PE-22-28 is a synthetic variant of the naturally occurring peptide Spadin. Spadin is a secreted peptide obtained from Sortilin. It appears to act as an antagonist of the TREK-1 (TWIK-related-potassium channel) receptor, a two-pore potassium channel identified as a potential target in the context of depression research and as a possible neurogenic regulator. Studies in mice have suggested that TREK-1 receptor deletion may make them resistant to depressive behavior and corresponding chemical imbalances in the brain.[1] Sortilin exposure may also lead to resistance by promoting neuronal growth and intersynaptic connections. PE-22-28 represents the group of synthetic Spadin analogs with potentially higher efficacy and stability than Spadin. Neurogenesis is a long-term consequence noted in prolonged research studies examining certain anti-depressant compounds. Neuronal growth indicates the efficacy of such substances. Research studies suggest PE-22-28 has the potential to act more rapidly, inducing neurogenesis after just four days. Research in animal models is ongoing.
OTHER KNOWN TITLES: Spadin Analog, PE2228, TREK-1 Antagonist, PE 22 28, Sortilin Derivative, PE 2228
SEQUENCE: GVSWGLR
MOLECULAR FORMULA: C35H55N11O9
MOLECULAR WEIGHT: 773.8947 g/mol
PE-22-28 AND TREK-1 RECEPTORS
TREK-1 is a cognate receptor for Spadin and, therefore, researchers suggest it may be for PE-22-28 as well. It is a two-pore potassium channel regulated by several different molecules and is considered to regulate neuronal excitability.[2] TREK-1 appears to be abundant in the prefrontal cortex, the amygdala, and the hippocampus. By reducing the neuron’s excitability, TREK-1 may help protect against excitotoxicity. Researchers suggest PE-22-28 has the potential to relieve neurogenic depression controlled by the TREK-1 channel. PE-22-28 may potentially reverse the loss of hippocampal volume by stimulating neurogenesis.[3,4]
PE-22-28 PEPTIDE AND POST-STROKE DEPRESSION
Post-stroke depression (PSD) is considered to be a common symptom of post-brain ischemia and may be caused by TREK-1 overexpression. In mouse model experiments, this upregulation may be suppressed or reversed via SSRI anti-depressant compounds as well as TREK-1 blockers like Spadin.[5]The researchers reveal that “These findings point out spadin as a putative antidepressant of new generation with a rapid onset of action. Spadin can be regarded as the first natural antidepressant peptide identified. It corresponds to a new concept to address … depression.”
PE-22-28 PEPTIDE AND NEUROGENESIS
PE-22-28 appears to promote neurogenesis but in a shorter duration of time. Studies in mice suggest that PE-22-28 has the potential to increase neurogenesis and synaptogenesis in as little as four days.[6] CREB (cAMP response element-binding protein) is a transcription factor associated with neuronal plasticity, memory formation, and the development of spatial memory.[7] CREB appears to be a necessary component in not just the growth of neurons but also in their protection. It has been suggested by research in animal models that removing the TREK-1 channel may be disastrous for the organism. In previous mouse models, knockout of TREK-1 increased the likelihood of seizure activity significantly and reduced the normal ability of this two-pore potassium channel to protect neurons from excitotoxicity. It came as a surprise then that neither Spadin nor PE-22-28 appeared to enhance seizure activity following these experiments. Even more interesting is the fact that mice exposed to Spadin were reported by researchers to appear more resistant to developing generalized seizures. Research in animal models is ongoing.
PE-22-28 PEPTIDE AND MUSCLE FUNCTION
There is some research to suggest that TREK-1 plays a role in the ability of a muscle to respond to mechanical stimulation.[8] Scientists note that “Application of negative pressure to cell-attached patches (-20 mmHg) caused a 19-fold increase in the open probability (NPo) of … TREK-1 channels.” In particular, TREK-1 blockade appears to increase contractility in muscle tissue, while activation of the channel appears to promote muscle relaxation. While this particular aspect of the TREK-1 channel is still in the early stages of the investigation, it is becoming increasingly important. There is hope that understanding the role of molecules like PE-22-28 in muscle contraction and relaxation may provide new research modalities for conditions like myogenic bladder dysfunction and may also open up new pathways for understanding the physiology of muscle performance.
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