Dataset Information

Deletion of Kcnj16 in Mice Does Not Alter Auditory Function.

ABSTRACT: Endolymphatic potential (EP) is the main driving force behind the sensory transduction of hearing, and K⁺ is the main charge carrier. Kir5.1 is a K⁺ transporter that plays a significant role in maintaining EP homeostasis, but the expression pattern and role of Kir5.1 (which is encoded by the Kcnj16 gene) in the mouse auditory system has remained unclear. In this study, we found that Kir5.1 was expressed in the mouse cochlea. We checked the inner ear morphology and measured auditory function in Kcnj16 ^-/- mice and found that loss of Kcnj16 did not appear to affect the development of hair cells. There was no significant difference in auditory function between Kcnj16 ^-/- mice and wild-type littermates, although the expression of Kcnma1, Kcnq4, and Kcne1 were significantly decreased in the Kcnj16 ^-/- mice. Additionally, no significant differences were found in the number or distribution of ribbon synapses between the Kcnj16 ^-/- and wild-type mice. In summary, our results suggest that the Kcnj16 gene is not essential for auditory function in mice.

SUBMITTER: Lv J

PROVIDER: S-EPMC7937937 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature

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Deletion of Kcnj16 in Mice Does Not Alter Auditory Function.

Lv Jun J Fu Xiaolong X Li Yige Y Hong Guodong G Li Peipei P Lin Jing J Xun Youfang Y Fang Lucheng L Weng Weibin W Yue Rongyu R Li Geng-Lin GL Guan Bing B Li He H Huang Yideng Y Chai Renjie R

Frontiers in cell and developmental biology 20210222

Endolymphatic potential (EP) is the main driving force behind the sensory transduction of hearing, and K+ is the main charge carrier. Kir5.1 is a K+ transporter that plays a significant role in maintaining EP homeostasis, but the expression pattern and role of Kir5.1 (which is encoded by the Kcnj16 gene) in the mouse auditory system has remained unclear. In this study, we found that Kir5.1 was expressed in the mouse cochlea. We checked the inner ear morphology and me ...[more]

PMID: 33693002

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Project description:Discrete calcium signals within the vascular endothelium decrease with age and contribute to impaired endothelial-dependent vasodilation. Calreticulin (Calr), a multifunctional calcium binding protein and endoplasmic reticulum (ER) chaperone, can mediate calcium signals and vascular function within the endothelial cells (ECs) of small resistance arteries. We found Calr protein expression significantly decreases with age in mesenteric arteries and examined the functional role of EC Calr in vasodilation and calcium mobilization in the context of aging. Third-order mesenteric arteries from mice with or without EC Calr knockdown were examined for calcium signals and constriction to phenylephrine (PE) or vasodilation to carbachol (CCh) after 75 wk of age. PE constriction in aged mice with or without EC Calr was unchanged. However, calcium signals and vasodilation to endothelial-dependent agonist carbachol were significantly impaired in aged EC Calr knockdown mice. Ex vivo incubation of arteries with the ER stress inhibitor tauroursodeoxycholic acid (TUDCA) significantly improved vasodilation in mice lacking EC Calr. Our data suggests diminished vascular Calr expression with age can contribute to the detrimental effects of aging on endothelial calcium regulation and vasodilation.NEW & NOTEWORTHY Calreticulin (Calr) is responsible for key physiological processes in endoplasmic reticulum, especially in aging tissue. In particular, endothelial Calr is crucial to vascular function. In this study, we deleted Calr from the endothelium and aged the mice up to 75 wk to examine changes in vascular function. We found two key differences: 1) calcium events in endothelium were severely diminished after muscarinic stimulation, which 2) corresponded with a dramatic decrease in muscarinic vasodilation. Remarkably, we were able to rescue the effect of Calr deletion on endothelial-dependent vasodilatory function using tauroursodeoxycholic acid (TUDCA), an inhibitor of endoplasmic reticulum stress that is currently in clinical trials.

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Deletion of Kcnj16 in Mice Does Not Alter Auditory Function.

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Deletion of <i>Kcnj16</i> in Mice Does Not Alter Auditory Function.

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