Alterations in cell morphology involve changes in the actin cytoskeleton and play crucial roles in determining chondrocyte phenotypes. Although the effects of simvastatin (SV) have been demonstrated in various cell types, the mechanisms and effects of SV on chondrocyte differentiation and actin cytoskeletal rearrangement are still unclear. Here, we investigated the roles of actin filament rearrangement on SV-induced differentiation of rabbit articular chondrocytes. Treatment with SV caused actin remodeling in comparison with that in untreated chondrocytes, as determined by immunofluorescence staining. Moreover, treatment with cytochalasin D (CD) and jasplakinolide (JAS), which modulate actin filament formation, resulted in reorganization of the actin cytoskeleton compared with that induced by SV in chondrocytes. In addition, CD synergistically enhanced the SV-induced increase in type II collagen expression, whereas JAS dramatically inhibited SV-induced differentiation. We also found that differentiation via SV-dependent actin cytoskeleton changes was regulated by the extracellular signal-regulated kinase (ERK)-1/2 and p38 kinase pathways. These results demonstrated that actin cytoskeletal rearrangement by SV regulated type II collagen expression and suggested that ERK-1/2 and p38 kinase pathways may play important roles in SV-induced type II collagen expression by altering actin cytoskeletal reorganization in rabbit articular chondrocytes.

译文

细胞形态的改变涉及肌动蛋白细胞骨架的改变,并在确定软骨细胞表型中起关键作用。尽管辛伐他汀 (SV) 的作用已在各种细胞类型中得到证实,但SV对软骨细胞分化和肌动蛋白细胞骨架重排的机制和作用仍不清楚。在这里,我们研究了肌动蛋白丝重排在SV诱导的兔关节软骨细胞分化中的作用。通过免疫荧光染色确定,与未处理的软骨细胞相比,SV治疗引起肌动蛋白重塑。此外,与SV诱导的软骨细胞相比,调节肌动蛋白丝形成的细胞松弛素D (CD) 和jasplakinolide (JAS) 治疗可导致肌动蛋白细胞骨架的重组。此外,CD协同增强SV诱导的II型胶原表达的增加,而JAS显着抑制SV诱导的分化。我们还发现,通过SV依赖性肌动蛋白细胞骨架变化的分化受细胞外信号调节激酶 (ERK)-1/2和p38激酶途径的调节。这些结果表明,SV引起的肌动蛋白细胞骨架重排调节了II型胶原的表达,并表明ERK-1/2和p38激酶途径可能通过改变兔关节软骨细胞的肌动蛋白细胞骨架重组在SV诱导的II型胶原表达中起重要作用。

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