ArticleAmerican journal of physiology. Cell physiology2010
Vasoconstriction resulting from dynamic membrane trafficking of TRPM4 in vascular smooth muscle cells.
Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 65 citations in OpenAlex.
- TRPM4 Couples Mechanical Force to Myogenic Constriction Throughout the Resistance Vasculature.bioRxiv : the preprint server for biology · 2026Article
- The TRP channels serving as chemical-to-electrical signal converter.Physiological reviews · 2025Review
- Transient Receptor Potential Channels in Vascular Mechanotransduction.American journal of hypertension · 2025Review
- Sodium-Permeable Ion Channels TRPM4 and TRPM5 are Functional in Human Gastric Parietal Cells in Culture and Modulate the Cellular Response to Bitter-Tasting Food Constituents.Journal of agricultural and food chemistry · 2024Article
- Cholinergic stimulation stabilizes TRPM4 in the plasma membrane of cortical pyramidal neurons.Frontiers in cell and developmental biology · 2024Article
- Vasodilators mobilize SK3 channels in endothelial cells to produce arterial relaxation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Endothelial cell TRPA1 activity exacerbates cerebral hemorrhage during severe hypertension.Frontiers in molecular biosciences · 2023Article
- Article
- Mechanosensitive Angiotensin II Receptor Signaling in Pressure-Induced Vasoconstriction.Journal of the American Heart Association · 2022Article
- Pharmacological Modulation and (Patho)Physiological Roles of TRPM4 Channel-Part 2: TRPM4 in Health and Disease.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Upregulation of transient receptor potential melastatin 4 (TRPM4) in ventricular fibroblasts from heart failure patients.Pflugers Archiv : European journal of physiology · 2021Article
- Transient receptor potential channel-dependent myogenic responsiveness in small-sized resistance arteries.Journal of exercise rehabilitation · 2021Review
- Age-dependent decrease in TRPM4 channel expression but not trafficking alters urinary bladder smooth muscle contractility.Physiological reports · 2021Article
- Nitric Oxide Signals Through IRAG to Inhibit TRPM4 Channels and Dilate Cerebral Arteries.Function (Oxford, England) · 2021Article
- Obligatory role for PKCδ in PIPThe Journal of physiology · 2020Article
- TRPML1 channels initiate CaScience signaling · 2020Article
- Increased TRPM4 Activity in Cerebral Artery Myocytes Contributes to Cerebral Blood Flow Reduction After Subarachnoid Hemorrhage in Rats.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Article
- The ion channel TRPM4 in murine experimental autoimmune encephalomyelitis and in a model of glutamate-induced neuronal degeneration.Molecular brain · 2018Article
- Angiotensin II reduces the surface abundance of KThe Journal of physiology · 2017Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The melastatin (M) transient receptor potential (TRP) channel TRPM4 mediates pressure and protein kinase C (PKC)-induced smooth muscle cell depolarization and vasoconstriction of cerebral arteries. We hypothesized that PKC causes vasoconstriction by stimulating translocation of TRPM4 to the plasma membrane. Live-cell confocal imaging and fluorescence recovery after photobleaching (FRAP) analysis was performed using a green fluorescent protein (GFP)-tagged TRPM4 (TRPM4-GFP) construct expressed in A7r5 cells. The surface channel was mobile, demonstrating a FRAP time constant of 168 +/- 19 s. In addition, mobile intracellular trafficking vesicles were readily detected. Using a cell surface biotinylation assay, we showed that PKC activation with phorbol 12-myristate 13-acetate (PMA) increased (approximately 3-fold) cell surface levels of TRPM4-GFP protein in <10 min. Similarly, total internal reflection fluorescence microscopy demonstrated that stimulation of PKC activity increased (approximately 3-fold) the surface fluorescence of TRPM4-GFP in A7r5 cells and primary cerebral artery smooth muscle cells. PMA also caused an elevation of cell surface TRPM4 protein levels in intact arteries. PMA-induced translocation of TRPM4 to the plasma membrane was independent of PKCalpha and PKCbeta activity but was inhibited by blockade of PKCdelta with rottlerin. Pressure-myograph studies of intact, small interfering RNA (siRNA)-treated cerebral arteries demonstrate that PKC-induced constriction of cerebral arteries requires expression of both TRPM4 and PKCdelta. In addition, pressure-induced arterial myocyte depolarization and vasoconstriction was attenuated in arteries treated with siRNA against PKCdelta. We conclude that PKCdelta activity causes smooth muscle depolarization and vasoconstriction by increasing the number of TRPM4 channels in the sarcolemma.
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