Figure 2: In vivo and in vitro impact of MMP11 on mitochondrial function.

(a) Rectal body temperature progression in Mmp11-Tg and WT mice placed during 4 h at 4 °C (n = 5/group); (b) Variation in rectal body temperature as a function of time after injection of the β3-adrenergic agonist BRL37344 in Mmp11-Tg and WT mice (n = 6/group); (c) TEM showed increased numbers of mitochondria and less fat in the BAT of Mmp11-Tg compared to WT mice. Many of the mitochondria displayed altered cristae (scale bar = 10 μm in left panels and 2 μm in right panels); the mitochondria count in the BAT is indicated (n = 5); (d) TBARS measurement in BAT of Mmp11-Tg and WT mice; (e) Glutathion peroxidase (GPx) and catalase enzymatic activities in the BAT of Mmp11-Tg and WT mice; (f) mRNA expression of genes involved in lactate metabolism and pyruvate metabolism (n = 6–8/group); (g) Study of mitochondria function in 3T3-L1 adipocytes treated 24 h with vehicle, active-MMP11 or inactive-MMP11 (OXPHOS = oxidative phosphorylation using Seahorse technology, TMRM = tetramethyl rhodamine methylester for mitochondrial permeability test); (h) Oxygen consumption rate (OCR) measurement at baseline and after sequential injection of oligomycin (ATP synthase inhibitor), FCCP (uncoupler agent), and Rotenone/antimycin A (complex I/complex III inhibitors, respectively) in vehicle-, active-MMP11- and inactive-MMP11-treated 3T3-L1 preadipocytes; (i) Relative mitochondrial activity parameters (spare respiratory capacity, proton leak and ATP turnover) in vehicle-, active-MMP11- and inactive-MMP11-treated 3T3-L1 preadipocytes; (j) Mitochondrial permeability test as measured by TMRM fluorescence intensity, which inversely correlates with the mitochondrial depolarization.