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Pregled bibliografske jedinice broj: 821729

Časopis

Autori: Ravichandran K; Wang Q; Ozkok A; Jani A; Li H; He Z; Galešić Ljubanović Danica; Weiser-Evans MC; Nemenoff RA; Edelstein CL
Naslov: CD4 T cell knockout does not protect against kidney injury and worsens cancer.
( CD4 T cell knockout does not protect against kidney injury and worsens cancer. )
Izvornik: Journal of molecular medicine (0946-2716) 94 (2016), 4; 443-455
Vrsta rada: članak
Ključne riječi: CD4 T cell knockout ; kidney injury ; cancer
( CD4 T cell knockout ; kidney injury ; cancer )
Sažetak:
Most previous studies of cisplatin-induced acute kidney injury (AKI) have been in models of acute, high-dose cisplatin administration that leads to mortality in non-tumor-bearing mice. The aim of the study was to determine whether CD4 T cell knockout protects against AKI and cancer in a clinically relevant model of low-dose cisplatin- induced AKI in mice with cancer. Kidney function, serum neutrophil gelatinase-associated lipocalin (NGAL), acute tubular necrosis (ATN), and tubular apoptosis score were the same in wild-type and CD4 -/- mice with AKI. The lack of protection against AKI in CD4 -/- mice was associated with an increase in extracellular signal-regulated kinase (ERK), p38, CXCL1, and TNF-α, mediators of AKI and fibrosis, in both cisplatin-treated CD4 -/- mice and wild-type mice. The lack of protection was independent of the presence of cancer or not. Tumor size was double, and cisplatin had an impaired therapeutic effect on the tumors in CD4 -/- vs. wild-type mice. Mice depleted of CD4 T cells using the GK1.5 antibody were not protected against AKI and had larger tumors and lesser response to cisplatin. In summary, in a clinically relevant model of cisplatin-induced AKI in mice with cancer, (1) CD4 -/- mice were not protected against AKI ; (2) ERK, p38, CXCL1, and TNF-α, known mediators of AKI, and interstitial fibrosis were increased in CD4 -/- kidneys ; and (3) CD4 -/- mice had faster tumor growth and an impaired therapeutic effect of cisplatin on the tumors. The data warns against the use of CD4 T cell inhibition to attenuate cisplatin-induced AKI in patients with cancer. KEY MESSAGE: A clinically relevant low-dose cisplatin model of AKI in mice with cancer was used. CD4 -/- mice were not functionally or histologically protected against AKI. CD4 -/- mice had faster tumor growth. CD4 -/- mice had an impaired therapeutic effect of cisplatin on the tumors. Mice depleted of CD4 T cells were not protected against AKI and had larger tumors.
Projekt / tema: 198-0000000-3355
Izvorni jezik: eng
Rad je indeksiran u
bazama podataka:
Current Contents Connect (CCC)
MEDLINE
Scopus
SCI-EXP, SSCI i/ili A&HCI
Science Citation Index Expanded (SCI-EXP) (sastavni dio Web of Science Core Collectiona)
Kategorija: Znanstveni
Znanstvena područja:
Kliničke medicinske znanosti
URL Internet adrese: http://link.springer.com/article/10.1007/s00109-015-1366-z
Broj citata:
Altmetric:
DOI: 10.1007/s00109-015-1366-z
URL cjelovitog teksta:
Google Scholar: CD4 T cell knockout does not protect against kidney injury and worsens cancer.
Upisao u CROSBI: Danica Ljubanović (danica.ljubanovic@zg.t-com.hr), 15. Lip. 2016. u 19:34 sati



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