Effects of long-term dehydration and quick rehydration on the camel kidney: pathological changes and modulation of the expression of solute carrier proteins and aquaporins.
Autor: | Damir HA; Department of Pharmacology, College of Medicine & Health Sciences, United Arab Emirates University, Al Ain, United Arab Emirates., Ali MA; Department of Pharmacology, College of Medicine & Health Sciences, United Arab Emirates University, Al Ain, United Arab Emirates., Adem MA; Department of Pharmacology, College of Medicine & Health Sciences, United Arab Emirates University, Al Ain, United Arab Emirates., Amir N; Department of Pharmacology, College of Medicine & Health Sciences, United Arab Emirates University, Al Ain, United Arab Emirates., Ali OM; Department of Pharmacology, College of Medicine & Health Sciences, United Arab Emirates University, Al Ain, United Arab Emirates., Tariq S; Department of Anatomy, College of Medicine & Health Sciences, Emirates University, Al-Ain, United Arab Emirates., Adeghate E; Department of Anatomy, College of Medicine & Health Sciences, Emirates University, Al-Ain, United Arab Emirates., Greenwood MP; Molecular Neuroendocrinology Research Group, Bristol Medical School, Translational Health Sciences, University of Bristol, Dorothy Hodgkin Building, Bristol, BS13NY, UK., Lin P; Molecular Neuroendocrinology Research Group, Bristol Medical School, Translational Health Sciences, University of Bristol, Dorothy Hodgkin Building, Bristol, BS13NY, UK., Alvira-Iraizoz F; Molecular Neuroendocrinology Research Group, Bristol Medical School, Translational Health Sciences, University of Bristol, Dorothy Hodgkin Building, Bristol, BS13NY, UK., Gillard B; Molecular Neuroendocrinology Research Group, Bristol Medical School, Translational Health Sciences, University of Bristol, Dorothy Hodgkin Building, Bristol, BS13NY, UK., Murphy D; Molecular Neuroendocrinology Research Group, Bristol Medical School, Translational Health Sciences, University of Bristol, Dorothy Hodgkin Building, Bristol, BS13NY, UK. D.Murphy@bristol.ac.uk., Adem A; Department of Pharmacology, College of Medicine & Health Sciences, United Arab Emirates University, Al Ain, United Arab Emirates. abdu.adem@ku.ac.ae.; Department of Pharmacology, College of Medicine and Health Sciences, Khalifa University, PO. Box 127788, Abu Dhabi, UAE. abdu.adem@ku.ac.ae. |
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Jazyk: | angličtina |
Zdroj: | BMC veterinary research [BMC Vet Res] 2024 Aug 16; Vol. 20 (1), pp. 367. Date of Electronic Publication: 2024 Aug 16. |
DOI: | 10.1186/s12917-024-04215-4 |
Abstrakt: | Background: Recurrent dehydration causes chronic kidney disease in humans and animal models. The dromedary camel kidney has remarkable capacity to preserve water and solute during long-term dehydration. In this study, we investigated the effects of dehydration and subsequent rehydration in the camel's kidney histology/ultrastructure and changes in aquaporin/solute carrier proteins along with gene expression. Results: In light microscopy, dehydration induced few degenerative and necrotic changes in cells of the cortical tubules with unapparent or little effect on medullary cells. The ultrastructural changes encountered in the cortex were infrequent during dehydration and included nuclear chromatin condensation, cytoplasmic vacuolization, mitochondrial swelling, endoplasmic reticulum/ lysosomal degeneration and sometimes cell death. Some mRNA gene expressions involved in cell stability were upregulated by dehydration. Lesions in endothelial capillaries, glomerular membranes and podocyte tertiary processes in dehydrated camels indicated disruption of glomerular filtration barrier which were mostly corrected by rehydration. The changes in proximal tubules brush borders after dehydration, were accompanied by down regulation of ATP1A1 mRNA involved in Na + /K + pump that were corrected by rehydration. The increased serum Na, osmolality and vasopressin were paralleled by modulation in expression level for corresponding SLC genes with net Na retention in cortex which were corrected by rehydration. Medullary collecting ducts and interstitial connective tissue were mostly unaffected during dehydration. CKD, a chronic nephropathy induced by recurrent dehydration in human and animal models and characterized by interstitial fibrosis and glomerular sclerosis, were not observed in the dehydrated/rehydrated camel kidneys. The initiating factors, endogenous fructose, AVP/AVPR2 and uric acid levels were not much affected. TGF-β1 protein and TGF-β1gene expression showed no changes by dehydration in cortex/medulla to mediate fibrosis. KCNN4 gene expression level was hardly detected in the dehydrated camel's kidney; to encode for Ca + + -gated KCa3.1 channel for Ca + + influx to instigate TGF-β1. Modulation of AQP 1, 2, 3, 4, 9 and SLC protein and/or mRNAs expression levels during dehydration/rehydration was reported. Conclusions: Long-term dehydration induces reversible or irreversible ultrastructural changes in kidney cortex with minor effects in medulla. Modulation of AQP channels, SLC and their mRNAs expression levels during dehydration/rehydration have a role in water conservation. Cortex and medulla respond differently to dehydration/rehydration. (© 2024. The Author(s).) |
Databáze: | MEDLINE |
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