In today’s article, we are going to discuss the biological applications of the B7-33 peptide. If you should learn more about this topic, keep reading.
Tissues develop into abnormally thick or deteriorate in patients with fibrosis. Those experiencing the “end stage” of severe, chronic diseases usually tend to develop fibrosis.
Although fibrosis may be treated in quite a lot of ways, from medication to surgery, it was shown in a clinical experiment in 2012 that a protein called H2-relaxin prevented the event of everlasting scarring in the center because of this of injury [v].
The natural protein H2-relaxin has an artificial equivalent referred to as B7-33 peptide. Based on research, B7-33, like H2-relaxin, has anti-fibrotic qualities and the opposite apparent advantages we are going to list below.
B7-33 Peptide: What Is It?
One chain peptide B7-33 is a shorter, structurally similar version of the naturally occurring relaxin protein [ii].
4 subunits comprise the relaxin peptide: the signal peptide, the B chain, the C chain, and the COOH terminus.
Several early attempts to duplicate these peptide structures failed miserably as a consequence of the problem of achieving solubility and activity.
Studies show that the B7-33 peptide was the primary soluble analog resulting from structural modifications made by scientists in 2016 after years of study. These included the production of a B chain and the extension of the COOH terminus [ii].
Peptide Mechanism of Motion
Based on research, the peptide differs from native proteins in structure and a couple of other ways which are somewhat helpful, especially when put next to H2-relaxin.
Studies show that the cAMP pathway is bypassed by the B7-33 peptide, which as an alternative exerts its effects via the pERK pathway.
Traditionally, H2-relaxin generates its anti-fibrotic activities via the cAMP pathway, which can promote tumor development. An important negative impact of relaxin therapy [i].
The RXFP-1 receptors are also a goal of high affinity for the peptide.
Research shows that the Matrix metalloproteinase-2 (MMP-2) chemical production is boosted after the peptide binds to RXFP-1 receptors and triggers the pERK pathway. Inhibiting scarring and avoiding fibrosis results from these pharmacological interventions [i].
B7-33 peptide has quite a lot of potential applications.
Studies on test subjects have shown that this peptide has practical medical applications.
- The power to inhibit fibrotic growth
- The power to stop damage to blood vessels
- Aids in preeclampsia treatment
- Utilization as an adornment for inserted medical devices.
Evidence of Vasoprotective Effects
Based on research, H2 relaxin’s efficacy against heart failure and fibrosis led to its recognition as a robust vasoprotective medication.
Nonetheless, as a consequence of the high price and time commitment of exogenous H2 relaxin production, it became increasingly vital to analyze whether its analog B7-33 peptide demonstrated the identical effects.
Research shows that administering sodium acetate, H2 relaxin, or B7-33 into the tails of male Wistar rats was the tactic of selection for this study [iii]published in 2017.
These animals’ mesenteric artery, renal artery, and abdominal aorta were primarily analyzed after 3 hours.
Although neither B7-33 nor H2 relaxin demonstrated enhanced vasodilatory capabilities within the renal artery or abdominal aorta, they did within the mesenteric artery, as per study results.
So as to gain a deeper insight, an additional investigation [iii] was conducted on female mice that were manipulated to have endothelium dysfunction within the lab. These mice got H2 relaxin.
Based on research results, each substances effectively reduced the severity of endothelial dysfunction and halted its progression in mice once therapy had concluded.
These findings show that B7-33 can prevent additional damage to blood vessels by mimicking the vasoprotective actions of H2 relaxin. The findings also suggest that the peptide has therapeutic promise for addressing cardiovascular disorders.
Prevention of Preeclampsia: Current Research
Preeclampsia is a condition of pregnancy marked by elevated maternal blood pressure and diminished fetal weight. This study [iv] aimed to analyze the efficacy of the B7-33 peptide in managing preeclampsia while pregnant.
On this experiment, cytotrophoblasts (CTBs) were grown within the lab. A specific form of cell called cytotrophoblasts exists throughout the innermost layer of the embryo’s cells.
These cells were exposed to a placebo, steroid, or glucose for two days. After a part of the cells were treated, they were exposed to a relaxin antagonist. B7-33 chemical was added to the cell culture medium, and all cells were treated.
Research showed that upon closer inspection, cells treated with B7-33 peptide were found to have increased levels of vascular endothelial growth factor (VEGF). Antibodies against relaxin decreased VEGF levels in treated cells.
Based on these findings, the peptide appears to have anti-glucose solid and anti-marinobufagenin properties, making it an efficient tool within the fight against preeclampsia.
Investigations into Anti-Fibrotic Properties
H2 relaxin is a naturally occurring protein that inhibits scar tissue formation. The cAMP pathway is crucial to their operation. The total-length H2 relaxin protein strain has been proven in studies [v,vi] to extend heart rate and promote the spread of cancerous cells when administered to review participants. The first explanation for that is that it really works by stimulating the cAMP pathway.
Thus, scientists sought a variant that will generate the identical anti-fibrosis biological effects without cAMP activation. The B7-33 peptide is the product of their research.
Mice with myocardial infarction got the peptide, showing nearly a 50% reduction in heart tissue fibrosis. Overall, heart function increased, and problems diminished because of this.
Analyses revealed that the peptide’s success was primarily as a consequence of its ability to spice up the body’s production of matrix metalloproteinase protein, which reduced the variety of collagen-damaging cells and averted fibrosis.
Coating material studies show promise.
The immune system is primed to defend against intruders vigorously. Fibrosis is the first mechanism by which the body rejects foreign objects, separating them in order that they cannot disrupt normal body function. This aspect is helpful when coping with antigens and disease-causing elements, nevertheless it becomes problematic when undergoing body implants.
As an illustration, the body may reject a cardiac stent because it is a foreign object, leading to potentially fatal complications, including blockage and heart attack.
Antagonistic Reactions to B7-33 Peptide
Since B7-33 remains to be relatively latest, there’s much room for exploration and testing, as researchers reveal. On account of the continued trials, experts don’t know the complete extent of potential antagonistic effects, nevertheless it’s reasonable to assume that some unwanted effects can be typical of other peptides. There are several, but some effects, in line with studies, are:
- Temporary pain and itching.
- Lack of salivation
- Dizziness
- Chills, fever, and other flu-like symptoms
- Hurting joints
You could find B7-33 on the market if you happen to are a researcher excited by further studying the potential of this wonder peptide.
References
[i] Mohammed Akhter Hossain et al., A single-chain derivative of the relaxin hormone is a functionally selective agonist of the G protein-coupled receptor, RXFP1, Drug Discovery Biology Pharmacology Monash Biomedicine Discovery Institute, Vol 7, 2016. https://research.monash.edu/en/publications/a-single-chain-derivative-of-the-relaxin-hormone-is-a-functionall
[ii] Nitin A Patil et al., Relaxin family peptides: structure–activity relationship studies, British Pharmacological Society, vol 174 issue 10, published 06 December 2016. https://doi.org/10.1111/bph.13684
[iii] Marshall SA, O’Sullivan K, Ng HH, Bathgate RAD, Parry LJ, Hossain MA, Leo CH. B7-33 replicates the vasoprotective functions of human relaxin-2 (serelaxin). Eur J Pharmacol. 2017 Jul 15;807:190-197. doi: 10.1016/j.ejphar.2017.05.005. Epub 2017 May 3. PMID:28478069. https://pubmed.ncbi.nlm.nih.gov/28478069/
[iv] S.H Afroze et al., Abstract P3042: Novel Peptide B7-33 and It’s Lipidated Derivative Protect Cytotrophoblasts From Preeclampsia Phenotype in a Cellular Model of the Syndrome, 4 Sep 2019. https://doi.org/10.1161/hyp.74.suppl_1.P3042
[v] Silvertown JD, Ng J, Sato T, Summerlee AJ, Medin JA. H2 relaxin overexpression increases in vivo prostate xenograft tumor growth and angiogenesis. Int J Cancer. 2006 Jan 1;118(1):62-73. https://pubmed.ncbi.nlm.nih.gov/16049981
[vi] Shu Feng, Irina U. Agoulnik, Natalia V. Bogatcheva, Aparna A. Kamat, Bernard Kwabi-Addo, Rile Li, Gustavo Ayala, Michael M. Ittmann and Alexander I. Agoulnik, Relaxin Promotes Prostate Cancer Progression, March 2007. https://clincancerres.aacrjournals.org/content/13/6/1695
