Short Waves‐induced Enhancement of Proliferation of Human Chondrocytes: Involvement of Extracellular Signal‐regulated Map‐kinase (Erk)

Abstract

1. Short-wave diathermy (SWD) is a form of radiofrequency radiation that is used therapeutically by physiotherapists. The cellular mechanisms of SWD are unclear. The present study was performed to explore the effect of different conditions of short-wave exposure on the proliferation of cultured human chondrocytes. 2. Cells exposed to short waves once per day for seven consecutive days exhibited a significant increase in proliferation by 42% compared with the control cells. In cells that were treated with short waves twice per day for seven consecutive days, or only once on Day 1 and then examined for proliferation on Day 7, cell proliferation was greater than the control cells by 40% and 30%, respectively. 3. Given the importance of mitogen-activated protein kinases (MAPK) in the proliferation of different cell types, efforts were extended to explore the role of three major types of MAPK; that is, extracellular signal-regulated kinase (ERK), c-Jun NH(2)-terminal protein kinase (JNK) and p38. 4. It was found that the level of phosphorylated ERK (phospho-ERK 1 and ERK 2) increased significantly within 5-120 min following consecutive exposure to short waves for 7 days. Exposure to short waves failed to alter the intensity of phosphorylated JNK and p38 within 0-240 min. 5. Cells were exposed to short waves once for seven consecutive days in the presence of 0, 10 micromol/L, 20 micromol/L or 50 micromol/L PD98059 (an ERK inhibitor). PD98059 totally inhibited short waves-induced enhancement of proliferation without altering normal control viability. In the presence of short waves and PD98059, the cell viability was lower than the normal control. Together, the data suggest that short waves could increase proliferation in human chondrocytes through activation of the ERK pathway, which is also involved in maintaining normal cell proliferation under physiological conditions.

Regulation of chondrocyte proliferation through GIT1‐Rac1‐mediated ERK1/2 pathway by PDGF

“…TGFα which is involved in MEK1/2‐ERK1/2 mediated signaling pathway induced degradation of articular cartilage (Appleton et al, ). Wang et al () also found that short‐wave treatment increases chondrocyte proliferation and ERK1/2 activation, since ERK1/2 signalling was important in this process. Analysis of the extracellular matrix gene expression of aggrecan, II collagen, fibronectin, MMP‐1, MMP‐9, MMP‐13 and ADAMTS4 were all dependent on signals of ERK1/2 and p38 (Fitzgerald et al, ).…”

Berberine regulates melanin synthesis by activating PI3K/AKT, ERK and GSK3β in B16F10 melanoma cells

“…In particular, the PI3K/AKT and ERK signaling pathways are known as key mediators of α-MSH-induced melanogenesis (23)(24)(25). The GSK3β signaling pathway, which has been widely induced in the regulation of cell homeostasis due to its ability to phosphorylate a broad range of substrates, including glycogen synthase, the microtubule-associated protein τ, and β-catenin, is also known to decrease the binding of MITF to the tyrosinase promoter (26).…”

“…Berberine inhibits the signaling pathways involved in α-MSH-induced melanogenesis. Since activation of the PI3K/AKT, ERK, and GSK3β signaling pathways is associated with the inhibition of hyperpigmentation by decreasing MITF and tyrosinase activity (23)(24)(25)(26), berberine may inhibit melanin synthesis by inducing the phosphorylation of PI3K/AKT and ERK. Using the specific inhibitors, LY 294002, PD 98059 and BIO, we found that berberine inhibited induced-melanin content, MITF and tyrosinase.…”

A 1.8-GHz radiofrequency radiation induces EGF receptor clustering and phosphorylation in cultured human amniotic (FL) cells

“…For RFR, Friedman et al (2007) found that ERK, but not JNK (c-jun N-terminal kinase) or p38 MAPK, was the downstream signaling pathway components of the EGF receptor aff ected. Similarly, exposure of chondrocytes to pulsed short-wave RFR at 27.12 MHz with a mean power intensity of 15 W for 20 min could enhance cell proliferation through ERK1/2 activation, but no signifi cant JNK and p38 MAPK phosphorylation was observed (Wang et al 2007). In human neuroblastoma cells, a 900-MHz RFR, after a short exposure, also could activate ERK (Buttiglione et al 2007).…”