JEWJITSU PEPTIDES Research Roundup: Oestrogen, ELP Cassette, and AcSDKP

This rat study examined how ovarian hormones and stress alter brain‑gut neurocircuitry. Using female Sprague‑Dawley rats, the authors report that gastric emptying was slower when oestrogen levels were high and that acute stress did not further slow emptying. Electrophysiology showed that oxytocin (OXT) suppressed GABAergic input to dorsal motor nucleus of the vagus (DMV) neurons under non‑stressed conditions regardless of oestrous stage, a pattern differing from prior male rat reports. Pharmacology with astressin implicated ongoing CRF1 receptor activity in some presynaptic OXT effects, and in vivo DMV microinjections indicated OXT reduced gastric tone and motility via vagal efferents involving vasoactive intestinal peptide and nitric oxide. The authors frame these findings as evidence for sex‑specific vagal organization and note a disconnect between central synaptic modulation and peripheral effector recruitment.

This methods paper addresses practical barriers to wider adoption of elastin‑like polypeptide (ELP) tags for recombinant peptide and protein production. The authors describe a modular expression cassette engineered to yield an ELP with a low inverse transition temperature (Tt of 27–31 °C) that aggregates under mild conditions and tolerates reduced salt (up to 0.5 M NaCl). They exploit the ELP’s thermo‑responsive aggregation to separate tag from target by filtration after enzymatic cleavage, reporting particular efficiency for small peptides where the size difference aids separation. The manuscript discusses remaining challenges for larger peptides and positions the cassette as a standardized option for labs wanting non‑chromatographic purification.

This study explores N‑acetyl‑seryl‑aspartyl‑lysyl‑proline (AcSDKP) in models of chronic kidney disease (CKD) and reports a compartment‑specific profile. In vitro work showed AcSDKP suppressed TGF‑β1–induced pericyte‑to‑myofibroblast transition and restored pericyte VEGF secretion, improving endothelial tubulogenesis. In a unilateral aristolochic acid CKD mouse model, early AcSDKP intervention (reported at Week 3) reduced fibrosis, preserved peritubular capillaries, and improved systemic renal markers compared with later intervention (Week 4). Transcriptomics implicated the VEGF/FGFR1 axis, but in injured tubular HK‑2 cells AcSDKP increased apoptosis despite FGFR1 upregulation; FGFR1 knockdown worsened apoptosis, suggesting FGFR1 upregulation was compensatory while AcSDKP’s epithelial toxicity involved Akt pathway inhibition. The authors highlight timing and delivery as critical for translating vascular benefits while limiting epithelial harm.