Université catholique de Louvain

About: Université catholique de Louvain is a education organization based out in Louvain-la-Neuve, Belgium. It is known for research contribution in the topics: Population & Catalysis. The organization has 25319 authors who have published 57360 publications receiving 2172080 citations. The organization is also known as: University of Louvain & UCLouvain.

Do Environmental CSR Initiatives Serve Organizations’Legitimacy in the Oil Industry? Exploring Employees’ Reactions Through Organizational Identification Theory

Abstract: Little is known about employees’ responses to their organizations’ initiatives in corporate social responsibility (CSR). Academics have already identified a few outcomes regarding CSR’s impact on employees’ attitudes and behaviours; however, studies explaining the underlying mechanisms that drive employees’ favourable responses to CSR remain largely unexplored. Based on organizational identification (OI) theory, this study surveyed 155 employees of a petrochemical organization to better elucidate why, how and under which circumstances employees might positively respond to organizations’ CSR initiatives in the controversial oil industry sector. Findings first support that perceived CSR (i.e. environmental CSR) positively relates to employees’ OI which is known as an important antecedent of employees’ outcomes (Riketta, J Vocat Behavior, 66(2):358, 2005). Furthermore, results highlighted that the relationship between perceived CSR and employees’ OI is mediated by organizational trust. Finally, this study also revealed that some contingency factors such as employees’ attributions of self-centred motives to their organization’s investment in environmental issues can moderate the relationship between perceived CSR and organizational trust. Based on these findings, it is argued that CSR initiatives can support organizations’ efforts to maintain a strong relationship with their employees, and gain their support even in a controversial industry sector.

Common noncoding UMOD gene variants induce salt-sensitive hypertension and kidney damage by increasing uromodulin expression

Abstract: Hypertension and chronic kidney disease (CKD) are complex traits representing major global health problems. Multiple genome-wide association studies have identified common variants in the promoter of the UMOD gene, which encodes uromodulin, the major protein secreted in normal urine, that cause independent susceptibility to CKD and hypertension. Despite compelling genetic evidence for the association between UMOD risk variants and disease susceptibility in the general population, the underlying biological mechanism is not understood. Here, we demonstrate that UMOD risk variants increased UMOD expression in vitro and in vivo. Uromodulin overexpression in transgenic mice led to salt-sensitive hypertension and to the presence of age-dependent renal lesions similar to those observed in elderly individuals homozygous for UMOD promoter risk variants. The link between uromodulin and hypertension is due to activation of the renal sodium cotransporter NKCC2. We demonstrated the relevance of this mechanism in humans by showing that pharmacological inhibition of NKCC2 was more effective in lowering blood pressure in hypertensive patients who are homozygous for UMOD promoter risk variants than in other hypertensive patients. Our findings link genetic susceptibility to hypertension and CKD to the level of uromodulin expression and uromodulin's effect on salt reabsorption in the kidney. These findings point to uromodulin as a therapeutic target for lowering blood pressure and preserving renal function.

Loss of chloride channel ClC-5 impairs endocytosis by defective trafficking of megalin and cubilin in kidney proximal tubules.

Abstract: Loss of the renal endosome-associated chloride channel, ClC-5, in Dent's disease and knockout (KO) mice strongly inhibits endocytosis of filtered proteins by kidney proximal tubular cells (PTC). The underlying mechanism remains unknown. We therefore tested whether this endocytic failure could primarily reflect a loss of reabsorption by the multiligand receptors, megalin, and cubilin, caused by a trafficking defect. Impaired protein endocytosis in PTC of ClC-5 KO mice was demonstrated by (i) a major decreased uptake of injected 125I-beta 2-microglobulin, but not of the fluid-phase tracer, FITC-dextran, (ii) reduced labeling of endosomes by injected peroxidase and for the endogenous megalin/cubilin ligands, vitamin D- and retinol-binding proteins, and (iii) urinary appearance of low-molecular-weight proteins and the selective cubilin ligand, transferrin. Contrasting with preserved mRNA levels, megalin and cubilin abundance was significantly decreased in kidney extracts of KO mice. Percoll gradients resolving early and late endosomes (Rab5a, Rab7), brush border (villin, aminopeptidase M), and a dense peak comprising lysosomes (acid hydrolases) showed a disappearance of the brush border component for megalin and cubilin in KO mice. Quantitative ultrastructural immunogold labeling confirmed the overall decrease of megalin and cubilin in PTC and their selective loss at the brush border. In contrast, total contents of the rate-limiting endocytic catalysts, Rab5a and Rab7, were unaffected. Thus, impaired protein endocytosis caused by invalidation of ClC-5 primarily reflects a trafficking defect of megalin and cubilin in PTC.