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A critical role of the KCa3.1 channel in mechanical stretch‐induced proliferation of rat bone marrow‐derived mesenchymal stem cells
A critical role of the KCa3.1 channel in mechanical stretch‐induced proliferation of rat bone marrow‐derived mesenchymal stem cells
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A critical role of the KCa3.1 channel in mechanical stretch‐induced proliferation of rat bone marrow‐derived mesenchymal stem cells
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A critical role of the KCa3.1 channel in mechanical stretch‐induced proliferation of rat bone marrow‐derived mesenchymal stem cells
A critical role of the KCa3.1 channel in mechanical stretch‐induced proliferation of rat bone marrow‐derived mesenchymal stem cells

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A critical role of the KCa3.1 channel in mechanical stretch‐induced proliferation of rat bone marrow‐derived mesenchymal stem cells
A critical role of the KCa3.1 channel in mechanical stretch‐induced proliferation of rat bone marrow‐derived mesenchymal stem cells
Journal Article

A critical role of the KCa3.1 channel in mechanical stretch‐induced proliferation of rat bone marrow‐derived mesenchymal stem cells

2020
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Overview
Mechanical stimulation is an important factor regulating mesenchymal stem cell (MSC) functions such as proliferation. The Ca2+‐activated K+ channel, KCa3.1, is critically engaged in MSC proliferation but its role in mechanical regulation of MSC proliferation remains unknown. Here, we examined the KCa3.1 channel expression and its role in rat bone marrow‐derived MSC (BMSC) proliferation in response to mechanical stretch. Application of mechanical stretch stimulated BMSC proliferation via promoting cell cycle progression. Such mechanical stimulation up‐regulated the KCa3.1 channel expression and pharmacological or genetic inhibition of the KCa3.1 channel strongly suppressed stretch‐induced increase in cell proliferation and cell cycle progression. These results support that the KCa3.1 channel plays an important role in transducing mechanical forces to MSC proliferation. Our finding provides new mechanistic insights into how mechanical stimuli regulate MSC proliferation and also a viable bioengineering approach to improve MSC proliferation.