Evidence map›Paper›PMID 39182017›Full record

ArticleBMC musculoskeletal disorders2024

Loss of BACH1 improves osteogenic differentiation in glucocorticoid-induced hBMSCs through restoring autophagy.

ShuYing Xiao, GuoJuan Li, MeiHua Tan, Wen Liu, WenJin Li

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC musculoskeletal disorders, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

ShuYing XiaoDepartment of Endocrinology, The Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, NO. 336, Dongfeng South Road, Zhuhui District, Hengyang, Hunan Province, 421002, China.
GuoJuan LiDepartment of Endocrinology, The Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, NO. 336, Dongfeng South Road, Zhuhui District, Hengyang, Hunan Province, 421002, China.
MeiHua TanDepartment of Endocrinology, The Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, NO. 336, Dongfeng South Road, Zhuhui District, Hengyang, Hunan Province, 421002, China.
Wen LiuDepartment of Endocrinology, The Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, NO. 336, Dongfeng South Road, Zhuhui District, Hengyang, Hunan Province, 421002, China.
WenJin LiDepartment of Nutrition, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, China. 278244750@qq.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlucocorticoid-induced osteoporosis (GIOP) is the most common type of secondary osteoporosis. Recently, autophagy has been found to be related with the development of various diseases, including osteoporosis and osteoblast differentiation regulations. BTB and CNC homology 1 (BACH1) was a previously confirmed regulator for osteoblast differentiation, but whether it's could involve in glucocorticoid-induced human bone mesenchymal stem cells (hBMSCs) differentiation and autophagy regulation remain not been elucidated.

methodshBMSCs were identified by flow cytometry method, and its differentiation ability were measured by ARS staining, oil O red, and Alcian blue staining assays. Gene and proteins were quantified via qRT-PCR and western blot assays, respectively. Autophagy activity was determined using immunofluorescence. ChIP and dual luciferase assay validated the molecular interactions.

resultsThe data revealed that isolated hBMSCs exhibited positive of CD29/CD44 and negative CD45/CD34. Moreover, BACH1 was abated gradually during osteoblast differentiation of hBMSCs, while dexamethasone (Dex) treatment led to BACH1 upregulation. Loss of BACH1 improved osteoblast differentiation and activated autophagy activity in Dex-challenged hBMSCs. Autophagy-related proteins (ATG3, ATG4, ATG5, ATG7, ATG12) were repressed after Dex treatment, while ATG3, ATG7 and BECN1 could be elevated by BACH1 knockdown, especially ATG7. Moreover, BACH1 could interact ATG7 promoter region to inhibit its transcription. Co-inhibition of ATG7 greatly overturned the protective roles of BACH1 loss on osteoblast differentiation and autophagy in Dex-induced hBMSCs.

conclusionTaken together, our results demonstrated that silencing of BACH1 mitigated Dex-triggered osteogenic differentiation inhibition by transcriptionally activating ATG7-mediated autophagy, suggesting that BACH1 may be a therapeutic target for GIOP treatment.

Indexed as

AutophagyBasic-Leucine Zipper Transcription FactorsCell DifferentiationDexamethasoneGlucocorticoidsMesenchymal Stem CellsOsteoblastsOsteogenesisCells, CulturedHumansOsteoporosisBACH1 protein, humanBasic-Leucine Zipper Transcription FactorsDexamethasoneGlucocorticoidsATG7AutophagyBACH1Glucocorticoid-induced osteoporosisOsteoblast differentiation

Identifiers

PMID39182017
PMCPMC11344390

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.