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The kidney injury caused by the onset of acute graft-versus-host disease is associated with down-regulation of alpha Klotho

Amin, Risul (author)
Karolinska Institutet
He, Rui (author)
Karolinska Institutet
Gupta, Dhanu (author)
Karolinska Institutet
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Zheng, Wenyi (author)
Karolinska Institutet
Burmakin, Mikhail (author)
Uppsala universitet,Institutionen för medicinsk cellbiologi
Mohammad, Dara K. (author)
Karolinska Institutet
DePierre, Joseph W. (author)
Stockholms universitet,Institutionen för biokemi och biofysik,Stockholm Univ, Arrhenius Labs Nat Sci, Dept Biochem & Biophys, SE-10691 Stockholm, Sweden
Sadeghi, Behnam (author)
Karolinska Institutet
Olauson, Hannes (author)
Karolinska Institutet
Wernerson, Annika (author)
Karolinska Institutet
El-Andaloussi, Samir (author)
Karolinska Institutet
Hassan, Moustapha (author)
Karolinska Institutet
Abedi-Valugerdi, Manuchehr (author)
Karolinska Institutet
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 (creator_code:org_t)
Elsevier BV, 2020
2020
English.
In: International Immunopharmacology. - : Elsevier BV. - 1567-5769 .- 1878-1705. ; 78
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  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Acute graft-versus-host disease (aGVHD) and kidney injury are the major complications after allogeneic hematopoietic stem cell transplantation (HSCT). Although the underlying mechanisms for the development of these complications are not yet fully understood, it has been proposed that emergence of aGVHD contributes to the development of kidney injury after HSCT. We have shown previously that aGVHD targets the kidney in a biphasic manner: at the onset, inflammatory genes are up-regulated, while when aGVHD becomes established, donor lymphocytes infiltrate the kidney. Here, we characterize renal manifestations at the onset of aGVHD. Mice receiving allogeneic bone marrow and spleen cells displayed symptoms of aGVHD and elevated serum levels of tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma) within 4 days. There was concurrent kidney injury with the following characteristics: (1) elevated expression of the kidney injury biomarker, neutrophil gelatinase-associated lipocalin (NGAL), (2) accumulation of hetero-lysosomes in proximal tubule epithelial cells, and (3) reductions in alpha Klotho mRNA and protein and increased serum levels of fibroblast growth factor 23 (Fgf23), phosphate and urea. This situation resembled acute renal injury caused by bacterial lipopolysaccharide. We conclude that the onset of aGVHD is associated with kidney injury involving down-regulation of alpha Klotho, a sight that may inspire novel therapeutic approaches.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Immunologi inom det medicinska området (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Immunology in the medical area (hsv//eng)
NATURVETENSKAP  -- Biologi -- Immunologi (hsv//swe)
NATURAL SCIENCES  -- Biological Sciences -- Immunology (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Urologi och njurmedicin (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Urology and Nephrology (hsv//eng)

Keyword

Acute graft versus host disease
Fibroblast growth factor 23
alpha Klotho
Hematopoietic stem cell transplantation
Interferon gamma
Kidney injury
Lysosome
Tumor necrosis factor alpha

Publication and Content Type

ref (subject category)
art (subject category)

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