HDAC4 was negatively correlated with Runx2 and col x (R1 = -0.576, P = 0.000; R2 = -0.382, P = 0.021).
The morphology and incidence of primary cilia on the surface of MOCC and negpc were observed by laser confocal microscope; Toluidine blue staining and sulfonyl rhodamine B Colorimetry (SRB) were used to observe the morphology and proliferation of MOCC and negpc chondrocytes; The functional maturity [alcian blue and alkaline phosphatase (ALP) staining] of chondrocytes in MOCC and negpc groups were compared by chemical staining.
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Results MOCC and negpc cells cultured in vitro were polygonal or spindle shaped, and purple metachromatic particles appeared in toluidine blue stained cells.
the reduction of primary cilia on the surface of Mo chondrocytes may lead to the decline of the proliferation, maturation and secretion of chondrocytes in the epiphyseal growth plate.
The decrease of HDAC4 may directly or indirectly lead to the up regulation of Runx2 and col X expression.
Conclusion the primary cilia on the surface of chondrocytes are closely related to the formation of mo.
The metastatic and invasive potential were analyzed by scratch method and invasive chamber method (Transwell).
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The incidence of primary cilia on the surface of MOCC cells [(25.265 ± 1.766)%] was lower than that of negpc cells [(53.943 ± 3.631)%], and the difference was statistically significant (F = 232.692, P = 0.000).
Conclusion p53 gene can inhibit the proliferation of osteosarcoma cells and reduce the possibility of migration through inositol phosphate 3 kinase / protein kinase B / mTOR signaling pathway..
Regulating HDAC4 expression is expected to be a new therapeutic target to delay and prevent endplate cartilage degeneration.
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The expression levels of AGN and col Ⅱ in degenerative group were significantly lower than those in normal group (AGN in degenerative group: 0.364 ± 0.054, AGN in normal group: 1.000 ± 0.049, t = 15.110, P = 0.000; col Ⅱ in degenerative group: 0.282 ± 0.063, col Ⅱ in normal group: 1.000 ± 0.280, t = 4.328, P = 0.012); The expression levels of Runx2, MMP-13 and col X in degenerative group were significantly higher than those in normal group (Runx2 in degenerative group: 2.676 ± 1.444, Runx2 in normal group: 1.000 ± 0.811, t = 4.480, P = 0.000; MMP-13 in degenerative group: 3.310 ± 2.207, MMP-13 in normal group: 1.000 ± 0.517, t = 5.624, P = 0.000; col X in degenerative group: 3.017 ± 1.872, col X in normal group: 1.000 ± 0.439, t = 5.789, P = 0.000).
Results when the concentration of p53 was 100 nmol / L, the scratch healing rates (%) of MG63 cell line and hFOB cell line were 22.37 ± 1.35 and 76.84 ± 0.97, respectively; The quantitative results of invasion inhibition were 417.35 ± 3.67 and 386.54 ± 2.78, respectively.
In vivo, p53 gene can effectively inhibit the cell proliferation of osteosarcoma cell line (MG63) and human normal osteoblast cell line (hfob1.19) in the range of 50 ~ 500 nmol / L.
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Results the expression level of HDAC4 in degenerative group was significantly lower than that in normal group (degenerative group: 0.324 ± 0.107, normal group: 1.000 ± 0.202, t = 9.260, P = 0.000).
By comparing the expression of histone deacetylase 4 (HDAC4) in normal and degenerative human endplate cartilage, to explore its role in the process of endplate cartilage degeneration.
Methods MOCC and negpc were cultured.
The results of Western blot and immunofluorescence were consistent with those of real time PCR.
Conclusion the expression of HDAC4 is significantly decreased in degenerative endplate cartilage.
Methods cell counting Kit (CCK-8) was used to evaluate the inhibitory effect of p53 on proliferation.
Methods 44 cases of abandoned endplate cartilage tissue were obtained, including 8 cases of cervical trauma as the normal group and 36 cases of multi-level cervical spondylotic myelopathy as the degenerative group (CDD).
The expression of HDAC4 in the normal group and degenerative group was detected by real-time quantitative polymerase chain reaction (real-time PCR), Western blot and immunofluorescence, Real time PCR was used to detect the expression of cartilage phenotype genes proteoglycan (AGN), type II collagen (Col Ⅱ), human sex determination region Y-box protein 9 (Sox9), runt related transcription factor 2 (Runx2), matrix metalloproteinase-13 (MMP-13) and type X collagen (Col x) in the two groups.
Alcian blue staining was lighter in MOCC cells and darker in negpc cells; The ALP staining area of MOCC cells [(7.387 ± 2.045) mm2] was lower than that of negpc [(14.768 ± 2.072) mm2], and the difference was statistically significant (F = 16.835, P = 0.020).
Finally, the expression of s2448p mammalian rapamycin target protein (mTOR) was detected by immunohistochemistry.
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With the extension of cell growth time, the absorbance (a) of chondrocytes in both groups increased, but MOCC cells were always lower than negpc cells.
Objective To observe the effect of p53 gene on the proliferation and migration of osteosarcoma cells and explore its possible mechanism.
The correlation between HDAC4 and cartilage phenotype genes in the degeneration group was compared.
Objective to compare the differences of primary cilia between chondrocytes of multiple osteochondroma (MOCC) and normal epiphyseal growth plate chondrocytes (negpc), and to explore the role of primary cilia on the surface of chondrocytes in multiple osteochondroma (MO).
