ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014
A molecular signature of tissues with pacemaker activity in the heart and upper urinary tract involves coexpressed hyperpolarization-activated cation and T-type Ca2+ channels.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Identifying peristaltic pacemaker cells in the upper urinary tract.The Journal of physiology · 2026Review
- In vitro generation of a ureteral organoid from pluripotent stem cells.Nature communications · 2025Article
- An evolutionarily conserved pacemaker role for HCN ion channels in smooth muscle.The Journal of physiology · 2023Article
- Understanding ureteropelvic junction obstruction: how far have we come?Frontiers in urology · 2023Review
- Innate Bacteriostatic Mechanisms Defend the Urinary Tract.Annual review of physiology · 2022Review
- Propagation of Pacemaker Activity and Peristaltic Contractions in the Mouse Renal Pelvis Rely on CaFunction (Oxford, England) · 2022Article
- Aging Changes in Bladder Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels Are Associated With Increasing Heterogeneity of Adrenergic/Mucosal Influence on Detrusor Control in the Mouse.The journals of gerontology. Series A, Biological sciences and medical sciences · 2021Article
- Identification and classification of interstitial cells in the mouse renal pelvis.The Journal of physiology · 2020Article
- Constitutively active HCN channels constrain detrusor excitability and modulate evoked contractions of human bladder.American journal of clinical and experimental urology · 2020Article
- Overactivity or blockade of transforming growth factor-β each generate a specific ureter malformation.The Journal of pathology · 2019Article
- TAF1-gene editing alters the morphology and function of the cerebellum and cerebral cortex.Neurobiology of disease · 2019Article
- The role of HCN channels in peristaltic dysfunction in human ureteral tuberculosis.International urology and nephrology · 2018Article
- Protein Kinase 2Journal of the American Society of Nephrology : JASN · 2018Article
- Interstitial cell modulation of pyeloureteric peristalsis in the mouse renal pelvis examined using FIBSEM tomography and calcium indicators.Pflugers Archiv : European journal of physiology · 2017Article
- Hyperpolarization-activated cation and T-type calcium ion channel expression in porcine and human renal pacemaker tissues.Journal of anatomy · 2016Article
- Interaction of Caveolin-3 and HCN is involved in the pathogenesis of diabetic cystopathy.Scientific reports · 2016Article
- Each niche has an actor: multiple stem cell niches in the preterm kidney.Italian journal of pediatrics · 2015Review
- Decreased expression of hyperpolarisation-activated cyclic nucleotide-gated channel 3 in Hirschsprung's disease.World journal of gastroenterology · 2015Article
- Inhibition by Benidipine of Contractility of Isolated Proximal and Distal Caprine Ureter.International journal of applied & basic medical researchArticle
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Renal pacemakers set the origin and frequency of the smooth muscle contractions that propel wastes from the kidney to the bladder. Although congenital defects impairing this peristalsis are a leading cause of pediatric renal failure, the mechanisms underlying renal pacemaker activity remain unknown. Using ratiometric optical mapping and video microscopy, we discovered that hyperpolarization-activated cation (HCN) channel block with the specific anatagonist ZD7288 (30 μm; IC50) abolished the pacemaker depolarizations that initiate murine upper urinary tract peristalsis. Optical mapping and immunohistochemistry indicate that pacemaker potentials are generated by cells expressing HCN isoform-3, and that HCN3(+) cells are coupled to definitive smooth muscle via gap junctions. Furthermore, we demonstrate that HCN3(+) cells coexpress T-type Ca(2+) (TTC) channels and that TTC channel inhibition with R(-)efonidipine or NNC55-0396 decreased contractile frequency in a dose-dependent manner. Collectively, these data demonstrate that HCN3(+)/TTC(+) cells are the pacemakers that set the origin and rate of upper urinary tract peristalsis. These results reveal a conserved mechanism controlling autorhythmicity in 2 distinct muscle types, as HCN and TTC channels also mediate cardiac pacemaker activity. Moreover, these findings have translational applications, including the development of novel diagnostics to detect fetal urinary tract motility defects prior to renal damage.-Hurtado, R., Bub, G., Herzlinger, D. A molecular signature of tissues with pacemaker activity in the heart and upper urinary tract involves coexpressed hyperpolarization-activated cation and T-type Ca(2+) channels.
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