The journal of sexual medicine · 2026
Activation of TRPV4 promotes transepithelial K+ secretion in rat vaginal epithelium.
СтатьяНазвание и аннотация: Перевод в очереди
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Zhou Yu-Yun, Sun Xin-Ni, Jiang Ping, Ye Yi-Ran, Chen Lei, Qu Su, Zhou Wen-Liang, Zhang Yi-Lin
Аннотация
BACKGROUND: Transient receptor potential vanilloid 4 (TRPV4) is a non-selective cation channel that regulates diverse biological processes, including osmoregulation, thermosensation, and ion transport. As a key component of the female reproductive tract, the vaginal epithelium plays a crucial role in maintaining luminal moisture and lubrication. However, the contribution of TRPV4 to vaginal epithelial function remains unclear.
AIM: To characterize the expression pattern of TRPV4 in vaginal epithelial cells and to elucidate its physiological role in regulating transepithelial ion transport and vaginal lubrication.
METHODS: Female SD rats were used in this study. Primary culture of rat vaginal epithelial cells was established. TRPV4 expression levels, transepithelial ion transport, and vaginal fluid secretion were measured.
OUTCOMES: The primary outcome of the study was the functional relationship between TRPV4 activation and vaginal lubrication.
RESULTS: TRPV4 was expressed in rat vaginal epithelial cells and that its activation promoted transepithelial K+ secretion across vaginal epithelium. Pharmacological blockade of large-conductance Ca2+-activated K+ channel (BKCa) but not ATP-sensitive K+ channel significantly attenuated TRPV4-mediated transepithelial K+ secretion, indicating functional coupling between TRPV4 and BKCa. In vivo studies revealed that activation of TRPV4 robustly enhanced vaginal fluid secretion in rats.
CLINICAL IMPLICATIONS: TRPV4-BKCa axis represents a potential molecular target for the treatment of female reproductive disorders characterized by vaginal dryness and impaired lubrication.
STRENGTHS AND LIMITATIONS: The combined in vitro and in vivo approaches provide mechanistic insight into TRPV4-mediated regulation of vaginal fluid secretion. However, the absence of human tissues or clinical data limits the direct translational extrapolation of these findings.
CONCLUSION: This study identifies TRPV4 as a key regulator of vaginal moistness and lubrication, providing novel insights into the physiological mechanisms governing female reproductive function and suggesting new therapeutic avenues for conditions associated with vaginal dryness.
AIM: To characterize the expression pattern of TRPV4 in vaginal epithelial cells and to elucidate its physiological role in regulating transepithelial ion transport and vaginal lubrication.
METHODS: Female SD rats were used in this study. Primary culture of rat vaginal epithelial cells was established. TRPV4 expression levels, transepithelial ion transport, and vaginal fluid secretion were measured.
OUTCOMES: The primary outcome of the study was the functional relationship between TRPV4 activation and vaginal lubrication.
RESULTS: TRPV4 was expressed in rat vaginal epithelial cells and that its activation promoted transepithelial K+ secretion across vaginal epithelium. Pharmacological blockade of large-conductance Ca2+-activated K+ channel (BKCa) but not ATP-sensitive K+ channel significantly attenuated TRPV4-mediated transepithelial K+ secretion, indicating functional coupling between TRPV4 and BKCa. In vivo studies revealed that activation of TRPV4 robustly enhanced vaginal fluid secretion in rats.
CLINICAL IMPLICATIONS: TRPV4-BKCa axis represents a potential molecular target for the treatment of female reproductive disorders characterized by vaginal dryness and impaired lubrication.
STRENGTHS AND LIMITATIONS: The combined in vitro and in vivo approaches provide mechanistic insight into TRPV4-mediated regulation of vaginal fluid secretion. However, the absence of human tissues or clinical data limits the direct translational extrapolation of these findings.
CONCLUSION: This study identifies TRPV4 as a key regulator of vaginal moistness and lubrication, providing novel insights into the physiological mechanisms governing female reproductive function and suggesting new therapeutic avenues for conditions associated with vaginal dryness.