Nerve injury induces concurrent up-regulation of the voltage-gated calcium channel subunit Ca<sub>v</sub> α<sub>2</sub> δ<sub>1</sub> and the extracellular matrix protein thrombospondin-4 (TSP4) in dorsal root ganglia and dorsal spinal cord, leading to the development of a neuropathic pain state.
Further, the bioinformatics analysis of the cancer genome atlas dataset suggested that there may be a positive correlation between THBS4 and KLF9 expression.
The effects of forced THBS4 knockdown and lncRNA‑THBS4‑003 knockdown in the two PCa cell lines, DU145 and PC‑3, were evaluated using cell migration and invasion assays, as well as using Western blot analysis.
In vitro cell viability, colony formation, and invasion and migration assays were performed to evaluate the effect of FGFR2-TSP4 axis on tumor cell activities.
Further, the bioinformatics analysis of the cancer genome atlas dataset suggested that there may be a positive correlation between THBS4 and KLF9 expression.
Plasma proteomic analysis showed 13 proteins increased more than 1.3 fold in the SCI patients, including proteins involved in hypercoagulability (α2-antiplasmin, fibrinogen-γ chain, thrombospondin-4), inflammation (α2-macroglobulin, complement C1s and C3), and atherosclerosis (apolipoprotein B-100).
Plasma proteomic analysis showed 13 proteins increased more than 1.3 fold in the SCI patients, including proteins involved in hypercoagulability (α2-antiplasmin, fibrinogen-γ chain, thrombospondin-4), inflammation (α2-macroglobulin, complement C1s and C3), and atherosclerosis (apolipoprotein B-100).
In previous work, we studied the role of TSP-4 in small arteries during hypertension using Ang II-treated Thrombospondin 4 knockout (Thbs4<sup>-/-</sup>) mice.
We found strong evidence for the presence of IgG isotype autoantibodies against the cartilage extracellular matrix proteins TSP-4, COMP and CLEC3A in OA.
We investigated the contributions of Ca<sub>v</sub> α<sub>2</sub> δ<sub>1</sub> subunits and TSP4 to synaptogenesis, and the pathways involved in vitro, and whether treatment with gabapentin could block this process and pain development in vivo.
This study is the first to identify THBS4 as a powerful marker for diffuse-type gastric adenocarcinomas and to provide an initial characterization of its expression in the course of this disease.
Similarly, deletion of <i>Thbs4</i> in the <i>mdx</i> mouse model of Duchenne muscular dystrophy enhances cardiomyocyte membrane instability and cardiomyopathy.
Differential expression was also highly significant (<i>P</i> < 10<sup>-20</sup>) for previously described TB markers, such as IP-10, LBP, FCG3B, and TSP4, and for many novel proteins not previously associated with TB.