Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Alerts
  • Advertising/recruitment
  • Subscribe
  • Contact
  • Current Issue
  • Past Issues
  • By specialty
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All...
  • Videos
    • Conversations with Giants in Medicine
    • Author's Takes
  • Reviews
    • View all reviews...
    • Mechanisms Underlying the Metabolic Syndrome (Oct 2019)
    • Reparative Immunology (Jul 2019)
    • Allergy (Apr 2019)
    • Biology of familial cancer predisposition syndromes (Feb 2019)
    • Mitochondrial dysfunction in disease (Aug 2018)
    • Lipid mediators of disease (Jul 2018)
    • Cellular senescence in human disease (Apr 2018)
    • View all review series...
  • Collections
    • Recently published
    • In-Press Preview
    • Commentaries
    • Concise Communication
    • Editorials
    • Viewpoint
    • Scientific Show Stoppers
    • Top read articles
  • Clinical Medicine
  • JCI This Month
    • Current issue
    • Past issues

  • About
  • Editors
  • Consulting Editors
  • For authors
  • Current issue
  • Past issues
  • By specialty
  • Subscribe
  • Alerts
  • Advertise
  • Contact
  • Conversations with Giants in Medicine
  • Author's Takes
  • Recently published
  • Brief Reports
  • Technical Advances
  • Commentaries
  • Editorials
  • Hindsight
  • Review series
  • Reviews
  • The Attending Physician
  • First Author Perspectives
  • Scientific Show Stoppers
  • Top read articles
  • Concise Communication
Top
  • View PDF
  • Download citation information
  • Send a letter
  • Terms of use
  • Standard abbreviations
  • Article usage
  • Citations to this article
  • Share this article
  • Need Help? E-mail the JCI
  • Top
  • Version history

Advertisement

CorrigendumCell biology Free access | 10.1172/JCI25461C1

Identification of thrombospondin 1 (TSP-1) as a novel mediator of cell injury in kidney ischemia

Charuhas V. Thakar, Kamyar Zahedi, Monica P. Revelo, Zhaohui Wang, Charles E. Burnham, Sharon Barone, Shannon Bevans, Alex B. Lentsch, Hamid Rabb, and Manoocher Soleimani

Find articles by Thakar, C. in: JCI | PubMed | Google Scholar

Find articles by Zahedi, K. in: JCI | PubMed | Google Scholar

Find articles by Revelo, M. in: JCI | PubMed | Google Scholar

Find articles by Wang, Z. in: JCI | PubMed | Google Scholar

Find articles by Burnham, C. in: JCI | PubMed | Google Scholar

Find articles by Barone, S. in: JCI | PubMed | Google Scholar

Find articles by Bevans, S. in: JCI | PubMed | Google Scholar

Find articles by Lentsch, A. in: JCI | PubMed | Google Scholar

Find articles by Rabb, H. in: JCI | PubMed | Google Scholar

Find articles by Soleimani, M. in: JCI | PubMed | Google Scholar

First published February 1, 2006 - More info

Published in Volume 116, Issue 2 on February 1, 2006
J Clin Invest. 2006;116(2):549–549. https://doi.org/10.1172/JCI25461C1.
© 2006 The American Society for Clinical Investigation
First published February 1, 2006 - Version history

Related article:

Identification of thrombospondin 1 (TSP-1) as a novel mediator of cell injury in kidney ischemia
Charuhas V. Thakar, … , Hamid Rabb, Manoocher Soleimani
Charuhas V. Thakar, … , Hamid Rabb, Manoocher Soleimani
Categories: Research Article Cell biology

Identification of thrombospondin 1 (TSP-1) as a novel mediator of cell injury in kidney ischemia

  • Text
  • PDF
Abstract

Thrombospondin 1 (TSP-1) is a matricellular protein that inhibits angiogenesis and causes apoptosis in vivo and in vitro in several cancerous cells and tissues. Here we identify TSP-1 as the molecule with the highest induction level at 3 hours of IR injury in rat and mouse kidneys subjected to ischemia/reperfusion (IR) injury using the DNA microarray approach. Northern hybridizations demonstrated that TSP-1 expression was undetectable at baseline, induced at 3 and 12 hours, and returned to baseline levels at 48 hours of reperfusion. Immunocytochemical staining identified the injured proximal tubules as the predominant sites of expression of TSP-1 in IR injury and showed colocalization of TSP-1 with activated caspase-3. Addition of purified TSP-1 to normal kidney proximal tubule cells or cells subjected to ATP depletion in vitro induced injury as demonstrated by cytochrome c immunocytochemical staining and caspase-3 activity. The deleterious role of TSP-1 in ischemic kidney injury was demonstrated directly in TSP-1 null mice, which showed significant protection against IR injury–induced renal failure and tubular damage. We propose that TSP-1 is a novel regulator of ischemic damage in the kidney and may play an important role in the pathophysiology of ischemic kidney failure.

Authors

Charuhas V. Thakar, Kamyar Zahedi, Monica P. Revelo, Zhaohui Wang, Charles E. Burnham, Sharon Barone, Shannon Bevans, Alex B. Lentsch, Hamid Rabb, Manoocher Soleimani

×

Original citation: J Clin Invest. 2005;115(8):3451–3459. doi:10.1172/JCI25461.

Citation for this corrigendum: J Clin Invest. 2006;116(2):549. doi:10.1172/JCI25461C1.

Figure ​6B was incorrect in that the top panels were identical. The correct version of ​Figure6B follows.

Figure 6

The authors regret this error.

Version history
  • Version 1 (February 1, 2006): No description

Article tools

  • View PDF
  • Download citation information
  • Send a letter
  • Terms of use
  • Standard abbreviations
  • Article usage
  • Citations to this article
  • Share this article
  • Need Help? E-mail the JCI

Go to:

  • Top
  • Version history
Advertisement
Advertisement
Follow JCI:
Copyright © 2019 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts