The thermosensitive TRPV3 channel contributes to rapid wound healing in oral epithelia

Aijima, Reona; Yamashita, Yoshio; Danjo, Atsushi; Kido, Mizuho A.; Goto, Masaaki

doi:10.1016/j.joms.2014.06.319

Cited by 20 publications

(38 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the present study, we confirmed TRPV4 protein expression by in situ hybridization, Western blotting, immunohistochemistry, and immunocytochemistry, in accord with our previous reports on TRPV4 mRNA expression in rats and mice . Antibody specificity against TRP channels has challenged many researchers, including us.…”

Section: Discussionsupporting

confidence: 91%

“…Recently, we showed that oral epithelia have thermosensitive properties mediated by TRPV3 and TRPV4 and wound‐healing processes regulated by TRPV3 . In the present study, we reveal marked TRPV4 expression in the junctional epithelium in addition to oral epithelia.…”

Section: Introductionsupporting

confidence: 68%

“…Primary cultures of oral epithelial cells were performed as previously described . Briefly, the palatal mucosa of neonatal mice (n = 8 per group) was incubated in 400 PU/mL dispase I (Godoshusei Ltd.) at 4°C overnight.…”

Section: Methodsmentioning

confidence: 99%

“…We previously reported that oral epithelia express thermosensitive transient receptor potential (TRP) channels . Activation of TRP channels allows cation influx into cells, leading to a variety of physiological or pathological consequences mediated by Ca 2+ ‐dependent processes.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Enhanced junctional epithelial permeability in TRPV4‐deficient mice

Kitsuki

Yoshimoto

Aijima

et al. 2019

J of Periodontal Research

View full text Add to dashboard Cite

Background and Objective As the interface between the oral cavity and the teeth, the junctional epithelial barrier is critical for gingival defense. The junctional epithelium is subject to mechanical stresses from biting force or external insults such as bacterial attacks, but little is known about the effects of mechanical stimuli on epithelial functions. Transient receptor potential vanilloid 4 (TRPV4) functions as a mechanosensitive nonselective cation channel. In the present study, based on marked expression of TRPV4 in the mouse junctional epithelium, we aimed to clarify the putative links between TRPV4 and junctional complexes in the junctional epithelium. Methods and Results Histological observations revealed that the junctional epithelium in TRPV4‐deficient (TRPV4−/−) mice had wider intercellular spaces than that in wild‐type (TRPV4+/+) mice. Exogenous tracer penetration in the junctional epithelium was greater in TRPV4−/− mice than in TRPV4+/+ mice, and immunoreactivity for adherens junction proteins was suppressed in TRPV4−/− mice compared with TRPV4+/+ mice. Analysis of a mouse periodontitis model showed greater bone volume loss in TRPV4−/− mice compared with TRPV4+/+ mice, indicating that an epithelial barrier deficiency in TRPV4−/− mice may be associated with periodontal complications. Conclusion The present findings identify a crucial role for TRPV4 in the formation of adherens junctions in the junctional epithelium, which could regulate its permeability. TRPV4 may be a candidate pharmacological target to combat periodontal diseases.

show abstract

Section: Discussionsupporting

confidence: 91%

Section: Introductionsupporting

confidence: 68%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Enhanced junctional epithelial permeability in TRPV4‐deficient mice

Kitsuki

Yoshimoto

Aijima

et al. 2019

J of Periodontal Research

View full text Add to dashboard Cite

show abstract

“…We used targetscan software to predict the downstream of miR‐103, and found that TRPV3 was the underlying target of miR‐103. TRPV3, a non‐selective cation channel, belongs to the Ca 2+ ‐permeant TRP channel family, and which functions in the formation of the skin barrier, hair growth, wound healing and temperature sensation . TRPV3 can be activated by warm temperatures above 33°C and natural herbs such as carvacrol and inhibited by ruthenium red.…”

Section: Introductionmentioning

confidence: 99%

MiR‐103 inhibiting cardiac hypertrophy through inactivation of myocardial cell autophagy via targeting TRPV3 channel in rat hearts

Ren

Mingyao

et al. 2019

J Cellular Molecular Medi

View full text Add to dashboard Cite

Cardiac hypertrophy is a common pathological change frequently accompanied by chronic hypertension and myocardial infarction. Nevertheless, the pathophysiological mechanisms of cardiac hypertrophy have never been elucidated. Recent studies indicated that miR‐103 expression was significantly decreased in heart failure patients. However, less is known about the role of miR‐103 in cardiac hypertrophy. The present study was designed to investigate the relationship between miR‐103 and the mechanism of pressure overload‐induced cardiac hypertrophy. TRPV 3 protein, cardiac hypertrophy marker proteins ( BNP and β‐ MHC ) and autophagy associated proteins (Beclin‐1 and LC 3‐ II ) were up‐regulated, as well as, miR‐103 expression and autophagy associated proteins (p62) were down‐regulated in cardiac hypertrophy models in vivo and in vitro respectively. Further results indicated that silencing TRPV 3 or forcing overexpression of miR‐103 could dramatically inhibit cell surface area, relative fluorescence intensity of Ca 2+ signal and the expressions of BNP , β‐ MHC , Beclin‐1 and LC 3‐ II , but promote p62 expression. Moreover, TRPV 3 protein was decreased in neonatal rat ventricular myocyte transfected with miR‐103, but increased by AMO ‐103. Co‐transfection of the miR‐103 with the luciferase reporter vector into HEK 293 cells caused a sharp decrease in luciferase activity compared with transfection of the luciferase vector alone. The miR‐103‐induced depression of luciferase activity was rescued by an AMO ‐103. These findings suggested that TRPV 3 was a direct target of miR‐103. In conclusion, miR‐103 could attenuate cardiomyocyte hypertrophy partly by reducing cardiac autophagy activity through the targeted inhibition of TRPV 3 signalling in the pressure‐overloaded rat hearts.

show abstract

Effects of Pulsed 810 nm Al‐Ga‐As Diode Laser on Wound Healing Under Immunosuppression: A Molecular Insight

et al. 2019

View full text Add to dashboard Cite

Background and Objectives Dysregulated inflammation is one of the major contributing factors for the prevalence of non‐healing chronic wound in immunosuppressed subjects. Photobiomodulation (PBM) has emerged as a potential non‐thermal, light‐based therapeutic healing intervention for the treatment of impaired wounds. Study Design/Materials and Methods The present study delineates the underlying molecular mechanisms of PBM 810 nm laser‐induced full‐thickness cutaneous wound repair in immunosuppressed rats at continuous and pulsed wave‐mode with power‐density of 40 mW/cm 2, fluence 22.6 J/cm 2 for 10 minutes daily for 7 post‐wounding days. Molecular markers were assessed using biochemical, enzyme‐linked immunosorbent assay quantification, enzyme kinetics and immunoblots analyses pertaining to inflammation, oxidative stress, cell survival, calcium signaling, and proliferation cascades. Results Results distinctly revealed that pulsed 810 nm (10 Hz) PBM potentially influenced the cell survival and proliferation signaling pathway by significantly upregulated phospho‐protein kinase B(phospho‐Akt), phospho‐extracellular‐signal‐regulated kinase 1 (ERK1), transient receptor potential vanilloid‐3 (TRPV3), Ca2+, calmodulin, transforming growth factor‐β1 (TGF‐β1), TGF‐βR3, and Na +/K +‐ATPase pump levels. PBM treatment resulted in reduction of exaggerated inflammatory responses evident by significantly repressed levels of interleukin‐1β (IL‐1β), IL‐6, cyclooxygenase 2 (COX‐2), and substance‐P receptor (SPR), as well as inhibited apoptotic cell death by decreasing p53, cytochrome C, and caspase 3 levels (P < 0.05), which, in turn, effectively augment the wound repair in immunosuppressed rats. PBM treatment also lowered 4‐hydroxynoneal (HNE) adduct level and NADP/NADPH ratio and upregulated the GRP78 expression, which might culminate into reduced oxidative stress and maintained the redox homeostasis. Conclusions Taken together, these findings would be helpful in better understanding of the molecular aspects involved in pulsed 810 nm laser‐mediated dermal wound healing in immunosuppressed rats through regulation of cell survival and proliferation via Ca2+‐calmodulin, Akt, ERK, and redox signaling. Lasers Surg. Med. © 2019 Wiley Periodicals, Inc.

show abstract

The thermosensitive TRPV3 channel contributes to rapid wound healing in oral epithelia

Cited by 20 publications

References 47 publications

Enhanced junctional epithelial permeability in TRPV4‐deficient mice

Enhanced junctional epithelial permeability in TRPV4‐deficient mice

MiR‐103 inhibiting cardiac hypertrophy through inactivation of myocardial cell autophagy via targeting TRPV3 channel in rat hearts

Effects of Pulsed 810 nm Al‐Ga‐As Diode Laser on Wound Healing Under Immunosuppression: A Molecular Insight

Contact Info

Product

Resources

About