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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/780
Title: Glomerular changes and alterations of zonula occludens-1 in the kidneys of Plasmodium falciparum malaria patients.
Authors: Benjamas Wichapoon
เบญจมาศ วิชาพูล
Chuchard Punsawad
ชูชาติ พันธ์สวัสดิ์
Urai Chaisri
อุไร ไชยศรี
Parnpen Viriyavejakul
พรรณเพ็ญ วิริยเวชกุล
Mahidol University. Faculty of Tropical Medicine. Department of Tropical Pathology
Parnpen Viriyavejakul
Keywords: Acute kidney injury;AKI;Glomeruli;Kidney;Plasmodium falciparum;Tight junction;Open Access article
Issue Date: 9-May-2014
Citation: Wichapoon B, Punsawad C, Chaisri U, Viriyavejakul P. Glomerular changes andalterations of zonula occludens-1 in the kidneys of Plasmodium falciparum malaria patients. Malar J. 2014 May 9;13:176.
Abstract: BACKGROUND: The process of cytoadhesion in Plasmodium falciparum malaria infection causes signaling processes that lead to structural and functional changes at the cellular level. Histopathological changes of acute kidney injury (AKI) in P. falciparum malaria often involve glomerular proliferation, thickening of the glomerular basement membrane, acute tubular necrosis, and interstitial inflammation. Focusing on the glomeruli, this study aimed to investigate glomerular and tight junction-associated protein- zonula occludens-1 (ZO-1) changes in P. falciparum malaria patients. METHODS: Kidney tissues were grouped into P. falciparum with AKI (Cr ≥ 265 μmol/L or 3 mg/dl), P. falciparum without AKI (Cr < 265 μmol/L), and normal kidney tissues (control group). Glomerular cells and the glomerular area were quantified and compared in three experimental groups. The tight junction was investigated immunohistochemically using tight junction-associated protein, ZO-1, protein marker. A further immunofluorescence study was performed in an endothelial cell (EC)-parasitized red blood cell (PRBC) co-culture system, to evaluate the tight junction protein. RESULTS: Glomerular cell proliferation was significant in P. falciparum with AKI (Cr ≥ 265 μmol/L). By contrast, the glomerular area decreased significantly. ZO-1 expression was significantly decreased in the AKI group compared with normal kidneys, and in kidney tissues without AKI (p < 0.05). This was further confirmed by the depletion in ZO-1 localization in ECs co-cultured with PRBCs. CONCLUSIONS: In P. falciparum malaria with AKI, the decrease in glomerular area, despite glomerular cell proliferation, could be due to the collapse of cellular structures secondary to damaged tight junction-associated protein, ZO-1.
URI: http://repository.li.mahidol.ac.th/dspace/handle/123456789/780
metadata.dc.identifier.url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4023169/pdf/1475-2875-13-176.pdf
ISSN: 1475-2875 (electronic)
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