Deciphering physiological role of the mechanosensitive TRPV4 channel in the distal nephron
Long-standing experimental evidence suggests that epithelial cells in the renal tubule are able to sense osmotic and pressure gradients caused by alterations in ultrafiltrate flow by elevating intracellular Ca(2+) concentration. These responses are viewed as critical regulators of a variety of proce...
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Published in | American journal of physiology. Renal physiology Vol. 308; no. 4; pp. F275 - F286 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
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United States
American Physiological Society
15.02.2015
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Abstract | Long-standing experimental evidence suggests that epithelial cells in the renal tubule are able to sense osmotic and pressure gradients caused by alterations in ultrafiltrate flow by elevating intracellular Ca(2+) concentration. These responses are viewed as critical regulators of a variety of processes ranging from transport of water and solutes to cellular growth and differentiation. A loss in the ability to sense mechanical stimuli has been implicated in numerous pathologies associated with systemic imbalance of electrolytes and to the development of polycystic kidney disease. The molecular mechanisms conferring mechanosensitive properties to epithelial tubular cells involve activation of transient receptor potential (TRP) channels, such as TRPV4, allowing direct Ca(2+) influx to increase intracellular Ca(2+) concentration. In this review, we critically analyze the current evidence about signaling determinants of TRPV4 activation by luminal flow in the distal nephron and discuss how dysfunction of this mechanism contributes to the progression of polycystic kidney disease. We also review the physiological relevance of TRPV4-based mechanosensitivity in controlling flow-dependent K(+) secretion in the distal renal tubule. |
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AbstractList | Long-standing experimental evidence suggests that epithelial cells in the renal tubule are able to sense osmotic and pressure gradients caused by alterations in ultrafiltrate flow by elevating intracellular Ca(2+) concentration. These responses are viewed as critical regulators of a variety of processes ranging from transport of water and solutes to cellular growth and differentiation. A loss in the ability to sense mechanical stimuli has been implicated in numerous pathologies associated with systemic imbalance of electrolytes and to the development of polycystic kidney disease. The molecular mechanisms conferring mechanosensitive properties to epithelial tubular cells involve activation of transient receptor potential (TRP) channels, such as TRPV4, allowing direct Ca(2+) influx to increase intracellular Ca(2+) concentration. In this review, we critically analyze the current evidence about signaling determinants of TRPV4 activation by luminal flow in the distal nephron and discuss how dysfunction of this mechanism contributes to the progression of polycystic kidney disease. We also review the physiological relevance of TRPV4-based mechanosensitivity in controlling flow-dependent K(+) secretion in the distal renal tubule. Long-standing experimental evidence suggests that epithelial cells in the renal tubule are able to sense osmotic and pressure gradients caused by alterations in ultrafiltrate flow by elevating intracellular Ca 2+ concentration. These responses are viewed as critical regulators of a variety of processes ranging from transport of water and solutes to cellular growth and differentiation. A loss in the ability to sense mechanical stimuli has been implicated in numerous pathologies associated with systemic imbalance of electrolytes and to the development of polycystic kidney disease. The molecular mechanisms conferring mechanosensitive properties to epithelial tubular cells involve activation of transient receptor potential (TRP) channels, such as TRPV4, allowing direct Ca 2+ influx to increase intracellular Ca 2+ concentration. In this review, we critically analyze the current evidence about signaling determinants of TRPV4 activation by luminal flow in the distal nephron and discuss how dysfunction of this mechanism contributes to the progression of polycystic kidney disease. We also review the physiological relevance of TRPV4-based mechanosensitivity in controlling flow-dependent K + secretion in the distal renal tubule. Long-standing experimental evidence suggests that epithelial cells in the renal tubule are able to sense osmotic and pressure gradients caused by alterations in ultrafiltrate flow by elevating intracellular Ca2+ concentration. These responses are viewed as critical regulators of a variety of processes ranging from transport of water and solutes to cellular growth and differentiation. A loss in the ability to sense mechanical stimuli has been implicated in numerous pathologies associated with systemic imbalance of electrolytes and to the development of polycystic kidney disease. The molecular mechanisms conferring mechanosensitive properties to epithelial tubular cells involve activation of transient receptor potential (TRP) channels, such as TRPV4, allowing direct Ca2+ influx to increase intracellular Ca2+ concentration. In this review, we critically analyze the current evidence about signaling determinants of TRPV4 activation by luminal flow in the distal nephron and discuss how dysfunction of this mechanism contributes to the progression of polycystic kidney disease. We also review the physiological relevance of TRPV4-based mechanosensitivity in controlling flow-dependent K+ secretion in the distal renal tubule. |
Author | Zaika, O O'Neil, R G Pochynyuk, O Mamenko, M Boukelmoune, N |
Author_xml | – sequence: 1 givenname: M surname: Mamenko fullname: Mamenko, M organization: Department of Integrative Biology and Pharmacology, University of Texas Health Science Center, Houston, Texas – sequence: 2 givenname: O surname: Zaika fullname: Zaika, O organization: Department of Integrative Biology and Pharmacology, University of Texas Health Science Center, Houston, Texas – sequence: 3 givenname: N surname: Boukelmoune fullname: Boukelmoune, N organization: Department of Integrative Biology and Pharmacology, University of Texas Health Science Center, Houston, Texas – sequence: 4 givenname: R G surname: O'Neil fullname: O'Neil, R G organization: Department of Integrative Biology and Pharmacology, University of Texas Health Science Center, Houston, Texas – sequence: 5 givenname: O surname: Pochynyuk fullname: Pochynyuk, O email: Oleh.M.Pochynyuk@uth.tmc.edu organization: Department of Integrative Biology and Pharmacology, University of Texas Health Science Center, Houston, Texas Oleh.M.Pochynyuk@uth.tmc.edu |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25503733$$D View this record in MEDLINE/PubMed |
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Keywords | mechanosensitive intracellular Ca2+ concentration signaling renal potassium excretion polycystic kidney disease flow sensitivity transient receptor potential cation channel subfamily V member 4 |
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SubjectTerms | Animals Calcium Calcium - metabolism Cell growth Cells Electrolytes Epithelial Cells - metabolism Homeostasis Humans Hyperkalemia - metabolism Hyperkalemia - physiopathology Kidney diseases Mechanotransduction, Cellular Nephrons - metabolism Nephrons - physiopathology Osmotic Pressure Polycystic Kidney Diseases - metabolism Polycystic Kidney Diseases - physiopathology Potassium - metabolism Pressure Reviews TRPV Cation Channels - chemistry TRPV Cation Channels - genetics TRPV Cation Channels - metabolism |
Title | Deciphering physiological role of the mechanosensitive TRPV4 channel in the distal nephron |
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