Fig 1: M2 macrophage-derived CCL17 reduced apoptosis of HNPCs. (A and B) Analysis of apoptosis of HNPCs using TUNEL staining, Scale bar, 50 µm. (C) Measurement of CCL17 secretion of THP-1-derived macrophage using ELISA. (D) Measurement of CCL17 overexpression efficiency in THP-1-derived macrophage via ELISA. (E) Analysis of the expression of Bcl-2 and Bax in HNPCs via western blotting. (F and G) Analysis of apoptosis of HNPCs via TUNEL staining. All data are mean ± SD from three independent experiment with each performed in triplicate. *P<0.05 vs. Control LV medium group; **P<0.05 vs. LV-CX3CL1 medium group. HNPCs, human nucleus pulposus cells; CCL17, C-C motif chemokine ligand 17; CX3CL1, CX3C chemokine ligand 1; LV, lentivirus.
Fig 2: Model for CX3CL1/CX3CR1 axis alleviating IDD progression. HNPC-derived CX3CL1 binds to monocyte CX3CR1 that leads to monocyte migration and M2 macrophage polarization via RhoA and JAK2/STAT3 signaling, respectively. M2-like macrophage promotes the production of anti-inflammatory cytokines from HNPCs and M2 macrophage-secreted CCL17 to inhibit apoptosis of HNPCs. CX3CL1, CX3C chemokine ligand 1; CX3CR1, CX3C motif chemokine receptor 1; IDD, intervertebral disc degeneration; HNPCs, human nucleus pulposus cells; RhoA, Ras homolog family member A; CCL17, C-C motif chemokine ligand 17.
Supplier Page from Abcam for Human TARC ELISA Kit (CCL17)