Instructions: Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.
Input: We have previously shown that advanced glycation-endproducts (AGEs) induced NFB activation in differentiated mouse podocytes. This NFB activation may contribute to the progression of renal disease and mediation of fibrosis by various mechanisms. This study was undertaken to test whether this detrimental response may be reversed by vitamin D3 or its analogue paricalcitol.', 'Differentiated mouse podocytes were challenged with glycated bovine serum albumin (AGE-BSA), or non-glycated control BSA (in the presence or absence of various concentrations of vitamin D3 (decostriol, 1,25-dihydroxyvitamin D3)) or its active analog paricalcitol. Quantitative mRNA expressions were measured by real-time PCR, whereas protein expressions were determined by Western blotting followed by densitometry. Cytoplasmic and nuclear protein expression of the NFB subunit p65 (Rel A) were determined by Western blotting. Furthermore, the ratio of phosphorylated to non-phosphorylated IB- was measured using specific antibodies. Electrophoretic mobility shift assays and a capture ELISA assay were used to assess NFB transactivation in vitro. In addition, NFB transactivation was also monitored in HEK-NFBIA reporter cells using live cell luminometry.', 'Podocytes expressed the receptor for vitamin D. The vitamins did not suppress receptor for AGEs (RAGE) expression; instead, they rather upregulated RAGE. Although vitamin D3 and paricalcitol partly and differentially modified some of the studied parameters, both hormones inhibited AGE-BSA-induced NFB transactivation, presumably by various mechanisms including the upregulation of IB- protein, keeping NFB sequestered in an inactive state in the cytoplasm.
Output:
Does vitamin D3 Partly antagonize Advanced-Glycation Endproducts-Induced NFB Activation in Mouse Podocytes?