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2021•Journal of Biochemical and Molecular ToxicologyRequires access

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Abstract

SNGH5 and TGFBR3 messenger RNA were downregulated while miR-181a-5p was upregulated in osteoarthritis tissues and models. Knockdown of SNGH5 impeded chondrocytes proliferation, while accelerated the apoptosis. However, miR-181a-5p had opposite effects. TGFBR3 was identified as a target gene of miR-181a-5p, which could be indirectly suppressed by SNGH5 knockdown. Taken together, downregulation of SNGH5 could inhibit the proliferation abilities of chondrocytes and facilitate apoptosis via regulating the miR-181a-5p/TGFBR3 axis

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What this paper is about

SNGH5 and TGFBR3 messenger RNA were downregulated while miR-181a-5p was upregulated in osteoarthritis tissues and models. Knockdown of SNGH5 impeded chondrocytes proliferation, while accelerated the apoptosis. However, miR-181a-5p had opposite effects. TGFBR3 was identified as a target gene of miR-181a-5p, which could be indirectly suppressed by SNGH5 knockdown. Taken together, downregulation of SNGH5 could inhibit the proliferation abilities of chondrocytes and facilitate apoptosis via regulating the miR-181a-5p/TGFBR3 axis

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Available abstract

SNGH5 and TGFBR3 messenger RNA were downregulated while miR-181a-5p was upregulated in osteoarthritis tissues and models. Knockdown of SNGH5 impeded chondrocytes proliferation, while accelerated the apoptosis. However, miR-181a-5p had opposite effects. TGFBR3 was identified as a target gene of miR-181a-5p, which could be indirectly suppressed by SNGH5 knockdown. Taken together, downregulation of SNGH5 could inhibit the proliferation abilities of chondrocytes and facilitate apoptosis via regulating the miR-181a-5p/TGFBR3 axis

Key concepts: Gene knockdown, Downregulation and upregulation, Apoptosis, Messenger RNA, Cell biology, Chemistry, microRNA, Cell growth

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