Journal: bioRxiv
Article Title: Amyloid β induces cardiac dysfunction and neuro-signaling impairment in the heart of an Alzheimer’s disease model
doi: 10.1101/2023.07.11.548558
Figure Lengend Snippet: ( A - B ): Representative immunoblots ( A ) and densitometric quantitative analysis ( B ) showing levels of NGF, BDNF, GAP-43, and DβH, in total cardiac (top panels) and cerebral cortex (bottom panels) lysates from WT and Tg2576 mice. ( C-D ): digital images (C, scale bar 100μm) and quantifications (D) showing cardiac adrenergic nerve fibers, labeled with anti-tyrosine-hydroxylase (TH, in green), and cardiac regenerating nerve endings, labeled with anti-neuronal regeneration marker (GAP-43, in red) in heart sections from WT and Tg2576 mice. n=3– 5 mice/group. Data are presented as a mean±SEM. *P<0.05, **P<0.01 and vs WT. Student t-tests have been performed between the 2 groups.
Article Snippet: Total lysates were used to evaluate the protein levels of NGF (AN-240; Alomone labs; 1:1000), BDNF (ANT-010; Alomone labs; 1:1000), GAP-43 (Millipore AB552; 1:1000), Cleaved Caspase-3- Asp175 (Cl-Casp-3- Cell Signaling- #94530; 1:200), dopamine β hydroxylase (DβH; AB1536; Millipore), human Aβ [mouse monoclonal anti-Aβ antibodies mixture composed of 4G8 epitope (residues Aβ18–22; SIG-39320; Covance) and 6E10 epitope (residues Aβ3–8; SIG-39220; Covance)], and GAPDH (sc-32233,6C5; Santa Cruz Biotechnology; 1: 2000), the latter which was used as the loading control.
Techniques: Western Blot, Labeling, Marker