Functions of the SNAI family in chondrocyte‐to‐osteocyte development

Razmara, Ehsan; Bitaraf, Amirreza; Karimi, Behrooz; Babashah, Sadegh

doi:10.1111/nyas.14668

Cited by 15 publications

(11 citation statements)

References 150 publications

(267 reference statements)

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“…Pth1r, Nkx3-4, Grem-1, Snai2, Chadl) that lead to an osteogenic lineage when suppressed (Fig. SI 5C) [41][42][43] . Overall, our results indicate that the presence of H3K9me3 does protect a subset of specific chondrogenic functional pathways, but the suppression of H3K9me3 does not significantly influence the dedifferentiation process.…”

Section: Suppressing Levels Of H3k9 Methylation Did Not Prevent Chromatin Architecture Remodeling or Dedifferentiationmentioning

confidence: 99%

Epigenetic remodeling during monolayer cell expansion reduces therapeutic potential

Scott

Casas

Schneider

et al. 2021

Preprint

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Understanding how cells remember previous mechanical environments to influence their fate, or mechanical memory, informs the design of biomaterials and therapies in medicine. Current regeneration therapies require two-dimensional (2D) cell expansion processes to achieve large cell populations critical for the repair of damaged (e.g. connective and musculoskeletal) tissues. However, the influence of mechanical memory on cell fate following expansion is unknown, and mechanisms defining how physical environments influence the therapeutic potential of cells remain poorly understood. Here, we show that the organization of histone H3 trimethylated at lysine 9 (H3K9me3) and expression of tissue-identifying genes in primary cartilage cells (chondrocytes) transferred to three-dimensional (3D) hydrogels depends on the number of previous population doublings on tissue culture plastic during 2D cell expansion. Decreased levels of H3K9me3 occupying promoters of dedifferentiation genes after the 2D culture were also retained in 3D culture. Suppression of H3K9me3 during expansion of cells isolated from a murine model similarly resulted in the loss of the chondrocyte phenotype and global remodeling of nuclear architecture. In contrast, increasing levels of H3K9me3 through inhibiting H3K9 demethylases partially rescued the chondrogenic nuclear architecture and gene expression, which has important implications for tissue repair therapies, where expansion of large numbers of phenotypically-suitable cells is required. Overall, our findings indicate mechanical memory in primary cells is encoded in the chromatin architecture, which impacts cell fate and the phenotype of expanded cells.SIGNIFICANCE STATEMENTTissue regeneration procedures, such as cartilage defect repair (e.g. Matrix-induced Autologous Chondrocyte Implantation) often require cell expansion processes to achieve sufficient cells to transplant into an in vivo environment. However, the chondrocyte cell expansion on 2D stiff substrates induces epigenetic changes that persist even when the chondrocytes are transferred to a different (e.g. 3D) or in vivo environment. Treatments to alter epigenetic gene regulation may be a viable strategy to improve existing cartilage defect repair procedures and other tissue engineering procedures that involve cell expansion.

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Section: Suppressing Levels Of H3k9 Methylation Did Not Prevent Chromatin Architecture Remodeling or Dedifferentiationmentioning

confidence: 99%

Epigenetic remodeling during monolayer cell expansion reduces therapeutic potential

Scott

Casas

Schneider

et al. 2021

Preprint

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“…In this context, long noncoding RNAs (lncRNAs) have been introduced as a novel class of molecules [7][8][9][10] that may have roles in ALL initiation, progression, and development. In fact, lncRNAs are a class of non-coding RNAs (with about 200 nucleotides in length) that can modulate target gene expression at multiple levels in pathophysiological conditions [11][12][13]. LncRNAs are of paramount importance for a broad range of cellular functions such as chromatin organization, mRNA stability, and the regulation of translation [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

“…LncRNAs are of paramount importance for a broad range of cellular functions such as chromatin organization, mRNA stability, and the regulation of translation [11][12][13]. In essence, lncRNAs contribute to various biological processes that are important in cancer biology such as the regulation of cell proliferation [14], differentiation [11], angiogenesis, apoptosis, and cell motility [11]. The aberrant expression of lncRNAs has been documented in different human diseases, particularly in cancer [10].…”

Section: Introductionmentioning

confidence: 99%

Upregulation of the long noncoding RNA GJA9-MYCBP and PVT1 is a potential diagnostic biomarker for Acute Lymphoblastic Leukemia

shahamiri

Alghasi

Saki

et al. 2023

Preprint

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Background Acute Lymphoblastic Leukemia (ALL) is the most common type of blood cancer in children. Aberrant expression of long non-coding RNAs may set stages for ALL development. LncRNAs are emerging as a novel diagnostic and prognostic biomarker for ALL. Herein, we aimed to evaluate the expression of lncRNA GJA9-MYCBP and PVT1 in blood samples of ALL and healthy individuals. Methods As a case-control study, 40 pairs of ALL and healthy individual samples were used. The expression of MYC and each candidate lncRNA was measured using quantitative real-time PCR. Any possible association between the expression of putative non-coding RNAs and clinicopathological characteristics was also evaluated. Results LncRNA GJA9-MYCBP and PVT1 were significantly upregulated in ALL samples compared with healthy ones. Similarly, mRNA levels of MYC were increased in ALL samples than control ones. Receiver operating characteristic curve analysis indicated a satisfactory diagnostic efficacy (P-value < 0.0001), suggesting that lncRNA GJA9-MYCBP and PVT1 may serve as a diagnostic biomarker for ALL. Linear regression analysis unveiled positive correlations between the expression level of MYC and lncRNA GJA9-MYCBP and PVT1 in ALL patients (P-values < 0.01). Conclusions In this study, we provided approval for the clinical diagnostic significance of lncRNA GJA9-MYCBP and PVT1that their upregulations may be a diagnostic biomarker for ALL.

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“…Among various biomarkers, non-coding RNAs, particularly microRNAs (miRNAs or miRs), have attracted much attention [10][11][12][13][14] . MiRNAs are a small noncoding RNA of 18-25 nt that functions as a gene expression regulator at the post-translational level [15,16] . In other words, miRNAs function by binding to their target mRNAs and by suppressing the protein expression [10,16] .…”

Section: Introductionmentioning

confidence: 99%

“…MiRNAs are a small noncoding RNA of 18-25 nt that functions as a gene expression regulator at the post-translational level [15,16] . In other words, miRNAs function by binding to their target mRNAs and by suppressing the protein expression [10,16] . Aberrant expression or dysregulation of miRNAs can cause malignancy in glioma cells and may gives rise to glioblastoma development [18] .…”

Section: Introductionmentioning

confidence: 99%

A Signature of Three microRNAs Is a Potential Diagnostic Biomarker for Glioblastoma

Yazdi

Zarrinpour²,

Moslemi³

et al. 2022

IBJ

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Background: Glioblastoma is the most common primary malignant neoplasm of the central nervous system. Despite progress in diagnosis and treatment, glioblastoma still has a poor prognosis. This study aimed to examine whether a signature of three candidate miRNAs (i.e. hsa-let-7c-5p, hsa-miR-206-5p, and hsa-miR-1909-5p) can be used as a diagnostic biomarker for distinguishing glioblastoma from healthy brain tissues. Methods: In this study, 50 FFPE glioblastoma tissue samples and 50 healthy tissue samples adjacent to tumor were included. The expression of each candidate miRNA (i.e. hsa-let-7c-5p, hsa-miR-206-5p, and hsa-miR-1909-5p) was measured using RT-qPCR. To show the roles of each miRNA and their biological effects on glioblastoma development and clinicopathological characteristics, in silico tools were used. ROC curves were performed to assess the diagnostic accuracy of each miRNA. Results: Based on the results, hsa-let-7c-5p and hsa-miR-206-5p were downregulated, while hsa-miR-1909-5p was upregulated in glioblastoma tumors compared to healthy samples. No association was detected between the expression of each candidate miRNA and sex. Except for hsa-let-7c-5p, other miRNAs did not correlate with age status. ROC curve analysis indicated that the signature of candidate miRNAs is a potential biomarker distinguishing between glioblastoma and healthy samples. Only hsa-miR-206-5p suggested the association with poor prognosis in glioblastoma patients. Conclusion: Our findings revealed that the signature of three miRNAs is capable of distinguishing glioblastoma tumor and healthy tissues. These results are beneficial for the clinical management of glioblastoma patients.

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Functions of the SNAI family in chondrocyte‐to‐osteocyte development

Cited by 15 publications

References 150 publications

Epigenetic remodeling during monolayer cell expansion reduces therapeutic potential

Epigenetic remodeling during monolayer cell expansion reduces therapeutic potential

Upregulation of the long noncoding RNA GJA9-MYCBP and PVT1 is a potential diagnostic biomarker for Acute Lymphoblastic Leukemia

A Signature of Three microRNAs Is a Potential Diagnostic Biomarker for Glioblastoma

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