Fig 1: Effects of SCH and OHT on NGF-mediated TrkA and p75NTR signaling pathway. NGF induces TrkA signaling pathway to increase neuronal proliferation. Pro-NGF, the precursor protein of NGF, can combine with p75NTR preferentially to enhance neuronal apoptosis. CREB, cAMP response element-binding protein; JNK, C-Jun N-terminal kinase; NGF, nerve growth factor; OHT, overt hypothyroidism; p75NTR, p75 neurotrophin receptor; SCH, subclinical hypothyroidism; TrkA, tropomyosin-related kinase A
Fig 2: Bioassay of recombinant human proNGF (rhproNGF) in the SH-SY5Y cells.Characterization of rhproNGF is shown by western blot (A). Positive expression of p75NTR and sortilin is detected in SH-SY5Y cells in both control and LPS stimulation conditions (B). MTT shows no significant change of SH-SY5Y cell viability after proNGF treatment at different concentrations (C). Hoechst/PI staining indicates cell damage of SH-SY5Y cells resulted from proNGF treatment at 10ng/ml and 40ng/ml (D). E, Immunoblot shows a slight increase of cleaved caspase-3 expression (mainly 19kDa) following proNGF treatment (E). TUNEL assay shows appearance and increase of apoptotic cell death in SH-SY5Y cells with proNGF treatment (F).
Fig 3: Expression of p75 neurotrophin receptor (p75NTR) (a), Bax (b), proapoptotic proteins p53 (c) and cleaved caspase-3 (d), and phospho-c-Jun N-terminal kinase (p-JNK) (e) in the hippocampus of pups (N = 6, PND7). *p < 0.05 versus CON group, #p < 0.05 versus SCH group; &p < 0.05 versus OHT group. CON, control; E, gestational day; OHT, overt hypothyroidism; SCH, subclinical hypothyroidism
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