Universität zu Köln

Grant, Michael P., Henley, Nathalie, Dubuissez, Marion, Chen, Nan ORCID: 0000-0002-0311-9264, Hartmann, Ursula, Royal, Virginie, Barbier, Olivier, Pichette, Vincent and Gerarduzzi, Casimiro ORCID: 0000-0001-7098-1455 (2022). Subchronic oral exposure of tungsten induces myofibroblast transformation and various markers of kidney fibrosis. Am. J. Physiol.-Cell Physiol., 322 (2). S. C205 - 13. Rockville: AMER PHYSIOLOGICAL SOC. ISSN 1522-1563

Full text not available from this repository.

Abstract

Tungsten is a naturally occurring transition element used in a broad range of applications. As a result of its extensive use, we are increasingly exposed to tungsten from our environment, including potable water, since tungsten can become bioaccessible in ground sources. The kidneys are particularly susceptible to tungsten exposure as this is the main site for tungsten excretion. In this study, we investigated the prolonged effects of tungsten on the kidneys and how this may impact injury and function. When mice were exposed to tungsten in their drinking water for 1 mo, kidney function had not significantly changed. Following 3-mo exposure, mice were presented with deterioration in kidney function as determined by serum and urine creatinine levels. During 3 mo of tungsten exposure, murine kidneys demonstrated significant increases in the myofibroblast marker a-smooth muscle actin (aSMA) and extracellular matrix products: fibronectin, collagen, and matricellular proteins. In addition, Masson's trichrome and hematoxylin-eosin (H&E) staining revealed an increase in fibrotic tissue and vacuolization of tubular epithelial cells, respectively, from kidneys of tungsten-treated mice, indicative of renal injury. In vitro treatment of kidney fibroblasts with tungsten led to increased proliferation and upregulation of transforming growth factor b1 (TGFb1), which was consistent with the appearance of fibroblast-to-myofibroblast transition (FMT) markers. Our data suggest that continuous exposure to tungsten impairs kidney function that may lead to the development of chronic kidney disease (CKD).

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Grant, Michael P. UNSPECIFIED UNSPECIFIED UNSPECIFIED Henley, Nathalie UNSPECIFIED UNSPECIFIED UNSPECIFIED Dubuissez, Marion UNSPECIFIED UNSPECIFIED UNSPECIFIED Chen, Nan UNSPECIFIED orcid.org/0000-0002-0311-9264 UNSPECIFIED Hartmann, Ursula UNSPECIFIED UNSPECIFIED UNSPECIFIED Royal, Virginie UNSPECIFIED UNSPECIFIED UNSPECIFIED Barbier, Olivier UNSPECIFIED UNSPECIFIED UNSPECIFIED Pichette, Vincent UNSPECIFIED UNSPECIFIED UNSPECIFIED Gerarduzzi, Casimiro UNSPECIFIED orcid.org/0000-0001-7098-1455 UNSPECIFIED
URN:	urn:nbn:de:hbz:38-686346
DOI:	10.1152/ajpcell.00277.2021
Journal or Publication Title:	Am. J. Physiol.-Cell Physiol.
Volume:	322
Number:	2
Page Range:	S. C205 - 13
Date:	2022
Publisher:	AMER PHYSIOLOGICAL SOC
Place of Publication:	Rockville
ISSN:	1522-1563
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language RESISTANT STAPHYLOCOCCUS-AUREUS; SODIUM TUNGSTATE; MATRICELLULAR PROTEINS; TUBULAR VACUOLATION; CHURCHILL COUNTY; ATSDR EVALUATION; DNA-DAMAGE; MECHANISMS; COILS; EMBOLIZATION Multiple languages Cell Biology; Physiology Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/68634