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RNASeq-based identification of extracellular matrix components impacted by FasL deficiency in osteoblasts

ABSTRACT: Osteoblasts and osteoclasts are two critical cell populations in bone remodelling. FasL is known from osteoblast-induced osteoclast apoptosis. Notably, FasL deficient (gld) mice display increased bone mass pointing to non-apoptotic functions of FasL. Some key extracellular matrix associated molecules, such as osteoprotegerin, osteocalcin, osteopontin and alkaline phosphatase were reported to be affected by FasL deficiency in osteoblasts but a complex insight has been missing. To fill this gap and provide a robust dataset, gld calva-derived cells were differentiated along with controls and subjected to RNASequencing. The analysis revealed statistically significant changes in expression of 1,710 genes. 15 % (263) out of them were associated with the extracellular matrix. This applied for the collagen components, but also non-collagenous proteoglycans including versican and aggrecan. This report provides enrichment analysis of statistically significant expression changes in calva-derived osteoblastic cells with focus on extracellular matrix components. The dataset further provides a solid background for further functional analyses revealing the exact mechanisms behind and consequences of such dysregulations in pathophysiology.

ORGANISM(S): Mus musculus

PROVIDER: GSE250608 | GEO | 2025/10/16

REPOSITORIES: GEO

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Project description:Arterial smooth muscle cells (ASMCs) undergo phenotypic changes during development and pathological processes in vivo and during cell culture in vitro. Our previous studies demonstrated that retrovirally-mediated expression of the versican V3 splice variant (V3) that lacks glycosaminoglycan chains by ASMCs retards cell proliferation and migration in vitro and reduces neointimal thickening, macrophage and lipid accumulation in animal models of vascular injury and atherosclerosis. However, the molecular pathways induced by V3 expression that are responsible for these changes are not yet clear. In the present study, we employed a microarray approach to examine how expression of V3 induced changes in gene expression and the molecular pathways in ASMCs. We found that forced expression of V3 by ASMCs affected expression of 521 genes by more than 1.5 fold. Gene ontology (GO) analysis shows that components of extracellular matrix were the most significantly affected by V3 expression, indicating that V3 expression elicits profound remodeling of extracellular matrix. In addition, genes regulating the formation of the cytoskeleton which also serve as markers of contractile smooth muscle cells were significantly upregulated. On the other hand, components of the complement system, chemokines, chemokine receptors, and transcription factors crucial for regulating inflammatory processes were among the genes most downregulated. Consistently, we found that the level of myocardin, a key transcription factor promoting contractile ASMC phenotype, was greatly increased while proinflammatory transcription factors NFkappaB1 and C/EBPβ were significantly attenuated in V3-expressing SMCs. Such results indicate that V3 expression reprograms ASMC into differentiated and anti-inflammatory phenotypes. Overall, these findings demonstrate that expression of V3 reprograms ASMCs promoting anti-inflammatory and differentiated smooth muscle cell phenotypes potentially by altering cell-ECM interaction and focal adhesion signaling pathways. Fischer rat ASMCs were transduced with either a retroviral vector expressing the Versican V3 splice variant (LV3SN) or an empty control vector (LXSN) in three independent experiments. In the first experiment, V3 and control transductions were performed with four technical replicates. In the subsequent two experiments, individual transductions were done for the V3 or control treatments. For data analysis, the technical replicates from the first experiment were averaged, and then data from the three experiments was evaluated in a paired manner.

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RNASeq-based identification of extracellular matrix components impacted by FasL deficiency in osteoblasts

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