The Antagonism of Neuropeptide Y Type I Receptor (Y1R) Reserves the Viability of Bone Marrow Stromal Cells in the Milieu of Osteonecrosis of Femoral Head (ONFH)

Ko, Jih‐Yang; Wang, Feng‐Sheng; Chen, Sung-Hsiung; Wu, Re‐Wen; Hsu, Chieh-Cheng; Kuo, Sheng‐Fong

doi:10.3390/biomedicines10112942

Cited by 3 publications

(3 citation statements)

References 30 publications

(36 reference statements)

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“…The assessment of gene transcription levels was conducted employing the reverse transcription-quantitative polymerase chain reaction (RT-qPCR) assay following our previous works (Ko et al 2022a , b , 2023a , b ). Tissues were pulverized under liquid nitrogen in the absence of RNase, and total RNA was extracted using the RiboPure RNA purification kit (Thermo Fisher Scientific, Waltham, MA, USA).…”

Section: Methodsmentioning

confidence: 99%

Dickkopf-1 (DKK1) blockade mitigates osteogenesis imperfecta (OI) related bone disease

Ko,

Wang,

Lian

et al. 2024

Mol Med

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Background The current treatment of osteogenesis imperfecta (OI) is imperfect. Our study thus delves into the potential of using Dickkopf-1 antisense (DKK1-AS) to treat OI. Methods We analysed serum DKK1 levels and their correlation with lumbar spine and hip T-scores in OI patients. Comparative analyses were conducted involving bone marrow stromal cells (BMSCs) and bone tissues from wild-type mice, untreated OI mice, and OI mice treated with DKK1-ASor DKK1-sense (DKK1-S). Results Significant inverse correlations were noted between serum DKK1 levels and lumbar spine (correlation coefficient = − 0.679, p = 0.043) as well as hip T-scores (correlation coefficient = − 0.689, p = 0.042) in OI patients. DKK1-AS improved bone mineral density (p = 0.002), trabecular bone volume/total volume fraction (p < 0.001), trabecular separation (p = 0.010), trabecular thickness (p = 0.001), trabecular number (p < 0.001), and cortical thickness (p < 0.001) in OI mice. DKK1-AS enhanced the transcription of collagen 1α1, osteocalcin, runx2, and osterix in BMSC from OI mice (all p < 0.001), resulting in a higher von Kossa-stained matrix area (p < 0.001) in ex vivo osteogenesis assays. DKK1-AS also reduced osteoclast numbers (p < 0.001), increased β-catenin and T-cell factor 4 immunostaining reactivity (both p < 0.001), enhanced mineral apposition rate and bone formation rate per bone surface (both p < 0.001), and decreased osteoclast area (p < 0.001) in OI mice. DKK1-AS upregulated osteoprotegerin and downregulated nuclear factor-kappa B ligand transcription (both p < 0.001). Bone tissues from OI mice treated with DKK1-AS exhibited significantly higher breaking force compared to untreated OI mice (p < 0.001). Conclusions Our study elucidates that DKK1-AS has the capability to enhance bone mechanical properties, restore the transcription of osteogenic genes, promote osteogenesis, and inhibit osteoclastogenesis in OI mice.

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Section: Methodsmentioning

confidence: 99%

Dickkopf-1 (DKK1) blockade mitigates osteogenesis imperfecta (OI) related bone disease

Ko,

Wang,

Lian

et al. 2024

Mol Med

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“…The mRNA expression levels of the assayed genes by the study group were expressed as 2 −∆∆Ct [23,24].…”

Section: Reverse Transcription-quantitative Polymerase Chain Reaction...mentioning

confidence: 99%

“…Between-group differences were assessed by the analysis of variance test and Tukey's HSD (Honestly Significant Difference) post hoc analysis employing GraphPad Prism v5.0 (GraphPad Software Inc., San Diego, CA, USA) [23].…”

Section: Statistical Analysesmentioning

confidence: 99%

Micro Ribonucleic Acid−29a (miR−29a) Antagonist Normalizes Bone Metabolism in Osteogenesis Imperfecta (OI) Mice Model

Wang

Chen

et al. 2023

Biomedicines

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Osteogenesis imperfecta (OI) is not curative nowadays. This study tried to unriddle the therapeutic potential of micro ribonucleic acid-29a (miR-29a) antagonist in treating OI in a mouse animal model (B6C3Fe a/a-Col1a2oim/J). We showed that the expression levels of miR-29a were higher in bone tissues obtained from the OI mice than from wild-type mice demonstrated by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and in situ hybridization assay. We established lentivirus-shuttled vector expressing miR-29a antisense oligonucleotide (miR-29a-AS) and miR-29a precursors (pre-miR-29a), showing that the inferior bony architecture in micro-computed tomography and pertinent morphometric parameters could be rescued by miR-29a-AS and deteriorated by pre-miR-29a. The decreased proliferating cell nuclear antigen (PCNA), increased Dickkopf-1 (DKK1), and decreased β-catenin expression in OI mice could be accentuated by pre-miR-29a and normalized by miR-29a-AS. The decreased osteogenesis and increased osteoclastogenesis in OI mice could also be accentuated by pre-miR-29a and normalized by miR-29a-AS. miR-29a-AS did not seem to possess severe hepatic or renal toxicities.

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Cartilage-specific knockout of miRNA-128a expression normalizes the expression of circadian clock genes (CCGs) and mitigates the severity of osteoarthritis

Wang

Lian

et al. 2024

Biomedical Journal

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The Antagonism of Neuropeptide Y Type I Receptor (Y1R) Reserves the Viability of Bone Marrow Stromal Cells in the Milieu of Osteonecrosis of Femoral Head (ONFH)

Cited by 3 publications

References 30 publications

Dickkopf-1 (DKK1) blockade mitigates osteogenesis imperfecta (OI) related bone disease

Dickkopf-1 (DKK1) blockade mitigates osteogenesis imperfecta (OI) related bone disease

Micro Ribonucleic Acid−29a (miR−29a) Antagonist Normalizes Bone Metabolism in Osteogenesis Imperfecta (OI) Mice Model

Cartilage-specific knockout of miRNA-128a expression normalizes the expression of circadian clock genes (CCGs) and mitigates the severity of osteoarthritis

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