Nitric oxide functions in stromal cell‑derived factor‑1‑induced cytoskeleton changes and the migration of Jurkat cells

Abstract

Stromal cell-derived factor-1 (SDF-1) regulates multiple cell signal pathways in a variety of cellular functions, including cell migration, proliferation, survival and angiogenesis. SDF-1-induced chemotaxis is an important step of lymphocyte migration. However, the molecular mechanisms that modulate SDF-1-mediated lymphocyte migration are not well identified. Nitric oxide (NO) has been found to function as a signaling molecule in a number of signaling pathways, including migration. In the present study, the potential role of NO in SDF-1-induced migration and the association between NO and the cytoskeletal changes of Jurkat cells was investigated. The present study demonstrated that Jurkat cells induced the production of NO by SDF-1 stimulation, using Griess reaction method and western blot analysis, and that NO was involved in SDF-1-induced rearrangement and polymerization of the cytoskeleton, using NOS inhibitor L-NMMA. Furthermore, NO was required for the migration of Jurkat cells. The research suggested that NO signaling pathways exerted a critical role in SDF-1-induced cytoskeleton changes and the migration of Jurkat cells. This work provides insight into the migration mechanism of acute lymphoblastic leukemia and provides an effective theoretical basis for therapy strategies for acute lymphoblastic leukemia.

The Combination of Tissue-Engineered Blood Vessel Constructs and Parallel Flow Chamber Provides a Potential Alternative to In Vivo Drug Testing Models

“…It is also possible that the SDF-1 CXCR4 axis is also involved in recruiting EPCs to sites of vascular injury. This theory is supported by the findings by Luo et al, 2018 [ 42 ]. They found that NO production was induced by SDF-1, which triggers multiple signalling pathways, resulting in chemokine-induced changes of the EPC cytoskeleton leading to enhanced cell migration [ 42 ].…”

“…This theory is supported by the findings by Luo et al, 2018 [ 42 ]. They found that NO production was induced by SDF-1, which triggers multiple signalling pathways, resulting in chemokine-induced changes of the EPC cytoskeleton leading to enhanced cell migration [ 42 ]. The value of our models is that various doses/concentrations of different drugs, as well as combinations of drugs, can be tested faster than conventional models and also allows for real-time monitoring without measures such as anaesthesia being needed.…”

Cell Trafficking at the Intersection of the Tumor–Immune Compartments

“…SDF-1α induces phosphorylation of WASP and FAK, along with a few other cytoskeletal proteins ( 146 ). SDF-1-induced cell migration has been attributed to reactive oxygen species (ROS) ( 143 ) and nitric oxide (NO) ( 147 ) signaling. SDF-1-induced actin filament rearrangement is abrogated by treating cells with ROS and NO synthase inhibitors, establishing the downstream role of ROS and NO in Jurkat cell migration.…”