Ask about this productRelated genes to: TRPV4 antibody
- Gene:
- TRPV4 NIH gene
- Name:
- transient receptor potential cation channel subfamily V member 4
- Previous symbol:
- -
- Synonyms:
- OTRPC4, TRP12, VROAC, VRL-2, VR-OAC, CMT2C
- Chromosome:
- 12q24.11
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-29
- Date modifiied:
- 2019-04-23
Related products to: TRPV4 antibody
Related articles to: TRPV4 antibody
- The swallowing reflex is essential for the safe transfer of food and liquids from the oral cavity to the esophagus. Water is a strong stimulus for triggering this reflex, yet the molecular mechanisms underlying water-induced activation remain unclear. The aim of this study was to evaluate whether transient receptor potential vanilloid 4 (TRPV4) channels contribute to the water-evoked swallowing reflex. We applied distilled water (DW) or saline to superior laryngeal nerve (SLN)-innervated swallowing-related regions in anesthetized rats, measured swallowing reflexes and SLN activity, and conducted immunohistochemical analyses of TRPV4 expression. DW elicited more frequent swallowing and greater SLN activation than saline. TRPV4 immunoreactivity was observed in epithelial cells, taste bud-like structures, and nerve fibers within the laryngopharyngeal and laryngeal mucosa. DW application also induced c-Fos expression in the nodose-petrosal-jugular ganglionic complex, with ~ 60% of activated neurons coexpressing TRPV4. Pretreatment with the TRPV4 antagonist RN9893 significantly attenuated DW-evoked swallowing and SLN activity. These findings provide integrated physiological, pharmacological, and immunohistochemical evidence that TRPV4 channels contribute to the initiation of water-evoked swallowing reflexes. Our study provides enhanced understanding of TRPV4-mediated sensory regulation of swallowing and suggests that TRPV4 is a potential therapeutic target for oropharyngeal dysphagia. - Source: PubMed
Publication date: 2026/04/29
Hossain Mohammad ZakirAndo HiroshiRoy Rita RaniKitagawa Junichi - - Source: PubMed
Publication date: 2026/02/01
Kamo AtsukoHotta MaoTominaga MitsutoshiTakamori Kenji - The swallowing reflex is essential for the safe transfer of food and liquids from the oral cavity to the esophagus. Water is a strong stimulus for triggering this reflex, yet the molecular mechanisms underlying water-induced activation remain unclear. The aim of this study was to evaluate whether transient receptor potential vanilloid 4 (TRPV4) channels contribute to the water-evoked swallowing reflex. We applied distilled water (DW) or saline to superior laryngeal nerve (SLN)-innervated swallowing-related regions in anesthetized rats, measured swallowing reflexes and SLN activity, and conducted immunohistochemical analyses of TRPV4 expression. DW elicited more frequent swallowing and greater SLN activation than saline. TRPV4 immunoreactivity was observed in epithelial cells, taste bud-like structures, and nerve fibers within the laryngopharyngeal and laryngeal mucosa. DW stimulation also induced c-Fos expression in the nodose-petrosal-jugular ganglionic complex, with ~ 60% of activated neurons coexpressing TRPV4. Pretreatment with the TRPV4 antagonist RN9893 significantly attenuated DW-evoked swallowing and SLN activity. These findings provide integrated physiological, pharmacological, and immunohistochemical evidence that TRPV4 channels contribute as molecular sensors initiating the water-induced swallowing reflex. Our study provides enhanced understanding of TRPV4-mediated sensory regulation of swallowing and suggests that TRPV4 is a potential therapeutic target for oropharyngeal dysphagia. - Source: PubMed
Publication date: 2026/02/04
Hossain Mohammad ZakirAndo HiroshiRoy Rita RaniKitagawa Junichi - Aminoglycoside (AG) antibiotics remain essential for treating life-threatening infections; however, their clinical use is limited by irreversible ototoxicity. The mechanisms of AG entry into the cochlea and its role in cochlear degeneration remain unclear. This study identified the transient receptor potential vanilloid 4 (TRPV4) channel as a key mediator of AG trafficking and ototoxicity. In an AG-induced ototoxicity mouse model, TRPV4 pharmacological inhibition reduced cochlear AG accumulation, preserving hearing, hair cell (HC) survival, and cochlear synaptic integrity. Conversely, TRPV4 pharmacological activation accelerated cochlear AG influx, exacerbating AG-induced ototoxicity. Cochlear explant experiments showed that TRPV4 agonists and antagonists modulated Texas Red-labeled gentamicin uptake and HC survival, suggesting that TRPV4 directly contributes to the regulation of HC permeability and survival in the explant preparation. Notably, TRPV4 modulation did not compromise AG antimicrobial activity in bacterial-killing assays, uncoupling therapeutic efficacy from ototoxicity. Collectively, these findings identify TRPV4 as a molecular gateway for AG trafficking into cochleae and demonstrate that its inhibition offers a strategy to protect hearing while maintaining antimicrobial potency. Thus, targeting TRPV4 may provide a clinically translatable approach to prevent AG-induced ototoxicity without undermining their life-saving benefits. - Source: PubMed
Publication date: 2026/04/25
Kong LingshuaiKurioka TakaomiMogi SachiyoNitta YoshihiroYamamoto KengoYamashita Taku - Aspiration pneumonia (AP) is a serious complication of achalasia; however, its risk factors and mechanisms remain unclear. We aimed to identify the clinical characteristics associated with AP and explore its underlying pathophysiology. - Source: PubMed
Publication date: 2026/04/24
Inamura KazukiWada MasafumiIhara EikichiHata YoshitakaTsuru HirotakaFukuya HirokiEsaki MitsuruMinoda YosukeBai XiaopengTanaka YoshimasaChinen TakatoshiOgino HarueiOgawa Yoshihiro