LL-37 suppresses sodium nitroprusside-induced apoptosis of systemic sclerosis dermal fibroblasts.
Kim. Hee Jung HJ; Cho. Dae Ho DH; Lee. Kyung Jin KJ; Cho. Chul Soo CS; Bang. Sa Ik SI; Cho. Baik Kee BK; Park. Hyun Jeong HJ
Key Findings
- LL‑37 levels are higher in skin samples from systemic sclerosis patients than in healthy people.
- Adding LL‑37 to diseased skin fibroblasts reduced cell death caused by a chemical stressor (sodium nitroprusside).
- LL‑37 increased the anti‑apoptotic protein Bcl‑2, decreased the pro‑apoptotic protein BAX, and lowered caspase‑3 activation.
- The peptide raised COX‑2 and prostaglandin E2 levels and activated the ERK signaling pathway; blocking ERK stopped LL‑37’s protective effect.
Practical Outcomes
- For most biohackers, this research doesn’t translate into a usable supplement or protocol, because it targets a specific disease process rather than general longevity or performance. It also suggests LL‑37 may promote fibroblast survival, which could be counter‑productive for anti‑fibrotic or anti‑aging goals. Until safety and systemic effects are clarified, there’s no actionable recommendation.
Summary
The study found that the natural peptide LL‑37 can stop skin cells from dying in a disease called systemic sclerosis. It does this by boosting survival proteins, lowering death proteins, and turning on certain cell‑signaling pathways. While interesting, the work is focused on a rare autoimmune condition, not on general health or performance.
Abstract
The human cathelicidin antimicrobial peptide LL-37 regulates apoptosis of several cell types. Defective apoptosis of skin fibroblasts may contribute to systemic sclerosis (SSc). Here, we show that LL-37 inhibited apoptosis of SSc fibroblasts and identified the signalling pathways by which LL-37 mediates apoptosis. Immunohistochemistry showed that cathelicidin expression was enhanced in SSc patients compared with healthy controls. In addition, LL-37 decreased sodium nitroprusside (SNP)-induced apoptosis of SSc fibroblasts. LL-37 significantly increased expression of Bcl-2 and decreased levels of BAX protein. Pretreatment with LL-37 decreased activation of caspase-3 following SNP-treatment. Moreover, exposure of SSc fibroblasts to LL-37 resulted in increased expression of COX-2 and stimulation of prostaglandin E(2) (PGE(2)). Furthermore, LL-37 induced phosphorylation of ERK and the ERK inhibitor PD98059 blocked the inhibitory effect of LL-37 on apoptosis. Our data indicate that LL-37 may be associated with skin sclerosis by inhibiting apoptosis of dermal fibroblasts.
Study Information
pubmed
2011
2011-07-07T00:00:00.000Z
10.1111/j.1600-0625.2011.01327.x
27
29