ArticleGenes and immunity2009
Mouse interleukin-20 receptor 1a targets renal epithelial cells and is associated with renal calcium deposition.
Article in Genes and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed, 3 citations in OpenAlex.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously identified a novel transcript, mouse (m)IL-20R1a, generated by alternative splicing of the mIL-20R1 gene and studied its possible in vitro functions. However, the function of mIL-20R1a in vivo is unknown. Overexpression of mIL-20R1a in transgenic FvB/N mice resulted in the pathological change of excess calcium deposited in the kidneys. The interplay between renal epithelial cells and calcium oxalate (CaOx) was important in the crystallization involved in the formation of renal stones (nephrolithiasis). Thus, we investigated and compared the responses of mouse renal proximal (TKPTS) and collecting (M-1) tubule cell lines to CaOx with or without mIL-20R1a. The renal epithelial cell lines exposed to CaOx in the presence of mIL-20R1a showed significantly increased lactate dehydrogenase release; loss of cell viability through apoptosis; increased CaOx internalization; higher tumor necrosis factor (TNF)-alpha, MCP-1 and RANTES expression; and higher reactive oxygen species production. Interleukin-6, TNF-alpha and MCP-1 were also upregulated in the kidneys of mIL-20R1a transgenic mice. These effects of mIL-20R1a on CaOx-exposed renal epithelial cells showed that mIL-20R1a functioned as an aggravating factor in promoting calcium deposition in kidney of mice.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.