ArticleKidney international2009
Mice that overexpress human heat shock protein 27 have increased renal injury following ischemia reperfusion.
Article in Kidney international, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- The STAT1/HMGB1/NF-κB pathway in chronic inflammation and kidney injury after cisplatin exposure.Theranostics · 2023Article
- Heat shock proteins in the kidney.Pediatric nephrology (Berlin, Germany) · 2016Review
- Nox2 is a mediator of ischemia reperfusion injury.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2015Article
- A minimally invasive, lentiviral based method for the rapid and sustained genetic manipulation of renal tubules.Scientific reports · 2015Article
- Class-specific histone/protein deacetylase inhibition protects against renal ischemia reperfusion injury and fibrosis formation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2015Article
- Immune cells in experimental acute kidney injury.Nature reviews. Nephrology · 2015Review
- Article
- Ischemic postconditioning prevents renal ischemia reperfusion injury through the induction of heat shock proteins in rats.Molecular medicine reports · 2014Article
- Mice with an absent stress response are protected against ischemic renal injury.Kidney international · 2014Article
- Critical role of interleukin-11 in isoflurane-mediated protection against ischemic acute kidney injury in mice.Anesthesiology · 2013Article
- The volatile anesthetic isoflurane induces ecto-5'-nucleotidase (CD73) to protect against renal ischemia and reperfusion injury.Kidney international · 2013Article
- Tubular expression of heat-shock protein 27 inhibits fibrogenesis in obstructive nephropathy.Kidney international · 2013Article
- Paneth cell-mediated multiorgan dysfunction after acute kidney injury.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Proximal tubule sphingosine kinase-1 has a critical role in A1 adenosine receptor-mediated renal protection from ischemia.Kidney international · 2012Article
- A1 adenosine receptor allosteric enhancer PD-81723 protects against renal ischemia-reperfusion injury.American journal of physiology. Renal physiology · 2012Article
- Heat shock protein 27 (HSP27): biomarker of disease and therapeutic target.Fibrogenesis & tissue repair · 2012Article
- Inhibition of the protein kinase MK-2 protects podocytes from nephrotic syndrome-related injury.American journal of physiology. Renal physiology · 2011Article
- Dangers within: DAMP responses to damage and cell death in kidney disease.Journal of the American Society of Nephrology : JASN · 2011Review
- Selective renal overexpression of human heat shock protein 27 reduces renal ischemia-reperfusion injury in mice.American journal of physiology. Renal physiology · 2010Article
- Protection against acute kidney injury via A(1) adenosine receptor-mediated Akt activation reduces liver injury after liver ischemia and reperfusion in mice.The Journal of pharmacology and experimental therapeutics · 2010Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
We previously showed that activation of the A1 adenosine receptor protected the kidney against ischemia-reperfusion injury by induction and phosphorylation of heat shock protein 27 (HSP27). Here, we used mice that overexpress human HSP27 (huHSP27) to determine if kidneys from these mice were protected against injury. Proximal tubule cells cultured from the transgenic mice had increased resistance to peroxide-induced necrosis compared to cells from wild-type mice. However, after renal ischemic injury, HSP27 transgenic mice had decreased renal function compared to wild-type mice, along with increased renal expression of mRNAs of pro-inflammatory cytokines (TNF-alpha, ICAM-1, MCP-1) and increased plasma and kidney keratinocyte-derived cytokine. Following ischemic injury, neutrophils infiltrated the kidneys earlier in the transgenic mice. Flow cytometric analysis of lymphocyte subsets showed that those isolated from the kidneys of transgenic mice had increased CD3(+), CD4(+), CD8(+), and NK1.1(+) cells 3 h after injury. When splenocytes or NK1.1(+) cells were isolated from transgenic mice and adoptively transferred into wild-type mice there was increased renal injury. Further, depletion of lymphocytes by splenectomy or neutralization of NK1.1(+) cells resulted in improved renal function in the transgenic mice following reperfusion. Our study shows that induction of HSP27 in renal tubular cells protects against necrosis in vitro, but its systemic increase counteracts this protection by exacerbating renal and systemic inflammation in vivo.
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