PTD-DBM – 5MG

PTD-DBM

The PTD-DBM peptide, which stands for Protein Transduction Domain-fused Dishevelled Binding Motif peptide, has been explored to induce follicle growth. The PTD is a small motif of amino acids that potentially enables the peptide to enter cells, and DBM is a domain sequence known to bind Dishevelled (Dvl) proteins that are important elements of Wnt/β-catenin signaling cascade. Researchers have speculated that PTD-DBM might inhibit the interaction between CXXC5 and Dishevelled (Dvl) proteins, which in turn could result in upregulation of Wnt/β-catenin signaling. Such a disruption is suggested to potentially promote β-catenin activity by studies. That enhanced activity was found to stimulate hair follicle growth and trigger the anagen phase, or growth phase, of the follicle in mice models. Specifically, combined exposure to PTD-DBM and alleged Wnt3a or valproic acid (VPA) activators of the Wnt/β-catenin pathway showed an apparent synergistic effect. With the up-regulation of β-catenin, alkaline phosphatase (ALP) and PCNA, respectively this was hypothesized from. These markers are tightly linked with cell proliferation, which is a measure of follicle health.

The PTD-DBM peptide seems to induce the Wnt signaling pathway in a complex network of proteins which can be potentially significant for ruling cell growth, mobility and differentiation throughout embryonic development as well as tissue homeostasis. It is also found to be important in processes like cell fate determination and it seems to have a role in follicle development and cell regeneration as well. It could activate stem cells located in hair follicles which cause hair to grow again and new follicles to sprout. The peptide could also improved blood microcirculation that is thought to enhance nutrient and oxygen delivery to follicles increasing the speed of growth.

The study suggests that Prostaglandin D2 (PGD2) may trigger hair loss from an investigation of the biological mechanisms associated with hair loss and a screen for potential exposures to compounds structurally similar to PTD-DBM. It is said to do this by upregulating activity of CXXC5, a negative modulator of the critical Wnt/β-catenin signaling pathway that has been implicated in hair follicle growth and recovery. Specific protein Dishevelled (Dvl) suppresses this pathway by interacting with CXXC5, and this suppression. may cause alopecia. The hypothesis is that PGD2 might act through the BMP signaling pathway to augment levels of CXXC5, a protein known to be involved in the regression of hair follicles during catagen. Mechanistically, the activation of Wnt/β-catenin signaling by PGD2 is inhibited due to this upregulation of CXXC5, which may consequently blunt follicle growth in contrast, sc -PTD-DBM, predicted to disrupt binding of CXXC5 with Dvl, seem to exert rescue activity on Wnt/β-catenin pathway and in turn possibly stimulates hair growth effects. This repair was supported by data from murine model experiments in which the gene for CXXC5 had been knocked out, or the animals were treated with PTD-DBM, indicating that inhibiting CXXC5 may have offset hair loss induced by PGD2. Moreover, the study also indicates that CXXC5 level is increased by DHT, another important factor in androgenic alopecia-induced hair loss, via activation of the PGD2-dependent pathways. This implies an intricate crosstalk involving DHT and PGD2 might cooperatively inhibit hair growth concomitant with a fine-tuning alteration of signaling pathways associated with CXXC5. Interestingly, the study suggests that dual inhibition targeting CXXC5 and a critical enzyme of the β-catenin degradation complex, Glycogen Synthase Kinase-3 beta (GSK-3β), may offer an effective strategy to enhance hair growth, rather than inhibiting the individual components.

Subsequent experiments have attempted to unravel the basis of its ability to inhibit CXXC5-Dvl protein-protein interaction. This is presumably mediated through sequestration of PTD-DBM to the PDZ domain of Dvl, and thereby perhaps release of the suppressive action of CXXC5 on Wnt/β‐catenin signalling. In addition, murine study also supported the possibility of hair induction and potentially WIHN by PTD-DBM as demonstrated with the experimental observation described above. This is where the process of wound formation gets blurred and new hair follicles are formed. Collectively, these findings indicate that PTD-DBM not only induces the anagen phase of the hair cycle but also plays a role in inducing de novo formation of follicles following skin damage.

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