Copper Peptide Chelator GHK
Resets Emphysema COPD Genes to Health
This information is for the use of medical researchers and persons interested in health sciences. It must be emphasized that GHK and other copper binding peptides have not been tested on human emphysema and COPD and are not approved for such uses.
Emphysema and attendant lung disease is the 2rd leading cause of death in the world. It is a deadly and painful disease of the lungs that causes difficulty in breathing. In people with emphysema, the tissues necessary to support the physical shape and function of the lungs are destroyed. Emphysema is most often caused by tobacco smoking and long-term exposure to air pollution. Emphysema is also a component of normal aging. As the lungs get older, the elastic properties decrease, and the tensions that develop can result in areas of emphysema.
In the study below, it was found that GHK, at a very low concentration (10 nanomolar) reversed the effects of emphysema on the genes of affected fibroblast cells from the patients. GHK shut down tissue destructive genes and increased genes that control wound repair and tissue remodeling.
Persons with severe emphysema use air inhalation systems that pump misty, water-filled air in and out of the lungs. Often steroids are added to the solution to suppress the lung inflammation, but while this provides short-term help, it also inhibits lung repair. In theory, GHK could be infused into the blood stream of patients to repair the lung tissue. In our wound healing studies we found that GHK-copper induced accelerated systemic healing through rats, mice , and pigs. Or it could be added to the misting solution or used in combination of a carrier like DMSO along with GHK in the misting solution. DMSO and GHK or GHK-copper always worked well together on wound healing.
The full article is available at no cost at www.genomemedicine.com/content/4/8/67.
Next-generation personalized drug discovery: the tripeptide GHK hits center stage in chronic obstructive pulmonary disease.
Meiners S, Eickelberg O. Genome Med. 2012 Sep 21;4(8):70. ABSTRACT Chronic lung diseases (CLDs), including chronic obstructive pulmonary disease (COPD), are the second leading cause of death worldwide. The first report of database-driven drug discovery in carefully phenotyped COPD specimens has now been published in Genome Medicine, combining gene expression data in defined emphysematous areas with connectivity-map-based compound discovery. This joint effort may lead the way to novel and potentially more efficient concepts of personalized drug discovery for COPD in particular, and CLD in general.
A gene expression signature of emphysema-related lung destruction and its reversal by the tripeptide GHK.
Campbell JD, McDonough JE, Zeskind JE, Hackett TL, Pechkovsky DV, Brandsma CA, Suzuki M, Gosselink JV, Liu G, Alekseyev YO, Xiao J, Zhang X, Hayashi S, Cooper JD, Timens W, Postma DS, Knight DA, Lenburg ME, Hogg JC, Spira A. Genome Med. 2012 Aug 31;4(8):67.Genome Med. 2012 Aug 31;4(8):67. [Epub ahead of print]
BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease consisting of emphysema, small airway obstruction, and/or chronic bronchitis that results in significant loss of lung function over time.
METHODS: In order to gain insights into the molecular pathways underlying progression of emphysema and explore computational strategies for identifying COPD therapeutics, we profiled gene expression in lung tissue samples obtained from regions within the same lung with varying amounts of emphysematous destruction from smokers with COPD (8 regions x 8 lungs = 64 samples). Regional emphysema severity was quantified in each tissue sample using the mean linear intercept (Lm) between alveolar walls from micro-CT scans.
RESULTS: We identified 127 genes whose expression levels were significantly associated with regional emphysema severity while controlling for gene expression differences between individuals. Genes increasing in expression with increasing emphysematous destruction included those involved in inflammation, such as the B-cell receptor signaling pathway, while genes decreasing in expression were enriched in tissue repair processes, including the transforming growth factor beta (TGF beta) pathway, actin organization, and integrin signaling. We found concordant differential expression of these emphysema severity-associated genes in four cross-sectional studies of COPD. Using the Connectivity Map, we identified GHK as a compound that can reverse the gene-expression signature associated with emphysematous destruction and induce expression patterns consistent with TGF beta pathway activation. Treatment of human fibroblasts with GHK recapitulated TGF beta-induced gene-expression patterns, led to the organization of the actin cytoskeleton, and elevated the expression of integrin beta1. Furthermore, addition of GHK or TGF beta restored collagen I contraction and remodeling by fibroblasts derived from COPD lungs compared to fibroblasts from former smokers without COPD.
CONCLUSIONS: These results demonstrate that gene-expression changes associated with regional emphysema severity within an individual's lung can provide insights into emphysema pathogenesis and identify novel therapeutic opportunities for this deadly disease. They also suggest the need for additional studies to examine the mechanisms by which TGF beta and GHK each reverse the gene-expression signature of emphysematous destruction and the effects of this reversal on disease progression.
It is also possible that GHK may improve lung regrowth in patients with COPD.
Exp Lung Res. 1986;10(2):115-36.
The effect of culture conditions on cytodifferentiation of fetal mouse lung respiratory passageways.
Hilfer SR, Schneck SL, Brown JW.
Differentiation of the respiratory region of fetal mouse lungs was investigated in serum-free medium supplemented with growth factors and hormones. Terminal buds from the margins of a lobe were removed from 16-day fetuses and organ cultures prepared either in submersion culture or at the air-medium interface. It was found that glycyl-L-histidyl-L-lysine, transferrin, and somatostatin were sufficient to promote branching in the absence of serum. However, type II pneumocytes containing lamellar bodies formed only in the presence of thyroxine or dexamethasone. At concentrations of these hormones slightly above the physiological range most of the cells became cuboidal and contained lamellar bodies; at lower concentrations regions of flattened cells appeared. In submersion culture a large, central cavity surrounded by saccules was formed rather than a branched tree. Thus, the pattern of differentiation is significantly influenced by culture conditions.
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