Journal: Brain Pathology

Article Title: Mitochondrial activity in the frontal cortex area 8 and angular gyrus in P arkinson's disease and P arkinson's disease with dementia

doi: 10.1111/bpa.12474

Figure Lengend Snippet: Western blot of mitochondrial‐enriched fractions in frontal cortex (FC) in MA cases and PD. (A) No differences in protein expression levels of monomeric α‐synuclein 17 kDa are seen between MA and PD. However, significant expression of oligomeric α‐synuclein of 37 and 50 kDa is found in PD when compared with MA. β‐actin is used as a marker of protein loading, and ATP5A as a mitochondrial marker. (B) Increased levels of neuroketal (NKT) protein adducts in mitochondrial‐enriched fractions in PD when compared with MA cases. (C) No significant differences of N‐Tyrosine levels are seen between the two groups. Student's T‐test *P < 0.05, **P < 0.01.

Article Snippet: Differences in protein loading were corrected with anti‐β‐actin (1:30 000, A5316; Sigma‐Aldrich); mitochondrial levels were assessed with anti‐oxidative phosphorylation‐ATP5A (1:10 000; MS601, Mitoscience, Eugene, OR, USA).

Techniques: Western Blot, Expressing, Marker

Journal: Molecular Metabolism

Article Title: PPARγ and PPARα synergize to induce robust browning of white fat in vivo

doi: 10.1016/j.molmet.2020.02.007

Figure Lengend Snippet: Dual PPARα/γ activators induce UCP1 in both mouse and human white adipocytes in vitro. (a) Ucp1 and Fabp4 mRNA expression in immortalized mouse white preadipocytes following 8 days of treatment with various dual PPARα/γ activators during differentiation ( n = 3/group). (b) Ucp1 mRNA expression in mouse white adipocytes (pre-differentiated from immortalized preadipocytes for 6 days) following 2 days of treatment ( n = 3/group). (c) UCP1 and FABP4 mRNA expression in primary human white preadipocytes following 12 days of treatment during differentiation ( n = 4–8/group). (d) UCP1 mRNA expression in freshly isolated mature human adipocytes following 7 days of treatment ( n = 4/group). All compounds in a-d were added at a final concentration of 10 μM. (e) qPCR analysis ( n = 3/group) of BAT-enriched genes (left panel) and lipid/glucose metabolism genes (right panel), (f) Western blot analysis of Pparγ, mitochondrial subunits and Ucp1 protein levels and (g) mitochondrial/nuclear DNA ratio ( n = 6/group), measured in primary mouse white preadipocytes after 8 days of treatment during differentiation with either vehicle or tesaglitazar (10 μM). Data presented as mean ± SEM: ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001 by two-tailed, unpaired Student's t-test.

Article Snippet: Primary antibodies were against PPARγ (SantaCruz, SC-7196), mitochondrial subunits (Mitoscience, MS601/F1208), UCP1 [ ], β-actin (Sigma, A5441), ERK (SantaCruz, SC-93), and GAPDH (Cell signaling, 2118).

Techniques: In Vitro, Expressing, Isolation, Concentration Assay, Western Blot, Two Tailed Test

Journal: Molecular Cell

Article Title: NADH Shuttling Couples Cytosolic Reductive Carboxylation of Glutamine with Glycolysis in Cells with Mitochondrial Dysfunction

doi: 10.1016/j.molcel.2018.01.034

Figure Lengend Snippet:

Article Snippet: Primary antibodies were: mouse anti-human GAPDH (Abcam cat. no. ab8245), mouse anti-human Mitochondria OXPHOS cocktail (Origene cat. no. MS601-360), rabbit anti-human LDH (Abcam cat. no. ab47010), rabbit anti-human MDH1 (Abcam cat. no. ab180152), rabbit anti-human Calnexin (Abcam cat. no. ab22595), rabbit anti-NDI-1 (Cambridge Research Biochemicals), mouse anti-human TOMM20 (Abcam cat. no. ab56783).

Techniques: Recombinant, Software