The Effect of Photobiomodulation on Human Mesenchymal Cells: A Literature Review.

Background: Mesenchymal stem cell-based therapy is known to have the potential to induce angiogenesis. However, there are still some limitations regarding their clinical application. Photomodulation/photobiomodulation is non-invasive and non-toxic phototherapy able to stimulate cell viability, proliferation, differentiation, and migration, when the right irradiation parameters are applied.

PTEN suppresses axon outgrowth by down-regulating the level of detyrosinated microtubules.

Inhibition of the phospholipid phosphatase and tumor suppressor PTEN leads to excessive polarized cell growth during directed cell migration and neurite outgrowth. These processes require the precise regulation of both the actin and microtubule cytoskeleton. While PTEN is known to regulate actin dynamics through phospholipid modulation, whether and how PTEN regulates microtubule dynamics is unknown.

Excitotoxicity induced by kainic acid provokes glycogen synthase kinase-3 truncation in the hippocampus.

In neuronal cultures, glycogen synthase kinase 3(GSK3) is truncated at the N-terminal end by calpain downstream of activated glutamate receptors. However, the in vivo biological significance of that truncation has not been explored. In an attempt to elucidate if GSK3 truncation has a pathophysiological relevance, we have used intraperitoneal injections of kainic acid (KA) in rats and intra-amygdala KA microinjections in mice as in vivo models of excitotoxicity.

Calpain regulates N-terminal interaction of GSK-3β with 14-3-3ζ, p53 and PKB but not with axin.

Calpain produces a truncation of GSK3β that removes the N-terminal inhibitory domain. Here we analyze the effect of that truncation on protein-protein interaction. We pulled down GST-tagged proteins in the presence of full length GSK-3β and calpain-cleaved GSK-3β.