Polyethylene glycol may be “pegylated” or “joined to another substance.” Keep reading for a Pegylated Mechano-Growth Factor research summary.
This pegylation is often considered to lessen the severity of an immune response or, as in the instance of PEG-MGF, to possibly lengthen the half-life of a molecule in the blood by decreasing its clearance in the kidneys.
PEG-MGF and Bone Marrow Stromal Cells
Studies suggest MGF may protect cells in a rat model of muscle damage by lowering inflammatory hormone expression and oxidative stress [i].
Sun et al. [ii] found similar results, suggesting that MGF may regulate muscle inflammation and enhance macrophage and neutrophil migration to the site of damage. Both investigations build on the fact that muscle damage brought on by exercise causes the production of the MGF-related growth factors IGF-1Ea and IGF-1Eb [iii].
Researchers in endocrinology worldwide have speculated that, like IGF-1, MGF may activate the insulin-like growth factor 1 receptor [iv]. Other studies have suggested activating this receptor may slow aging, boost lean body mass, and improve energy balance. PEG-MGF’s potential to mimic IGF-1’s actions may promote muscle regeneration, boost fat metabolism, and boost lean body mass.
According to the literature, MGF has been speculated to enhance mean muscle fiber size in exercise mice by 25% [v].
PEG-MGF and Heart Muscle
Studies by the University of Illinois’s bioengineering department suggest that MGF may prevent cardiac muscle cells from undergoing programmed cell death in response to hypoxia. In addition, the peptide seems to entice cardiac stem cells to the site of damage, which may aid in regeneration and repair after a heart attack.
Researchers speculated that when MGF was given to rats within eight hours of hypoxia, they appeared to have significantly reduced cell death and significantly more stem cell recruitment than controls who did not receive MGF [vi].
As suggested by the study’s principal author, Dr. Doroudian, giving MDF in the context of cardiac injury may offer the potential for targeted, long-term mitigation with the bioactive peptide.
Similar studies have suggested that MGF may reduce pathologic hypertrophy and improve ventricular function after a heart attack. PEG-MGF appeared to improve hemodynamics and reduce cardiac remodeling in the study animals compared to control rats [vii].
Similar results have been suggested when MGF was given to subjects with acute myocardial infarction; Carpenter et al. speculated that MGF might reduce cardiomyocyte damage by 35%.
PEG-MGF and Bone Formation
According to studies conducted on rabbits, scientists hypothesize that bone healing may be sped up since PEG-MGF may stimulate the growth of osteoblasts, the cells responsible for bone mineralization. Research suggests MGF appeared to accelerate recovery in rabbits, with results comparable to those found in controls six weeks after it was given. [viii].
PEG-MGF and Bone
Chondrocytes are the cells considered by scientists to be largely responsible for cartilage health and deposition, and studies suggest that MGF may increase their function. As mouse studies suggest, MGF may promote chondrocyte migration from the bone, where the cells originate, to the cartilage, where they may exert potential action.
PEG-MGF and Teeth
Studies on periodontal ligament cells cultured in the lab have suggested that PEG-MGF may increase osteogenic differentiation and MMP-1 and MMP-2 expression [ix]. These characteristics may help the ligaments that hold teeth in place to heal after trauma, which might mean not having to get rid of natural teeth. PEG-MGF has even been hypothesized to aid in the survival of surgically re-implanted teeth.
PEG-MGF and the Brain
BioMed Central’s Editorial Assistant, Alexander Walker, recently evaluated research examining the impact of elevated MGF levels on the brain and central nervous system over time. The research suggested that mice with elevated MGF levels may better maintain their cognitive abilities and peak cognitive performance far into old age.
Walker suggests that “the efficacy of MGF in the brain may be age-dependent” since earlier overexpression of MGF in the research mice appeared to have better outcomes immediately and in the long run [x].
Muscle growth factor (MGF) has also been hypothesized to lessen muscle weakness and minimize motor-neuron loss in ALS mice models [xi]. Dluzniewska et al. speculated that after hypoxic damage, MGF may be overexpressed in brain areas with the highest rates of neuron regeneration.
Despite the continuing illness process, MGF may mitigate the action of various neurological disfunctions without inducing any change in the underlying cause of the ailment by possibly delaying the death of neurons in the brain and spinal cord.
More investigation is required to explore the peptide’s potential in scientific research, and these studies must continue. Only academic and scientific institutions are allowed to use PEG-MGF peptides.
If you are a licensed professional interested in to buy peptides for your clinical studies, visit Biotech Peptides. Please note that none of the items mentioned are approved for human or animal consumption.
Laboratory research chemicals are only for in-vitro and in-lab use. Any kind of physical introduction is illegal. Only authorized academics and working professionals may make purchases. The content of this article is intended only for instructional purposes.
[i] X. Liu, Z. Zeng, L. Zhao, P. Chen, and W. Xiao, “Impaired Skeletal Muscle Regeneration Induced by Macrophage Depletion Could Be Partly Ameliorated by MGF Injection,” Front. Physiol., vol. 10, p. 601, 2019. [PubMed]
[ii] K.-T. Sun, K.-K. Cheung, S. W. N. Au, S. S. Yeung, and E. W. Yeung, “Overexpression of Mechano-Growth Factor Modulates Inflammatory Cytokine Expression and Macrophage Resolution in Skeletal Muscle Injury,” Front. Physiol., vol. 9, 2018. [PMC]
[iii] A. Philippou et al., “Expression of IGF-1 isoforms after exercise-induced muscle damage in humans: characterization of the MGF E peptide actions in vitro,” Vivo Athens Greece, vol. 23, no. 4, pp. 567–575, Aug. 2009. [PubMed]
[iv] J. A. M. J. L. Janssen, L. J. Hofland, C. J. Strasburger, E. S. R. van den Dungen, and M. Thevis, “Potency of Full- Length MGF to Induce Maximal Activation of the IGF-I R Is Similar to Recombinant Human IGF-I at High Equimolar Concentrations,” PLoS ONE, vol. 11, no. 3, Mar. 2016. [PLoS ONE]
[v] G. Goldspink, “Research on mechano growth factor: its potential for optimising physical training as well as misuse in doping,” Br. J. Sports Med., vol. 39, no. 11, pp. 787–788, Nov. 2005. [BMJ Journals]
[vi] G. Doroudian, J. Pinney, P. Ayala, T. Los, T. A. Desai, and B. Russell, “Sustained delivery of MGF peptide from microrods attracts stem cells and reduces apoptosis of myocytes,” Biomed. Microdevices, vol. 16, no. 5, pp. 705–715, Oct. 2014. [PubMed]
[vii] J. R. Peña, J. R. Pinney, P. Ayala, T. A. Desai, and P. H. Goldspink, “Localized delivery of mechano-growth factor E-domain peptide via polymeric microstructures improves cardiac function following myocardial infarction,” Biomaterials, vol. 46, pp. 26–34, Apr. 2015. [PubMed]
[viii] M. Deng et al., “Mechano growth factor E peptide promotes osteoblasts proliferation and bone-defect healing in rabbits,” Int. Orthop., vol. 35, no. 7, pp. 1099–1106, Jul. 2011. [PubMed]
[ix] J.-T. Chen, Y. Wang, Z.-F. Zhou, and K.-W. Wei, “[Mechano-growth factor regulated cyclic stretch-induced osteogenic differentiation and MMP-1, MMP-2 expression in human periodontal ligament cells by activating the MEK/ERK1/2 pathway],” Shanghai Kou Qiang Yi Xue Shanghai J. Stomatol., vol. 28, no. 1, pp. 6–12, Feb. 2019. [PubMed]
[x] A. W. graduated from the U. of L. with a Bs. in Z. in 2015 H. joined B. C. as E. A. for the L. S. department in May 2017, I. P. I. in Parasitology, entomology, and E. Biology, “Hearts and Minds of Mice and Men: Mechano Growth Factor a new tool in the battle against age-related neuron loss?,” On Biology, 20-Jul-2017. [Online]. Available: https://blogs.biomedcentral.com/on-biology/2017/07/20/hearts-minds-mice-men-mechano-growth-factor-new-tool-battle-age-related-neuron-loss/
[xi] J. Dluzniewska et al., “A strong neuroprotective effect of the autonomous C-terminal peptide of IGF-1 Ec (MGF) in brain ischemia,” FASEB J. Off. Publ. Fed. Am. Soc. Exp. Biol., vol. 19, no. 13, pp. 1896–1898, Nov. 2005. [PubMed]