Anoctamin 1 controls bone resorption by coupling Cl− channel activation with RANKL-RANK signaling transduction

Osteoclast over-activation leads to bone loss and chloride homeostasis is fundamental importance for osteoclast function. The calcium-activated chloride channel Anoctamin 1 (also known as TMEM16A) is an important chloride channel involved in many physiological processes. However, its role in osteocl...

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Published inNature communications Vol. 13; no. 1; pp. 2899 - 15
Main Authors Sun, Weijia, Guo, Shuai, Li, Yuheng, Li, JianWei, Liu, Caizhi, Chen, Yafei, Wang, Xuzhao, Tan, Yingjun, Tian, Hua, Wang, Cheng, Du, Ruikai, Zhong, Guohui, Shi, Sai, Ma, Biao, Qu, Chang, Fu, Jingxuan, Jin, Xiaoyan, Zhao, Dingsheng, Zhan, Yong, Ling, Shukuan, An, Hailong, Li, Yingxian
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 24.05.2022
Nature Publishing Group
Nature Portfolio
Subjects
13/1
13/109
13/89
14/19
38/61
631/337
631/80/304
631/80/86/1999
64/110
64/60
9/74
Animals
Anoctamin-1 - metabolism
Biomedical materials
Bone loss
Bone mass
Bone resorption
Bone Resorption - metabolism
Calcium chloride
Channel gating
Chloride
Chloride channels (calcium-gated)
Chloride ions
Coupling
Deletion
Female
Homeostasis
Humanities and Social Sciences
Humans
Ion channels
Mice
Mice, Inbred C57BL
multidisciplinary
NFATC Transcription Factors - metabolism
Osteoclasts - metabolism
Osteogenesis - genetics
Osteoporosis
Osteoporosis - metabolism
Ovariectomy
RANK Ligand - genetics
RANK Ligand - metabolism
Science
Science (multidisciplinary)
Signal transduction
Signaling
Therapeutic targets
TRANCE protein
Online AccessGet full text
ISSN2041-1723
2041-1723
DOI10.1038/s41467-022-30625-9

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Abstract Osteoclast over-activation leads to bone loss and chloride homeostasis is fundamental importance for osteoclast function. The calcium-activated chloride channel Anoctamin 1 (also known as TMEM16A) is an important chloride channel involved in many physiological processes. However, its role in osteoclast remains unresolved. Here, we identified the existence of Anoctamin 1 in osteoclast and show that its expression positively correlates with osteoclast activity. Osteoclast-specific Anoctamin 1 knockout mice exhibit increased bone mass and decreased bone resorption. Mechanistically, Anoctamin 1 deletion increases intracellular Cl − concentration, decreases H + secretion and reduces bone resorption. Notably, Anoctamin 1 physically interacts with RANK and this interaction is dependent upon Anoctamin 1 channel activity, jointly promoting RANKL-induced downstream signaling pathways. Anoctamin 1 protein levels are substantially increased in osteoporosis patients and this closely correlates with osteoclast activity. Finally, Anoctamin 1 deletion significantly alleviates ovariectomy induced osteoporosis. These results collectively establish Anoctamin 1 as an essential regulator in osteoclast function and suggest a potential therapeutic target for osteoporosis. Osteoclast over-activation leads to bone loss and chloride homeostasis is important for osteoclast function. Here, the authors show that Anoctamin 1 controls bone resorption by coupling Cl − channel activation with RANKL-RANK signaling transduction.
AbstractList Osteoclast over-activation leads to bone loss and chloride homeostasis is important for osteoclast function. Here, the authors show that Anoctamin 1 controls bone resorption by coupling Cl− channel activation with RANKL-RANK signaling transduction.
Osteoclast over-activation leads to bone loss and chloride homeostasis is fundamental importance for osteoclast function. The calcium-activated chloride channel Anoctamin 1 (also known as TMEM16A) is an important chloride channel involved in many physiological processes. However, its role in osteoclast remains unresolved. Here, we identified the existence of Anoctamin 1 in osteoclast and show that its expression positively correlates with osteoclast activity. Osteoclast-specific Anoctamin 1 knockout mice exhibit increased bone mass and decreased bone resorption. Mechanistically, Anoctamin 1 deletion increases intracellular Cl − concentration, decreases H + secretion and reduces bone resorption. Notably, Anoctamin 1 physically interacts with RANK and this interaction is dependent upon Anoctamin 1 channel activity, jointly promoting RANKL-induced downstream signaling pathways. Anoctamin 1 protein levels are substantially increased in osteoporosis patients and this closely correlates with osteoclast activity. Finally, Anoctamin 1 deletion significantly alleviates ovariectomy induced osteoporosis. These results collectively establish Anoctamin 1 as an essential regulator in osteoclast function and suggest a potential therapeutic target for osteoporosis.
Osteoclast over-activation leads to bone loss and chloride homeostasis is fundamental importance for osteoclast function. The calcium-activated chloride channel Anoctamin 1 (also known as TMEM16A) is an important chloride channel involved in many physiological processes. However, its role in osteoclast remains unresolved. Here, we identified the existence of Anoctamin 1 in osteoclast and show that its expression positively correlates with osteoclast activity. Osteoclast-specific Anoctamin 1 knockout mice exhibit increased bone mass and decreased bone resorption. Mechanistically, Anoctamin 1 deletion increases intracellular Cl − concentration, decreases H + secretion and reduces bone resorption. Notably, Anoctamin 1 physically interacts with RANK and this interaction is dependent upon Anoctamin 1 channel activity, jointly promoting RANKL-induced downstream signaling pathways. Anoctamin 1 protein levels are substantially increased in osteoporosis patients and this closely correlates with osteoclast activity. Finally, Anoctamin 1 deletion significantly alleviates ovariectomy induced osteoporosis. These results collectively establish Anoctamin 1 as an essential regulator in osteoclast function and suggest a potential therapeutic target for osteoporosis. Osteoclast over-activation leads to bone loss and chloride homeostasis is important for osteoclast function. Here, the authors show that Anoctamin 1 controls bone resorption by coupling Cl − channel activation with RANKL-RANK signaling transduction.
Osteoclast over-activation leads to bone loss and chloride homeostasis is fundamental importance for osteoclast function. The calcium-activated chloride channel Anoctamin 1 (also known as TMEM16A) is an important chloride channel involved in many physiological processes. However, its role in osteoclast remains unresolved. Here, we identified the existence of Anoctamin 1 in osteoclast and show that its expression positively correlates with osteoclast activity. Osteoclast-specific Anoctamin 1 knockout mice exhibit increased bone mass and decreased bone resorption. Mechanistically, Anoctamin 1 deletion increases intracellular Cl concentration, decreases H secretion and reduces bone resorption. Notably, Anoctamin 1 physically interacts with RANK and this interaction is dependent upon Anoctamin 1 channel activity, jointly promoting RANKL-induced downstream signaling pathways. Anoctamin 1 protein levels are substantially increased in osteoporosis patients and this closely correlates with osteoclast activity. Finally, Anoctamin 1 deletion significantly alleviates ovariectomy induced osteoporosis. These results collectively establish Anoctamin 1 as an essential regulator in osteoclast function and suggest a potential therapeutic target for osteoporosis.
Osteoclast over-activation leads to bone loss and chloride homeostasis is fundamental importance for osteoclast function. The calcium-activated chloride channel Anoctamin 1 (also known as TMEM16A) is an important chloride channel involved in many physiological processes. However, its role in osteoclast remains unresolved. Here, we identified the existence of Anoctamin 1 in osteoclast and show that its expression positively correlates with osteoclast activity. Osteoclast-specific Anoctamin 1 knockout mice exhibit increased bone mass and decreased bone resorption. Mechanistically, Anoctamin 1 deletion increases intracellular Cl− concentration, decreases H+ secretion and reduces bone resorption. Notably, Anoctamin 1 physically interacts with RANK and this interaction is dependent upon Anoctamin 1 channel activity, jointly promoting RANKL-induced downstream signaling pathways. Anoctamin 1 protein levels are substantially increased in osteoporosis patients and this closely correlates with osteoclast activity. Finally, Anoctamin 1 deletion significantly alleviates ovariectomy induced osteoporosis. These results collectively establish Anoctamin 1 as an essential regulator in osteoclast function and suggest a potential therapeutic target for osteoporosis.Osteoclast over-activation leads to bone loss and chloride homeostasis is important for osteoclast function. Here, the authors show that Anoctamin 1 controls bone resorption by coupling Cl− channel activation with RANKL-RANK signaling transduction.
Osteoclast over-activation leads to bone loss and chloride homeostasis is fundamental importance for osteoclast function. The calcium-activated chloride channel Anoctamin 1 (also known as TMEM16A) is an important chloride channel involved in many physiological processes. However, its role in osteoclast remains unresolved. Here, we identified the existence of Anoctamin 1 in osteoclast and show that its expression positively correlates with osteoclast activity. Osteoclast-specific Anoctamin 1 knockout mice exhibit increased bone mass and decreased bone resorption. Mechanistically, Anoctamin 1 deletion increases intracellular Cl- concentration, decreases H+ secretion and reduces bone resorption. Notably, Anoctamin 1 physically interacts with RANK and this interaction is dependent upon Anoctamin 1 channel activity, jointly promoting RANKL-induced downstream signaling pathways. Anoctamin 1 protein levels are substantially increased in osteoporosis patients and this closely correlates with osteoclast activity. Finally, Anoctamin 1 deletion significantly alleviates ovariectomy induced osteoporosis. These results collectively establish Anoctamin 1 as an essential regulator in osteoclast function and suggest a potential therapeutic target for osteoporosis.Osteoclast over-activation leads to bone loss and chloride homeostasis is fundamental importance for osteoclast function. The calcium-activated chloride channel Anoctamin 1 (also known as TMEM16A) is an important chloride channel involved in many physiological processes. However, its role in osteoclast remains unresolved. Here, we identified the existence of Anoctamin 1 in osteoclast and show that its expression positively correlates with osteoclast activity. Osteoclast-specific Anoctamin 1 knockout mice exhibit increased bone mass and decreased bone resorption. Mechanistically, Anoctamin 1 deletion increases intracellular Cl- concentration, decreases H+ secretion and reduces bone resorption. Notably, Anoctamin 1 physically interacts with RANK and this interaction is dependent upon Anoctamin 1 channel activity, jointly promoting RANKL-induced downstream signaling pathways. Anoctamin 1 protein levels are substantially increased in osteoporosis patients and this closely correlates with osteoclast activity. Finally, Anoctamin 1 deletion significantly alleviates ovariectomy induced osteoporosis. These results collectively establish Anoctamin 1 as an essential regulator in osteoclast function and suggest a potential therapeutic target for osteoporosis.
ArticleNumber 2899
Author Du, Ruikai
Shi, Sai
Fu, Jingxuan
An, Hailong
Tian, Hua
Qu, Chang
Guo, Shuai
Sun, Weijia
Zhong, Guohui
Li, JianWei
Ling, Shukuan
Chen, Yafei
Ma, Biao
Li, Yuheng
Wang, Cheng
Tan, Yingjun
Wang, Xuzhao
Jin, Xiaoyan
Zhao, Dingsheng
Zhan, Yong
Liu, Caizhi
Li, Yingxian
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/35610255$$D View this record in MEDLINE/PubMed
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Snippet Osteoclast over-activation leads to bone loss and chloride homeostasis is fundamental importance for osteoclast function. The calcium-activated chloride...
Osteoclast over-activation leads to bone loss and chloride homeostasis is important for osteoclast function. Here, the authors show that Anoctamin 1 controls...
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SubjectTerms 13/1
13/109
13/89
14/19
38/61
631/337
631/80/304
631/80/86/1999
64/110
64/60
9/74
Animals
Anoctamin-1 - metabolism
Biomedical materials
Bone loss
Bone mass
Bone resorption
Bone Resorption - metabolism
Calcium chloride
Channel gating
Chloride
Chloride channels (calcium-gated)
Chloride ions
Coupling
Deletion
Female
Homeostasis
Humanities and Social Sciences
Humans
Ion channels
Mice
Mice, Inbred C57BL
multidisciplinary
NFATC Transcription Factors - metabolism
Osteoclasts - metabolism
Osteogenesis - genetics
Osteoporosis
Osteoporosis - metabolism
Ovariectomy
RANK Ligand - genetics
RANK Ligand - metabolism
Science
Science (multidisciplinary)
Signal transduction
Signaling
Therapeutic targets
TRANCE protein
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Title Anoctamin 1 controls bone resorption by coupling Cl− channel activation with RANKL-RANK signaling transduction
URI https://link.springer.com/article/10.1038/s41467-022-30625-9
https://www.ncbi.nlm.nih.gov/pubmed/35610255
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https://pubmed.ncbi.nlm.nih.gov/PMC9130328
https://doaj.org/article/ad9a828c99b74de39cdca2c41f2000f0
Volume 13
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