TRPV4 activation in mouse submandibular gland modulates Ca<sup>2+</sup>influx and salivation

Zhang, Yan; Catalán, Marcelo A.; Melvin, James E.

doi:10.1152/ajpgi.00366.2012

Cited by 11 publications

(13 citation statements)

References 41 publications

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“…However, to our surprise, we did not detect saliva or tear secretion upon stimulation of salivary glands and LGs with a selective TRPV4 agonist alone (Supplemental Fig. 6), which is in contrast to a report by Zhang et al (30) showing that TRPV4 activation by GSK elicited saliva secretion in an ex vivo assay. Although the reason for this discrepancy is unclear, differences in experimental conditions could account in part for the different outcomes.…”

Section: Discussioncontrasting

confidence: 99%

“…Previous reports suggested that TRPV4 is involved in the regulatory volume decrease process in salivary glands and stimulates saliva secretion (29, 30). We first determined whether TRPV4 stimulation was sufficient to induce saliva and tear secretion in ex vivo and in vivo tissues from mice and found that GSK application alone did not promote fluid secretion from either SMG or LG (Supplemental Fig.…”

Section: Resultsmentioning

confidence: 99%

“…To further confirm TRPV4‐mediated cell shrinkage, we performed similar experiments in SMG cells loaded with calcein, a fluorescent dye that allows more accurate cell volume estimations (Fig. 2 F‐H ) (29, 30). In the standard sodium chloride bath solution, a significant calcein fluorescence increase (~10%; Fig.…”

Section: Resultsmentioning

confidence: 99%

“…1 B‐D ). Previous reports showed contrasting TRPV4 expression patterns in that the channel was first detected in the apical region of mouse SMG acinar cells (29) but in later studies was also found to localize in the basolateral and cytoplasmic regions (30). These results, combined with our observations, suggest that, in the absence of stimulation, TRPV4 is equally distributed between the membrane and cytoplasm of acinar cells.…”

Section: Discussionmentioning

confidence: 98%

“…TRPV4 was reported to contribute to the regulatory volume decrease mechanism in the salivary gland and to promote calcium‐dependent saliva secretion in mice, but the precise mechanism involved in this secretion was not clear (29, 30). Therefore, we investigated the possible interaction between TRPV4 and ANO1 in salivary gland acinar cells.…”

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confidence: 99%

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TRPV4 heats up ANO1‐dependent exocrine gland fluid secretion

et al. 2018

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Several ion channels and transporters regulate fluid secretion in salivary and lacrimal glands. In salivary glands, the major anion channel involved in fluid secretion is the calcium-activated chloride channel anoctamin 1 (ANO1). Several members of the transient receptor potential (TRP) channel superfamily regulate ANO1 activity. Here, we report a functional interaction between thermosensitive TRP vanilloid (TRPV)4 and ANO1 in acinar cells isolated from mouse salivary and lacrimal glands. TRPV4 activation induced chloride currents and shrinkage of acinar cells by increasing intracellular calcium concentrations. The chloride currents evoked by a TRPV4-specific activator (GSK1016790A) were identified as ANO1-mediated currents. Moreover, TRPV4 activation by an inositol 1,4,5-trisphosphate (IP)-dependent mechanism was found to contribute to the muscarinic pathway of fluid secretion. Muscarinic stimulation of saliva and tear secretion was down-regulated in both TRPV4-deficient mice and in acinar cells treated with a TRPV4-specific antagonist (HC-067047). Furthermore, the temperature dependence of muscarinic salivation was shown to depend mainly on TRPV4. Our results suggest that TRPV4 interacts with IP receptors and ANO1 to regulate the muscarinic pathway that mediates salivation and lacrimation.-Derouiche, S., Takayama, Y., Murakami, M., Tominaga, M. TRPV4 heats up ANO1-dependent exocrine gland fluid secretion.

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Section: Discussioncontrasting

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 98%

mentioning

confidence: 99%

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TRPV4 heats up ANO1‐dependent exocrine gland fluid secretion

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Immunolocalization and distribution of functional temperature-sensitive TRP channels in salivary glands

et al. 2013

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Transient receptor potential (TRP) cation channels are unique cellular sensors involved in multiple cellular functions. Their role in salivary secretion remains to be elucidated. The expression and localization of temperature-sensitive TRP channels in salivary (submandibular, sublingual and parotid) glands were analyzed by immunohistochemistry and quantitative real-time reverse transcription plus the polymerase chain reaction (RT-PCR). The effects of various TRP channel agonists on carbachol (CCh)-induced salivary secretion in the submandibular gland and on the intracellular Ca(2+) concentration ([Ca(2+)]i) in a submandibular epithelial cell line were also investigated. Immunohistochemistry revealed the expression of TRP-melastatin subfamily member 8 (TRPM8) and TRP-ankyrin subfamily member 1 (TRPA1) in myoepithelial, acinar and ductal cells in the sublingual, submandibular and parotid glands. In addition, TRP-vanilloid subfamily member 1 (TRPV1), TRPV3 and TRPV4 were also expressed in myoepithelial, acinar and ductal cells in all three types of gland. Quantitative real-time RT-PCR results demonstrated the mRNA expression of TRPV1, TRPV3, TRPV4, TRPM8 and TRPA1 in acinar and ductal cells in these salivary glands. Perfusion of the entire submandibular gland with the TRPV1 agonist capsaicin (1 μM) via the submandibular artery significantly increased CCh-induced salivation, whereas perfusion with TRPM8 and TRPA1 agonists (0.5 μM WS12 and 100 μM allyl isothiocyanate) decreased it. Application of agonists for each of the thermosensitive TRP channels increased [Ca(2+)]i in a submandibular epithelial cell line. These results indicate that temperature-sensitive TRP channels are localized and distributed in acinar, ductal and myoepithelial cells in salivary glands and that they play a functional role in the regulation and/or modulation of salivary secretion.

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Moderate High Temperature Condition Induces the Lactation Capacity of Mammary Epithelial Cells Through Control of STAT3 and STAT5 Signaling

Kobayashi

Tsugami

Matsunaga

et al. 2018

J Mammary Gland Biol Neoplasia

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In lactating mammary glands, alveolar mammary epithelial cells (MECs) synthesize and secrete milk components. MECs also form less permeable tight junctions (TJs) to prevent the leakage of milk components. During lactation, MECs are exposed to temperature changes by metabolic heat production and air ambient temperature. In this study, we investigated whether temperature changes influence milk production ability and TJ barriers in MECs by using two lactating culture models. The results showed that 39 °C treatment activated milk production and enhanced the formation of less-permeable TJs. In contrast, 41 °C treatment caused adverse effects on the TJ barrier and cell viability, although the milk production ability of MECs was temporarily up-regulated. MECs cultured at 37 °C showed relatively low milk production ability and high proliferation activity. Furthermore, we investigated three kinds of transcription factors relating to lactogenesis, signal transducer and activator of transcription 5 (STAT5), STAT3 and glucocorticoid receptor (GR). STAT5 signaling was activated at 39 and 41 °C by an increase in total STAT5. However, long-term treatment led to a decrease in total STAT5. STAT3 signaling was inactivated by high temperature treatment through a decrease in total STAT3 and inhibited phosphorylation of STAT3. GR signaling was continuously activated regardless of temperature. These results indicate that a moderate high temperature condition at 39 °C induces a high lactation capacity of MECs through control of STAT5 and STAT3 signaling. In contrast, long-term exposure at 41 °C leads to a decline in milk production capacity by inactivation of STAT5 and a decrease in the total number of MECs.

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TRPV4 activation in mouse submandibular gland modulates Ca²⁺influx and salivation

Abstract: Zhang Y, Catalán MA, Melvin JE. TRPV4 activation in mouse submandibular gland modulates Ca 2ϩ influx and salivation.

Cited by 11 publications

References 41 publications

TRPV4 heats up ANO1‐dependent exocrine gland fluid secretion

TRPV4 heats up ANO1‐dependent exocrine gland fluid secretion

Immunolocalization and distribution of functional temperature-sensitive TRP channels in salivary glands

Moderate High Temperature Condition Induces the Lactation Capacity of Mammary Epithelial Cells Through Control of STAT3 and STAT5 Signaling

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TRPV4 activation in mouse submandibular gland modulates Ca2+influx and salivation

Abstract: Zhang Y, Catalán MA, Melvin JE. TRPV4 activation in mouse submandibular gland modulates Ca 2ϩ influx and salivation.

Cited by 11 publications

References 41 publications

TRPV4 heats up ANO1‐dependent exocrine gland fluid secretion

TRPV4 heats up ANO1‐dependent exocrine gland fluid secretion

Immunolocalization and distribution of functional temperature-sensitive TRP channels in salivary glands

Moderate High Temperature Condition Induces the Lactation Capacity of Mammary Epithelial Cells Through Control of STAT3 and STAT5 Signaling

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TRPV4 activation in mouse submandibular gland modulates Ca²⁺influx and salivation