microRNA-126 inhibits vascular cell adhesion molecule-1 and interleukin-1beta in human dental pulp cells.

microRNA-126 inhibits vascular cell adhesion molecule-1 and interleukin-1beta in human dental pulp cells.
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DOI:
10.1002/jcla.24371
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发表时间:
2022-05
影响因子:
2.7
通讯作者:
--
中科院分区:
医学4区
文献类型:
--
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血管细胞粘附分子(VCAM-1)通过调节白细胞介素(IL)-1 β介导牙髓炎。据报道,microRNA(miR)-126在许多不同的病理生理学情况下调节VCAM-1。我们研究了炎症患者牙髓组织中miR-126和VCAM-1的变化,并使用体外培养的人牙髓细胞(hDPC)确定了miR-126在牙髓炎中的潜在作用。我们使用qRT-PCR定量测量了炎症人牙髓组织中miR-126和VCAM-1的转录,并与健康人牙髓组织中的转录进行了比较。此外,我们使用由聚乙烯亚胺(PEI)纳米颗粒递送的编码miR-126的质粒DNA(pDNA)在hDPC中转染miR-126。不可逆性牙髓炎显著降低了牙髓组织中miR-126的表达,并增加了VCAM-1的转录(p < 0.05)。编码miR-126的pDNA递送PEI纳米颗粒并有效上调hDPC中miR-126的表达(p < 0.05)。miR-126过表达可有效抑制Pg-LPS诱导的DPC中VCAM-1和IL-1β的转录和蛋白水平(p < 0.05)。 miR-126参与牙髓炎并下调DPC中的VCAM-1和IL-1β。miR-126可能是减轻牙髓炎炎症的潜在靶点。在人类牙髓组织中,不可逆性牙髓炎下调miR-126并增加VCAM-1。*p < 0.05,n = 6。
Vascular cell adhesion molecule (VCAM‐1) mediates pulpitis via regulating interleukin (IL)‐1β. microRNA (miR)‐126 was reported to regulate the VCAM‐1 under many different pathophysiological circumstances. We investigated variations of miR‐126 and VCAM‐1 in inflamed patient pulp tissues and determined potential roles of miR‐126 in pulpitis using human dental pulp cells (hDPCs) in vitro. We quantitatively measured the transcripts of miR‐126 and VCAM‐1 in inflamed human pulp tissues using qRT‐PCR and compared with those from healthy human pulp tissues. In addition, we transfected miR‐126 in hDPCs using plasmid DNA (pDNA)‐encoding miR‐126 delivered by polyethylenimine (PEI) nanoparticles. The irreversible pulpitis significantly reduced miR‐126 and increased the transcript of VCAM‐1 in pulp tissues (p < 0.05). pDNA‐encoding miR‐126 delivered PEI nanoparticles and effectively upregulated the expression of miR‐126 in hDPCs (p < 0.05). The overexpression of miR‐126 could effectively suppress the transcripts and protein levels of VCAM‐1 and IL‐1β induced by Pg‐LPS at 100ng/mL in DPCs (p < 0.05). miR‐126 is involved in pulpitis and downregulated the VCAM‐1 and IL‐1β in DPCs. miR‐126 may be a potential target to attenuate the inflammation of pulpitis. Irreversible pulpitis downregulated miR‐126 and increased VCAM‐1 in human pulpal tissues. *p < 0.05, n = 6.
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