Table 1.
Summary of Involvement of ATP and ERK1/2 Signaling Pathways in Cx43 HC- or GJ-Regulated Genes.
| Cx43-independent Genes | Cx43 GJ-regulated Genes | Cx43 HC-regulated Genes | ||||
|---|---|---|---|---|---|---|
| TIMP-2 EDA-FN EDB-FN Cx45 | ERK1/2-mediated | Not ERK1/2- mediated | ATP-dependent | Not ATP-dependent | ||
| TIMP-1 TIMP-3 Cadherin-2 | FMOD | ERK1/2- mediated | Not ERK1/2- mediated | ERK1/2- mediated | Not ERK1/2- mediated | |
| MMP-1 | MMP-14 | TGFβ−1 | DCN | |||
| MMP-3 | CXCL12 | |||||
| MMP-10 | ||||||
| Collagen- type I | ||||||
| TN-C | ||||||
| α-SMA | ||||||
| NMMIIB | ||||||
| VEGF-A | ||||||
Table shows a summary of expression changes of key wound healing-associated genes whose regulation was mediated by Cx43 GJs (genes that were only responsive to Gap27 but not to TAT-Gap19) or by Cx43 HCs (genes that were responsive to both Gap27 and TAT-Gap19 treatments) in human GFBLs. These genes are further categorized based on whether or not their expression change was inhibited by apyrase (ATP-regulated genes) or ERK1/2 inhibitor (ERK1/2-mediated). Results were obtained from qPCR analysis of relative amount of mRNA in confluent GFBL-DC cultures treated with Gap27 (150 μM) or TAT-Gap19 (400 μM) with or without MEK1/2 signaling pathway inhibitor (PD184352; 10 μM), and with ATP inhibitor (apyrase; 1 U/mL) for 24 h, and show results relative to control peptide/vehicle treated samples. EDA-FN: Extra Domain A-Fibronectin; EDB-FN: Extra Domain B-Fibronectin; FMOD: Fibromodulin; TN-C: Tenascin-C; α-SMA: α-Smooth Muscle Actin; NMMIIB: Non-Muscle Myosin IIB; VEGF-A: Vascular Endothelial Growth Factor-A; DCN: Decorin.