Extended Data Fig. 4: Cav1-mutant mice exhibit normal SMC integrity and function.
From: Caveolae in CNS arterioles mediate neurovascular coupling
a, In vivo two-photon microscopy images of hydrazide (magenta) and DsRed (red) from Cav1+/+NG2DsRED+ and Cav1−/−NG2DsRED+ mice. b, Quantification of DsRED+ SMCs per 100 μm as shown in a, in Cav1+/+ (n = 3 mice, 27 arterioles) and Cav1−/− (n = 3 mice, 28 arterioles) mice. c, Immunostaining for SMC contractile proteins, including SMA, MYH11, TAGLN and desmin on brain arterioles from Cav1+/+ and Cav1−/− mice. d–g, Normalized fluorescence quantification of the various contractile proteins from Cav1+/+ and Cav1−/− mice. h, Still frame images of arterioles labelled with hydrazide (magenta) in ex vivo acute brain slices from Cav1+/+ and Cav1−/− mice using two-photon microscopy. Left, arterioles during baseline; middle, arterioles during U46619 (thromboxane agonist) treatment; right, arterioles during DEA NONOate (NO donor) treatment. White hashes outline the arterioles during baseline based on time = 0 min. i, j, Maximum arteriolar contraction by U46619 (i) and maximum arteriolar dilation by DEA NONOate (j) on acute brain slices from Cav1+/+ (n = 5 mice, 19 arterioles) and Cav1−/− (n = 5 mice, 22 arterioles). k, In vivo images of arterioles labelled with hydrazide (magenta) from Cav1+/+ and Cav1−/− mice using two-photon microscopy. Left, arterioles during baseline; right, arterioles during DEA NONOate superfusion. White hashes outline the arterioles during baseline based on time = 0 s. l, Quantification of maximum arteriolar dilation during DEA NONOate superfusion in vivo (n = 5 mice for both genotypes). Statistical significance was determined by nested, unpaired, two-tailed t-test for b, d–g, i, j, and by two-tailed Mann–Whitney U test for l. Data shown as mean ± s.e.m.
