ArticlePloS one2014
Gpr48 deficiency induces polycystic kidney lesions and renal fibrosis in mice by activating Wnt signal pathway.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Review
- The Role of LGR4 (GPR48) in Normal and Cancer Processes.International journal of molecular sciences · 2021Review
- Emerging Roles for LGR4 in Organ Development, Energy Metabolism and Carcinogenesis.Frontiers in genetics · 2021Review
- R-spondin signalling is essential for the maintenance and differentiation of mouse nephron progenitors.eLife · 2020Article
- LGR4 modulates breast cancer initiation, metastasis, and cancer stem cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Identifying the localization and exploring a functional role for Gprc5c in the kidney.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Snail1 is positively correlated with atrial fibrosis in patients with atrial fibrillation and rheumatic heart disease.Experimental and therapeutic medicine · 2017Article
- Unsung renal receptors: orphan G-protein-coupled receptors play essential roles in renal development and homeostasis.Acta physiologica (Oxford, England) · 2017Review
- Dickkopf-1 has an Inhibitory Effect on Mesenchymal Stem Cells to Fibroblast Differentiation.Chinese medical journal · 2016Article
- Activation of glycogen synthase kinase 3β ameliorates diabetes-induced kidney injury.The Journal of biological chemistry · 2014Article
- Extra sensory perception: the role of Gpr receptors in the kidney.Current opinion in nephrology and hypertension · 2014Review
- Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
G protein-coupled receptor 48 (Gpr48/Lgr4) is essential to regulate the development of multiple tissues in mice. The notion that Gpr48 functions in renal development prompted us to investigate the relation between Gpr48 and renal diseases. Using a Gpr48 knockout mice model, we observed that 66.7% Gpr48 null mice developed polycystic lesions in the kidney, while no cysts were observed in the kidneys of wild-type mice. Polycystic kidney disease 1 (PKD1) and PKD2 expressions were also markedly decreased in the Gpr48 knockout mice. Abnormal expressions of exra-cellular matrix protein lead to the progression of polycystic kidney disease and the formation of renal fibrosis in the Gpr48 null mice. The expressions of several Wnt molecules and its receptors were increased and marked β-catenin nuclear accumulation was observed in the Gpr48 null mice. The inhibitors of Wnt/β-catenin signal pathway such as GSK3β and axin2 were loss of function. The Wnt/PCP signaling pathway is also activated in Gpr48 null mice. However, TGF-β expression and phosphorylated Smad2/3 levels were not altered. Collectively, our results showed that Gpr48 null mice are at a greater risk of suffering from polycystic lesions and renal fibrosis. Moreover, the formation of polycystic lesions and renal fibrosis induced by Gpr48 deficiency involves the activation of Wnt signaling pathway but not the TGF-β/Smad pathway.
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