A new hypothesis of sex-differences in temporomandibular disorders: Estrogen enhances hyperalgesia of inflamed TMJ through modulating voltage-gated sodium channel 1.7 in trigeminal ganglion?

Bi, Rui-Yun; Ding, Yun; Gan, Ye‐Hua

doi:10.1016/j.mehy.2014.12.010

Cited by 28 publications

(25 citation statements)

References 32 publications

(44 reference statements)

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“…Our previous study also showed that mRNA and protein expressions of trigeminal ganglionic Nav1.7 were upregulated by TMJ inflammation, whereas trigeminal ganglionic Nav1.3 was not changed and trigeminal ganglionic Nav1.8 and Nav1.9 were only slightly upregulated [20]. Based on the importance of Nav1.7 in pain perception and inflammatory pain, we hypothesized that trigeminal ganglionic Nav1.7 might be involved in estradiol-enhanced TMJ inflammatory pain as described previously in detail [21]. …”

Section: Introductionmentioning

confidence: 77%

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Estradiol upregulates voltage-gated sodium channel 1.7 in trigeminal ganglion contributing to hyperalgesia of inflamed TMJ

Meng

Zhang

et al. 2017

PLoS ONE

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BackgroundTemporomandibular disorders (TMDs) have the highest prevalence in women of reproductive age. The role of estrogen in TMDs and especially in TMDs related pain is not fully elucidated. Voltage-gated sodium channel 1.7 (Nav1.7) plays a prominent role in pain perception and Nav1.7 in trigeminal ganglion (TG) is involved in the hyperalgesia of inflamed Temporomandibular joint (TMJ). Whether estrogen could upregulate trigeminal ganglionic Nav1.7 expression to enhance hyperalgesia of inflamed TMJ remains to be explored.MethodsEstrous cycle and plasma levels of 17β-estradiol in female rats were evaluated with vaginal smear and enzyme linked immunosorbent assay, respectively. Female rats were ovariectomized and treated with 17β-estradiol at 0 μg, 20 μg and 80 μg, respectively, for 10 days. TMJ inflammation was induced using complete Freund’s adjuvant. Head withdrawal thresholds and food intake were measured to evaluate the TMJ nociceptive responses. The expression of Nav1.7 in TG was examined using real-time PCR and western blot. The activity of Nav1.7 promoter was examined using luciferase reporter assay. The locations of estrogen receptors (ERα and ERβ), the G protein coupled estrogen receptor (GPR30), and Nav1.7 in TG were examined using immunohistofluorescence.ResultsUpregulation of Nav1.7 in TG and decrease in head withdrawal threshold were observed with the highest plasma 17β-estradiol in the proestrus of female rats. Ovariectomized rats treated with 80 μg 17β-estradiol showed upregulation of Nav1.7 in TG and decrease in head withdrawal threshold as compared with that of the control or ovariectomized rats treated with 0 μg or 20 μg. Moreover, 17β-estradiol dose-dependently potentiated TMJ inflammation-induced upregulation of Nav1.7 in TG and also enhanced TMJ inflammation-induced decrease of head withdrawal threshold in ovariectomized rats. In addition, the estrogen receptor antagonist, ICI 182,780, partially blocked the 17β-estradiol effect on Nav1.7 expression and head withdrawal threshold in ovariectomized rats. ERα and ERβ, but not GPR30, were mostly co-localized with Nav1.7 in neurons in TG. In the nerve growth factor-induced and ERα-transfected PC12 cells, 17β-estradiol dose-dependently enhanced Nav1.7 promoter activity, whereas mutations of the estrogen response element at -1269/-1282 and -1214/-1227 in the promoter completely abolished its effect on the promoter activity.ConclusionEstradiol could upregulate trigeminal ganglionic Nav1.7 expression to contribute to hyperalgesia of inflamed TMJ.

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Section: Introductionmentioning

confidence: 77%

“…The estrogen–ER complex binds to ERE in the promoter region of some gene, and then modulates the levels of associated mRNA and protein [21]. The essential ERE has the consensus sequence GGTCAnnnTGACC, a 13-nucleotide segment with 10 nucleotides forming an inverted repeat [7].…”

Section: Resultsmentioning

confidence: 99%

Estradiol upregulates voltage-gated sodium channel 1.7 in trigeminal ganglion contributing to hyperalgesia of inflamed TMJ

Meng

Zhang

et al. 2017

PLoS ONE

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“…Similarly, two ERE-like sequences have been found in the promoter region of human Nav1.7 (SCN9A). Therefore, it is highly likely that estrogens regulate Nav1.7 mRNA expression [133]. It is also important to note that activation of estrogen receptor rapidly rescues the impairment of neuronal excitability through BK K+ channel-mediated mechanism in brain slices after oxygen-glucose deprivation [134], suggesting that this rapid signaling is also neuroprotective.…”

Section: Cooperation Of the Genomic And Rapid Nongenomic Actions Of Ementioning

confidence: 99%

Cooperation of Genomic and Rapid Nongenomic Actions of Estrogens in Synaptic Plasticity

Lai

Zhang

et al. 2016

Mol Neurobiol

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Neuroplasticity refers to the changes in the molecular and cellular processes of neural circuits that occur in response to environmental experiences. Clinical and experimental studies have increasingly shown that estrogens participate in the neuroplasticity involved in cognition, behavior, and memory. It is generally accepted that estrogens exert their effects through genomic actions that occur over a period of hours to days. However, emerging evidence indicates that estrogens also rapidly influence the neural circuitry through nongenomic actions. In this review, we provide an overview of the genomic and nongenomic actions of estrogens and discuss how these actions may cooperate in synaptic plasticity. We then summarize the role of epigenetic modifications, synaptic protein synthesis, and posttranslational modifications, and the splice variants of estrogen receptors in the complicated network of estrogens. The combination of genomic and nongenomic mechanisms endows estrogens with considerable diversity in modulating neural functions including synaptic plasticity.

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“…These disorders are 2-3times more frequently affect women than men, moreover the range of symptoms in women is clearly wider than in the opposite sex. [5][6][7] The most common symptoms of temporomandibular joints disorders include pain, independent or during mandibular movement and acustic signs, derange pattern and range of mandibular movement , problems with chewing foodthe . 8 However, the most common reason why patients seek help is pain of the masticatory muscles, headaches and pain in the neck.…”

Section: Introductionmentioning

confidence: 99%

Relationship of temporomandibular disorders with selected systemic diseases

Gruca¹,

Tysiąc-Miśta²,

Czelakowska³

et al. 2019

Prosthodontics

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Schorzenia skroniowo-żuchwowe (ang. temporomandibular disorders, TMD) są zespołem zaburzeń charakteryzujących się między innymi bólem mięśni w obrębie twarzy, głowy i szyi, bólami stawu skroniowo-żuchwowego (ssż), objawami akustycznymi czy też zaburzeniami toru oraz zakresu ruchów żuchwy. Zaburzenia w obrębie narządu żucia mogą w pewnym okresie życia dotyczyć nawet 50-75% populacji. Etiologia TMD nie jest do końca znana. Występowanie schorzeń jest zdeterminowane występowaniem wielu czynników, m.in. czynnikami wrodzonymi, zewnętrznymi, emocjami. Celem tego poglądowego artykułu jest zgłębienie informacji o TMD, jako schorzeniu pojawiającym się w przebiegu wielu chorób i zaburzeń stanu organizmu. Należy

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A new hypothesis of sex-differences in temporomandibular disorders: Estrogen enhances hyperalgesia of inflamed TMJ through modulating voltage-gated sodium channel 1.7 in trigeminal ganglion?

Cited by 28 publications

References 32 publications

Estradiol upregulates voltage-gated sodium channel 1.7 in trigeminal ganglion contributing to hyperalgesia of inflamed TMJ

Estradiol upregulates voltage-gated sodium channel 1.7 in trigeminal ganglion contributing to hyperalgesia of inflamed TMJ

Cooperation of Genomic and Rapid Nongenomic Actions of Estrogens in Synaptic Plasticity

Relationship of temporomandibular disorders with selected systemic diseases

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