ArticleInternational urology and nephrology2019
Mitochondrial TRPC3 promotes cell proliferation by regulating the mitochondrial calcium and metabolism in renal polycystin-2 knockdown cells.
Article in International urology and nephrology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- A Millimeter-Scale Implantable Magneto-Mechano-Electric Transducer Based on BTO Piezoelectric Ceramics for Remote Wireless Electrical Stimulation of Injured Sciatic Nerves.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Role of Mitochondria in Polycystic Kidney Disease.International journal of molecular sciences · 2026Review
- TRPC Channels in the Physiology and Pathophysiology of the Renal Tubular System: What Do We Know?International journal of molecular sciences · 2022Review
- Overexpression of DJ-1 alleviates autosomal dominant polycystic kidney disease by regulating cell proliferation, apoptosis, and mitochondrial metabolismAnnals of translational medicine · 2020Article
- Role of Transient Receptor Potential Canonical Channel 6 (TRPC6) in Diabetic Kidney Disease by Regulating Podocyte Actin Cytoskeleton Rearrangement.Journal of diabetes research · 2020Review
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Authors and funding
6 authors at 2 institutions in 1 country.
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Abstract
purposePrevious studies indicate that autosomal dominant polycystic kidney disease (ADPKD) cells exhibited dysregulated calcium homeostasis and enhanced cell proliferation. TRPC3 has been shown to function in the modulation of calcium and sodium entry, but whether TRPC3 plays a role in cellular abnormalities of ADPKD cells has not been defined.
methodsHuman conditionally immortalized proximal tubular epithelial cells and mouse IMCD3 cells were used with polycystin-2 (PC2, TRPP2) knockdown. Cell proliferation assay was used to detect the cell proliferations upon different treatments. QRT-PCR and western blotting were used to measure the expression profiles of TRPP2 and other proteins. High-resolution respirometry, enzymic activities and ROS levels were detected to reflect the mitochondrial functions. Calcium and sodium uptakes were measured using Fura2-AM and SBFI dyes.
resultsWe showed that PC2 knockdown promoted cell proliferation, ROS productions and ERK phosphorylation, compared with negative control. Meanwhile, we demonstrated that receptor-operated calcium entry (ROCE) exhibited less reductions compared with store-operated calcium entry (SOCE) upon PC2 knockdown. Inhibition of ROCE and SOCE by specific inhibitors partially reversed the enhanced cell proliferation, ROS productions and ERK phosphorylation induced by PC2 knockdown. Moreover, TRPC3 upregulation was observed upon PC2 knockdown, which acted as both SOC and ROC, promoting cation entry, cell proliferation and ERK phosphorylation. Furthermore, we showed that mitochondrial located TRPC3 was upregulated and modulating mitochondrial calcium uptake, thus promoting the ROS productions in the presence of PC2 knockdown.
conclusionsWe demonstrated that TRPC3 upregulation upon PC2 knockdown aggravated the mitochondrial abnormalities and cell proliferation by modulating mitochondrial calcium uptake. Targeting TRPC3 might be a promising target for ADPKD treatment.
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