IGF-1 LR3

Engel MG, Narayan S, Cui MH, Branch CA, Zhang X, Gandy SE, et al.

Journal of Alzheimer's disease : JAD

In a 5XFAD transgenic mouse model of Alzheimer's-type amyloid pathology, seven months of intranasal LR3-IGF-1 administration altered cortical amyloid-beta plaque morphology (reduced filamentous plaques, increased inert plaques, reduced low-molecular-weight oligomers) and enhanced BV-2 microglial cell uptake of amyloid-beta peptide in vitro, with transcriptomic changes implicating actin-remodeling and endocytosis pathways; cognitive and memory measures were not improved in this rodent model.

Lu Z, Liu N, Huang H, Wang Y, Tu T, Qin X, et al.

Applied microbiology and biotechnology

Reports recombinant production of human IGF-1 and its analog LR3 IGF-1 as xylanase fusion proteins in a Pichia pastoris yeast expression system; purified LR3 IGF-1 showed cell-proliferation bioactivity comparable to standard IGF-1 in an in vitro assay, with scalable yields (up to ~1 g/L) achieved via bioreactor fermentation.

Hadsell DL, Parlow AF, Torres D, George J, Olea W

The Journal of endocrinology

In a mouse model of lactation, subcutaneous administration of long-R3-IGF-I increased mammary-gland phospho-Akt signaling and SOCS3 gene expression and produced a modest increase in litter weight gain (a lactation-capacity measure), illustrating IGF-1 receptor pathway activation in mammary epithelial tissue.

Xi G, Kamanga-Sollo E, Pampusch MS, White ME, Hathaway MR, Dayton WR

Journal of cellular physiology

In the L6 rat myogenic cell line, recombinant porcine IGF-binding protein-3 (IGFBP-3) suppressed both IGF-I- and Long-R3-IGF-I-stimulated cell proliferation, but unlike native IGF-I, Long-R3-IGF-I's differentiation-promoting effect was NOT suppressed by IGFBP-3 — indicating an IGFBP-3-independent signaling mechanism specific to differentiation, useful for studying myoblast differentiation signaling in vitro.

Sundgren NC, Giraud GD, Schultz JM, Lasarev MR, Stork PJ, Thornburg KL

American journal of physiology. Regulatory, integrative and comparative physiology

In fetal sheep and cultured fetal sheep cardiomyocytes, LR3 IGF-1 stimulated cardiomyocyte proliferation (BrdU incorporation) via the IGF-1 receptor, an effect fully blocked by pharmacological inhibition of either ERK or PI3K signaling, establishing that both pathways are required downstream of IGF-1 receptor activation in this developmental cardiac model.