miR-188-3p targets skeletal endothelium coupling of angiogenesis and osteogenesis during ageing

A specific bone capillary subtype, namely type H vessels, with high expression of CD31 and endomucin, was shown to couple angiogenesis and osteogenesis recently. The number of type H vessels in bone tissue declines with age, and the underlying mechanism for this reduction is unclear. Here, we report...

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Published inCell death & disease Vol. 13; no. 5; pp. 494 - 13
Main Authors He, Wen-Zhen, Yang, Mi, Jiang, Yangzi, He, Chen, Sun, Yu-Chen, Liu, Ling, Huang, Mei, Jiao, Yu-Rui, Chen, Kai-Xuan, Hou, Jing, Huang, Min, Xu, Yi-Li, Feng, Xu, Liu, Ya, Guo, Qi, Peng, Hui, Huang, Yan, Su, Tian, Xiao, Ye, Li, Yusheng, Zeng, Chao, Lei, Guanghua, Luo, Xiang-Hang, Li, Chang-Jun
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 25.05.2022
Springer Nature B.V
Nature Publishing Group
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ISSN2041-4889
2041-4889
DOI10.1038/s41419-022-04902-w

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Abstract A specific bone capillary subtype, namely type H vessels, with high expression of CD31 and endomucin, was shown to couple angiogenesis and osteogenesis recently. The number of type H vessels in bone tissue declines with age, and the underlying mechanism for this reduction is unclear. Here, we report that microRNA-188-3p (miR-188-3p) involves this process. miRNA-188-3p expression is upregulated in skeletal endothelium and negatively regulates the formation of type H vessels during ageing. Mice with depletion of miR-188 showed an alleviated age-related decline in type H vessels. In contrast, endothelial-specific overexpression of miR-188-3p reduced the number of type H vessels, leading to decreased bone mass and delayed bone regeneration. Mechanistically, we found that miR-188 inhibits type H vessel formation by directly targeting integrin β3 in endothelial cells. Our findings indicate that miR-188-3p is a key regulator of type H vessel formation and may be a potential therapeutic target for preventing bone loss and accelerating bone regeneration.
AbstractList A specific bone capillary subtype, namely type H vessels, with high expression of CD31 and endomucin, was shown to couple angiogenesis and osteogenesis recently. The number of type H vessels in bone tissue declines with age, and the underlying mechanism for this reduction is unclear. Here, we report that microRNA-188-3p (miR-188-3p) involves this process. miRNA-188-3p expression is upregulated in skeletal endothelium and negatively regulates the formation of type H vessels during ageing. Mice with depletion of miR-188 showed an alleviated age-related decline in type H vessels. In contrast, endothelial-specific overexpression of miR-188-3p reduced the number of type H vessels, leading to decreased bone mass and delayed bone regeneration. Mechanistically, we found that miR-188 inhibits type H vessel formation by directly targeting integrin β3 in endothelial cells. Our findings indicate that miR-188-3p is a key regulator of type H vessel formation and may be a potential therapeutic target for preventing bone loss and accelerating bone regeneration.
A specific bone capillary subtype, namely type H vessels, with high expression of CD31 and endomucin, was shown to couple angiogenesis and osteogenesis recently. The number of type H vessels in bone tissue declines with age, and the underlying mechanism for this reduction is unclear. Here, we report that microRNA-188-3p (miR-188-3p) involves this process. miRNA-188-3p expression is upregulated in skeletal endothelium and negatively regulates the formation of type H vessels during ageing. Mice with depletion of miR-188 showed an alleviated age-related decline in type H vessels. In contrast, endothelial-specific overexpression of miR-188-3p reduced the number of type H vessels, leading to decreased bone mass and delayed bone regeneration. Mechanistically, we found that miR-188 inhibits type H vessel formation by directly targeting integrin β3 in endothelial cells. Our findings indicate that miR-188-3p is a key regulator of type H vessel formation and may be a potential therapeutic target for preventing bone loss and accelerating bone regeneration.A specific bone capillary subtype, namely type H vessels, with high expression of CD31 and endomucin, was shown to couple angiogenesis and osteogenesis recently. The number of type H vessels in bone tissue declines with age, and the underlying mechanism for this reduction is unclear. Here, we report that microRNA-188-3p (miR-188-3p) involves this process. miRNA-188-3p expression is upregulated in skeletal endothelium and negatively regulates the formation of type H vessels during ageing. Mice with depletion of miR-188 showed an alleviated age-related decline in type H vessels. In contrast, endothelial-specific overexpression of miR-188-3p reduced the number of type H vessels, leading to decreased bone mass and delayed bone regeneration. Mechanistically, we found that miR-188 inhibits type H vessel formation by directly targeting integrin β3 in endothelial cells. Our findings indicate that miR-188-3p is a key regulator of type H vessel formation and may be a potential therapeutic target for preventing bone loss and accelerating bone regeneration.
Abstract A specific bone capillary subtype, namely type H vessels, with high expression of CD31 and endomucin, was shown to couple angiogenesis and osteogenesis recently. The number of type H vessels in bone tissue declines with age, and the underlying mechanism for this reduction is unclear. Here, we report that microRNA-188-3p (miR-188-3p) involves this process. miRNA-188-3p expression is upregulated in skeletal endothelium and negatively regulates the formation of type H vessels during ageing. Mice with depletion of miR-188 showed an alleviated age-related decline in type H vessels. In contrast, endothelial-specific overexpression of miR-188-3p reduced the number of type H vessels, leading to decreased bone mass and delayed bone regeneration. Mechanistically, we found that miR-188 inhibits type H vessel formation by directly targeting integrin β3 in endothelial cells. Our findings indicate that miR-188-3p is a key regulator of type H vessel formation and may be a potential therapeutic target for preventing bone loss and accelerating bone regeneration.
ArticleNumber 494
Author Su, Tian
Liu, Ling
He, Wen-Zhen
Zeng, Chao
Huang, Yan
Yang, Mi
Lei, Guanghua
Hou, Jing
Luo, Xiang-Hang
Li, Chang-Jun
Jiao, Yu-Rui
Chen, Kai-Xuan
Xiao, Ye
Feng, Xu
Li, Yusheng
Xu, Yi-Li
Huang, Mei
He, Chen
Huang, Min
Sun, Yu-Chen
Jiang, Yangzi
Liu, Ya
Guo, Qi
Peng, Hui
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  publication-title: Cell Tissue Res
  doi: 10.1007/s00441-010-0994-4
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Snippet A specific bone capillary subtype, namely type H vessels, with high expression of CD31 and endomucin, was shown to couple angiogenesis and osteogenesis...
Abstract A specific bone capillary subtype, namely type H vessels, with high expression of CD31 and endomucin, was shown to couple angiogenesis and...
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SubjectTerms 13/31
14/19
38/39
631/80/509
64/110
64/60
692/699/2743/316/801
Aging
Aging - genetics
Angiogenesis
Animals
Antibodies
Biochemistry
Biomedical and Life Sciences
Bone growth
Bone loss
Bone mass
Cell Biology
Cell Culture
Endothelial cells
Endothelial Cells - metabolism
Endothelium
Immunology
Life Sciences
Mice
MicroRNAs
MicroRNAs - genetics
MicroRNAs - metabolism
miRNA
Neovascularization, Pathologic
Osteogenesis
Osteogenesis - genetics
Regeneration
Therapeutic targets
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Title miR-188-3p targets skeletal endothelium coupling of angiogenesis and osteogenesis during ageing
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