Journal
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
Volume 282, Issue 1, Pages C84-C93Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpcell.2002.282.1.C84
Keywords
P2 purinergic receptor; cervix; epithelium; paracellular permeability; transport
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Funding
- NIA NIH HHS [AG-15955] Funding Source: Medline
- NICHD NIH HHS [HD-29924, HD-00977] Funding Source: Medline
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [K08HD000977, R29HD029924] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG015955, R55AG015955] Funding Source: NIH RePORTER
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Micromolar concentrations of ATP stimulate biphasic change in transepithelial conductance across CaSki cultures on filters, an acute transient increase (phase I response; triggered by P2Y(2) receptor and mediated by calcium mobilization-dependent cell volume decrease) followed by a slower decrease in permeability (phase II response). Phase II response is mediated by augmented calcium influx and protein kinase C-dependent increase in tight junctional resistance. The objective of the study was to determine the role of P2X(4) receptor as a mediator of phase II response. Human cervical epithelial cells express P2X(4) receptor mRNA (1.4-, 2.2-, and 4.4-kb isoforms by Northern blot analysis) and P2X(4) protein. Depletion of vitamin A reversibly downregulated P2X(4) receptor mRNA and protein and ATP-induced calcium influx. Depletion of vitamin A abrogated phase II response, and the effect could be partially reversed only with retinoic acid receptor (RAR)-selective retinoids but not retinoid X receptor (RXR) agonists. Depletion of vitamin A also abrogated protein kinase C increase in tight junctional resistance, and the effect could not be reversed with retinoids. Depletion of vitamin A also abrogated phase I increase in permeability and reversibly downregulated P2Y(2) receptor mRNA and ATP-induced calcium mobilization. However, in contrast to phase II response, both RAR and RXR agonists could fully reverse those effects. These results suggest that phase II response is mediated by a P2X(4) receptor mechanism.
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