Understanding hormone and hormone therapies' impact on the auditory system

Williamson, Tanika T.; Liu, Hanjun; Pineros, Jennifer; Ding, Bo; Frisina, Robert D.

doi:10.1002/jnr.24588

Cited by 10 publications

(7 citation statements)

References 82 publications

(112 reference statements)

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“…Given this neuroprotective role, it is perhaps unsurprising that there is a wealth of literature that estrogen, the classical estrogen receptors (ERs), and the estrogen-related receptors (ERRs) play a critical role in maintaining auditory function (Charitidi, Meltser, Meltser, Tahera, & Canlon, 2009;Delhez, Lefebvre, Lefebvre, Pequeux, Malgrange, & Delacroix, 2020;Hultcrantz, Simonoska, Simonoska, & Stenberg, 2006;Shuster, Depireux, Depireux, Mong, & Hertzano, 2019;Williamson, Zhu, Zhu, Pineros, Ding, & Frisina, 2020). Despite this, our understanding of the modes of action of estrogen in the cochlea are far from clear.…”

Section: Estrogen-far More Than a Sex Hormonementioning

confidence: 99%

Age‐related hearing loss: Why we need to think about sex as a biological variable

Nolan

2020

J of Neuroscience Research

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It has long been known that age‐related hearing loss (ARHL) is more common, more severe, and with an earlier onset in men compared to women. Even in the absence of confounding factors such as noise exposure, these sexdifferences in susceptibility to ARHL remain. In the last decade, insight into the pleiotrophic nature by which estrogen signaling can impact multiple signaling mechanisms to mediate downstream changes in gene expression and/or elicit rapid changes in cellular function has rapidly gathered pace, and a role for estrogen signaling in the biological pathways that confer neuroprotection is becoming undeniable. Here I review the evidence why we need to consider sex as a biological variable (SABV) when investigating the etiology of ARHL. Loss of auditory function with aging is frequency‐specific and modulated by SABV. Evidence also suggests that differences in cochlear physiology between women and men are already present from birth. Understanding the molecular basis of these sex differences in ARHL will accelerate the development of precision medicine therapies for ARHL.

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Section: Estrogen-far More Than a Sex Hormonementioning

confidence: 99%

Age‐related hearing loss: Why we need to think about sex as a biological variable

Nolan

2020

J of Neuroscience Research

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“…Hearing impairment includes both transient partial conductive hearing loss [118] and bilateral SNHL due to mutations in POU3F4, which cause X-linked sensorineural deafness DFN3 [119]. In 2017, Muus et al, performed an auditory study to evaluate the prevalence, type, and severity of hearing impairment in children with untreated GH deficiency, finding that 83% of young patients presented with conductive, mixed or SNHL with a predisposition to be bilateral [120,121].…”

Section: Human Hearing Loss Syndromes and Involvement Of Ghmentioning

confidence: 99%

Insulin-like Growth Factor 1 Signaling in Mammalian Hearing

García-Mato

Cervantes

Murillo-Cuesta

et al. 2021

Genes

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Insulin-like growth factor 1 (IGF-1) is a peptide hormone belonging to the insulin family of proteins. Almost all of the biological effects of IGF-1 are mediated through binding to its high-affinity tyrosine kinase receptor, (IGF1R), a transmembrane receptor belonging to the insulin receptor family. Factors, receptors and IGF-binding proteins form the IGF system, which has multiple roles in mammalian development, adult tissue homeostasis, and aging. Consequently, mutations in genes of the IGF system, including downstream intracellular targets, underlie multiple common pathologies and are associated with multiple rare human diseases. Here we review the contribution of the IGF system to our understanding of the molecular and genetic basis of human hearing loss by describing, (i) the expression patterns of the IGF system in the mammalian inner ear; (ii) downstream signaling of IGF-1 in the hearing organ; (iii) mouse mutations in the IGF system, including upstream regulators and downstream targets of IGF-1 that inform cochlear pathophysiology; and (iv) human mutations in these genes causing hearing loss.

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“…There are gender differences in the damage of presbycusis, with men developing presbycusis earlier than women (Helzner et al 2005;Park et al 2016), and estrogen (E2) replacement therapy can delay presbycusis (Hederstierna et al 2007;Williamson et al 2020). Some studies have shown that E2 is related to apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Estrogen inhibits apoptosis of pericytes in the cochlea stria vascularis through downregulating TMEM16A

Zhang

Chen

Feng

et al. 2020

Preprint

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Background: Currently, the specific mechanism of estrogen (E2) in protecting presbycusis is not clear. This study aimed to investigate whether E2 could affect the apoptosis of capillary pericytes (PCs) of cochlear stria vascularis (SV) in aged C57BL/6J mice by regulating transmembrane member 16A (TMEM16A), such that it plays a protective role in presbycusis.Methods: The model of C57BL/6J ovariectomized mice was established, and E2 was administered for 2 months. The hearing threshold was measured by auditory brainstem response (ABR). The changes in the cochlea were measured using hematoxylin-eosin (HE) and electron microscopy. qRT-PCR was used to examine the expression of TMEM16A and apoptosis-related protein mRNA. The PCs were cultured in vitro, and the cell senescence model was established by the continuous passage method. TMEM16A expression was assessed using immunofluorescence. Flow cytometry was performed to explore the apoptosis rate.Results: The results of animal experiments showed that E2 intervention could reduce hearing loss and improve the atrophy of cochlear SV, loss of PC chromatin organelles, cytoplasmic swelling and nuclear porosity in aged mice. E2 also decreased the mRNA expression of TMEM16A, Caspase-3 and Bax in cochlear SV of aged mice and upregulated the expression of Bcl-2 mRNA. Cellular experiments showed that E2 could downregulate the expression of TMEM16A, and E2 or T16Ainh-A01(a specific blocker of TMEM16A) could reduce the apoptosis rate of PCs in aged mice.Conclusions: E2 may inhibit the apoptosis of PCs through downregulating the expression of TMEM16A, which plays a protective role in presbycusis. This study may provide a novel potential treatment and prevention method for presbycusis.

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Understanding hormone and hormone therapies' impact on the auditory system

Cited by 10 publications

References 82 publications

Age‐related hearing loss: Why we need to think about sex as a biological variable

Age‐related hearing loss: Why we need to think about sex as a biological variable

Insulin-like Growth Factor 1 Signaling in Mammalian Hearing

Estrogen inhibits apoptosis of pericytes in the cochlea stria vascularis through downregulating TMEM16A

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