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Your search keyword '"Katrina M. Mirabito Colafella"' showing total 3 results
Start Over Author "Katrina M. Mirabito Colafella" Journal scientific reports
3 results on '"Katrina M. Mirabito Colafella"'

1. Thrombomodulin is upregulated in the kidneys of women with pre-eclampsia

Author

Cleo C. L. van Aanhold, Manon Bos, Katrina M. Mirabito Colafella, Marie-Louise P. van der Hoorn, Ron Wolterbeek, Jan A. Bruijn, Kitty W. M. Bloemenkamp, Anton H. van den Meiracker, A. H. Jan Danser, and Hans J. Baelde

Subjects
Medicine, Science
Abstract

Abstract The endothelial glycoprotein thrombomodulin regulates coagulation, vascular inflammation and apoptosis. In the kidney, thrombomodulin protects the glomerular filtration barrier by eliciting crosstalk between the glomerular endothelium and podocytes. Several glomerular pathologies are characterized by a loss of glomerular thrombomodulin. In women with pre-eclampsia, serum levels of soluble thrombomodulin are increased, possibly reflecting a loss from the glomerular endothelium. We set out to investigate whether thrombomodulin expression is decreased in the kidneys of women with pre-eclampsia and rats exposed to an angiogenesis inhibitor. Thrombomodulin expression was examined using immunohistochemistry and qPCR in renal autopsy tissues collected from 11 pre-eclamptic women, 22 pregnant controls and 11 hypertensive non-pregnant women. Further, kidneys from rats treated with increasing doses of sunitinib or sunitinib in combination with endothelin receptor antagonists were studied. Glomerular thrombomodulin protein levels were increased in the kidneys of women with pre-eclampsia. In parallel, in rats exposed to sunitinib, glomerular thrombomodulin was upregulated in a dose-dependent manner, and the upregulation of glomerular thrombomodulin preceded the onset of histopathological changes. Selective ETAR blockade, but not dual ETA/BR blockade, normalised the sunitinib-induced increase in thrombomodulin expression and albuminuria. We propose that glomerular thrombomodulin expression increases at an early stage of renal damage induced by antiangiogenic conditions. The upregulation of this nephroprotective protein in glomerular endothelial cells might serve as a mechanism to protect the glomerular filtration barrier in pre-eclampsia.

Published
2021
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2. Zinc is a critical regulator of placental morphogenesis and maternal hemodynamics during pregnancy in mice

Author

Katrina M Mirabito Colafella, Claire T. Roberts, Sam Buckberry, Stephen Pederson, Cuong D. Tran, Zona Goh, Tanja Jankovic-Karasoulos, Gabriela E. Leghi, Rebecca L. Wilson, Sarah A. Robertson, Tina Bianco-Miotto, Jessica A. Phillips, Shalem Leemaqz, Dale McAninch, and Sean T. O’Leary

Subjects
0301 basic medicine, medicine.medical_specialty, Offspring, Placenta, lcsh:Medicine, Biology, Article, Mice, 03 medical and health sciences, Pregnancy, Internal medicine, Morphogenesis, medicine, Animals, lcsh:Science, 2. Zero hunger, Fetus, 030109 nutrition & dietetics, Multidisciplinary, lcsh:R, Hemodynamics, medicine.disease, Micronutrient, Placentation, Diet, Trace Elements, Zinc, 030104 developmental biology, Endocrinology, medicine.anatomical_structure, In utero, Zinc deficiency, Gestation, Female, lcsh:Q
Abstract

Zinc is an essential micronutrient in pregnancy and zinc deficiency impairs fetal growth. We used a mouse model of moderate zinc deficiency to investigate the physiological mechanisms by which zinc is important to placental morphogenesis and the maternal blood pressure changes during pregnancy. A 26% reduction in circulating zinc (P = 0.005) was exhibited in mice fed a moderately zinc-deficient diet. Zinc deficiency in pregnancy resulted in an 8% reduction in both near term fetal and placental weights (both P in utero programming of offspring growth and development largely through effects to the placenta and maternal cardiovascular system.

Published
2017
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3. Chronic recurrent dehydration associated with periodic water intake exacerbates hypertension and promotes renal damage in male spontaneously hypertensive rats

Author

Katrina M Mirabito Colafella, Reetu R. Singh, Antony Vinh, Victor G. Puelles, Grant R Drummond, Connie P. C. Ow, Louise L. Bulmer, Roger G. Evans, Lucinda M Hilliard, Tracey Gaspari, and Kate M. Denton

Subjects
medicine.medical_specialty, Multidisciplinary, business.industry, Urinary system, 030232 urology & nephrology, Renal function, 030204 cardiovascular system & hematology, medicine.disease, Article, End stage renal disease, 03 medical and health sciences, 0302 clinical medicine, Endocrinology, Blood pressure, Internal medicine, medicine, Urine osmolality, Renal fibrosis, Dehydration, business, Kidney disease
Abstract

Epidemiological evidence links recurrent dehydration associated with periodic water intake with chronic kidney disease (CKD). However, minimal attention has been paid to the long-term impact of periodic water intake on the progression of CKD and underlying mechanisms involved. Therefore we investigated the chronic effects of recurrent dehydration associated with periodic water restriction on arterial pressure and kidney function and morphology in male spontaneously hypertensive rats (SHR). Arterial pressure increased and glomerular filtration rate decreased in water-restricted SHR. This was observed in association with cyclic changes in urine osmolarity, indicative of recurrent dehydration. Additionally, water-restricted SHR demonstrated greater renal fibrosis and an imbalance in favour of pro-inflammatory cytokine-producing renal T cells compared to their control counterparts. Furthermore, urinary NGAL levels were greater in water-restricted than control SHR. Taken together, our results provide significant evidence that recurrent dehydration associated with chronic periodic drinking hastens the progression of CKD and hypertension, and suggest a potential role for repetitive bouts of acute renal injury driving renal inflammatory processes in this setting. Further studies are required to elucidate the specific pathways that drive the progression of recurrent dehydration-induced kidney disease.

Published
2016

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