IgA nephropathy |
---|---|
Authors | |
Keywords | Mesangial Cell Tubulointerstitial Injury Tumor Necrosis Factor-Α |
Issue Date | 2008 |
Citation | American Journal Of Physiology - Renal Physiology, 2008, v. 294 n. 4, p. F945-F955 How to Cite? |
Abstract | We have previously documented that human mesangial cell (HMC)-derived TNF-α is an important mediator involved in the glomerulo-tubular communication in the development of interstitial damage in IgA nephropathy (IgAN). With the strategic position of podocytes, we further examined the role of mesangial cells in the activation of podocytes in IgAN. There was no binding of IgA from patients with IgAN to podocytes. Podocytes cultured with IgA from patients with IgAN did not induce the release of growth factors or cytokines. Furthermore, podocytes did not express mRNA of known IgA receptors. In contrast, IgA-conditioned medium (IgA-HMC medium) prepared by culturing HMC with IgA from patients with IgAN for 48 h significantly increased the gene expression and protein synthesis of TNF-α by podocytes with a 17-fold concentration above that of IgA-HMC medium. The upregulation of TNF-α expression by podocyte was only abolished by a neutralizing antibody against TNF-α but not by other antibodies. Exogenous TNF-α upregulated the synthesis of TNF-α by podocytes in an autocrine fashion. IgA-HMC medium prepared with IgA from patients with IgAN also significantly upregulated the expression of both TNF-α receptor 1 and 2 in podocytes. Our in vitro finding suggests podocytes may play a contributory role in the development of interstitial damage in IgAN by amplifying the activation of tubular epithelial cells with enhanced TNF-α synthesis after inflammatory changes of HMC. Copyright © 2008 the American Physiological Society. |
Persistent Identifier | http://hdl.handle.net/10722/163175 |
ISSN | |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lai, KN | en_US |
dc.contributor.author | Leung, JCK | en_US |
dc.contributor.author | Chan, LYY | en_US |
dc.contributor.author | Saleem, MA | en_US |
dc.contributor.author | Mathieson, PW | en_US |
dc.contributor.author | Lai, FM | en_US |
dc.contributor.author | Tang, SCW | en_US |
dc.date.accessioned | 2012-09-05T05:28:26Z | - |
dc.date.available | 2012-09-05T05:28:26Z | - |
dc.date.issued | 2008 | en_US |
dc.identifier.citation | American Journal Of Physiology - Renal Physiology, 2008, v. 294 n. 4, p. F945-F955 | en_US |
dc.identifier.issn | 0363-6127 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/163175 | - |
dc.description.abstract | We have previously documented that human mesangial cell (HMC)-derived TNF-α is an important mediator involved in the glomerulo-tubular communication in the development of interstitial damage in IgA nephropathy (IgAN). With the strategic position of podocytes, we further examined the role of mesangial cells in the activation of podocytes in IgAN. There was no binding of IgA from patients with IgAN to podocytes. Podocytes cultured with IgA from patients with IgAN did not induce the release of growth factors or cytokines. Furthermore, podocytes did not express mRNA of known IgA receptors. In contrast, IgA-conditioned medium (IgA-HMC medium) prepared by culturing HMC with IgA from patients with IgAN for 48 h significantly increased the gene expression and protein synthesis of TNF-α by podocytes with a 17-fold concentration above that of IgA-HMC medium. The upregulation of TNF-α expression by podocyte was only abolished by a neutralizing antibody against TNF-α but not by other antibodies. Exogenous TNF-α upregulated the synthesis of TNF-α by podocytes in an autocrine fashion. IgA-HMC medium prepared with IgA from patients with IgAN also significantly upregulated the expression of both TNF-α receptor 1 and 2 in podocytes. Our in vitro finding suggests podocytes may play a contributory role in the development of interstitial damage in IgAN by amplifying the activation of tubular epithelial cells with enhanced TNF-α synthesis after inflammatory changes of HMC. Copyright © 2008 the American Physiological Society. | en_US |
dc.language | eng | en_US |
dc.relation.ispartof | American Journal of Physiology - Renal Physiology | en_US |
dc.subject | Mesangial Cell | en_US |
dc.subject | Tubulointerstitial Injury | en_US |
dc.subject | Tumor Necrosis Factor-Α | en_US |
dc.title | Activation of podocytes by mesangial-derived TNF-α: Glomerulo-podocytic communication in IgA nephropathy | en_US |
dc.type | Article | en_US |
dc.identifier.email | Lai, KN:knlai@hku.hk | en_US |
dc.identifier.email | Leung, JCK:jckleung@hku.hk | en_US |
dc.identifier.email | Tang, SCW:scwtang@hku.hk | en_US |
dc.identifier.authority | Lai, KN=rp00324 | en_US |
dc.identifier.authority | Leung, JCK=rp00448 | en_US |
dc.identifier.authority | Tang, SCW=rp00480 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1152/ajprenal.00423.2007 | en_US |
dc.identifier.scopus | eid_2-s2.0-44949252210 | en_US |
dc.identifier.hkuros | 143111 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-44949252210&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 294 | en_US |
dc.identifier.issue | 4 | en_US |
dc.identifier.spage | F945 | en_US |
dc.identifier.epage | F955 | en_US |
dc.identifier.isi | WOS:000254623200031 | - |
dc.identifier.f1000 | 721990771 | - |
dc.identifier.scopusauthorid | Lai, KN=7402135706 | en_US |
dc.identifier.scopusauthorid | Leung, JCK=7202180349 | en_US |
dc.identifier.scopusauthorid | Chan, LYY=8108378300 | en_US |
dc.identifier.scopusauthorid | Saleem, MA=7103095853 | en_US |
dc.identifier.scopusauthorid | Mathieson, PW=7005677484 | en_US |
dc.identifier.scopusauthorid | Lai, FM=7202559720 | en_US |
dc.identifier.scopusauthorid | Tang, SCW=7403437082 | en_US |
dc.identifier.issnl | 0363-6127 | - |