Figure 1. Neonatal Mmp14-deficient mice have small and weak tendons.

(A) Weight of wild type (WT) and Mmp14 knockout (Mmp14 KO) littermates at birth (P0) and at 3 days postnatal (P3). (B) The cross-sectional transverse area of P0 Mmp14 KO tendons is significantly smaller than WT tendons. (C) TEM images of P0 tail tendon demonstrate that KO tendons are smaller and show dysmorphic, enlarged bundles of collagen fibrils (arrowhead). Scale bars 5 μm. (D) KO tendons have fewer, larger fibril bundles, but the FVF is not different to WT tendons. (E) KO tendons are weaker than WT tendons but have normal mechanical properties after adjusting for differences in size. (F) Analysis of Col1a1 mRNA by qPCR in P0 tendons revealed no difference in gene expression. (G) ¹⁴C-proline labeling of collagen demonstrated normal collagen processing at P7 in WT and KO tail tendon. (H) Fibril diameter distributions of KO and WT tail tendon at P0 revealed significantly increased fibril diameters in KO mice. Bars show SEM. *p < 0.05, ^†p > 0.05 (t-tests).

DOI: http://dx.doi.org/10.7554/eLife.09345.003

Figure 1—figure supplement 1. Cell number and type I collagen synthesis in neonatal WT and Mmp14 KO tail tendon.

3D reconstruction from SBF-SEM analysis of P0 (A) WT and (B) Mmp14 KO tendons. Green/turquoise, outline of the tendon. Red/pink spheres, cell nuclei. Scale bars 10 µm. (C) Estimated mean cell number per unit volume of tissue shows that the absence of MMP14 does not affect cell number at birth. Bars show SEM. ^†p > 0.05 (t-test). (D) Densitometry data for P7 tail tendons were labeled with ¹⁴C-proline for 1 hr and separate extracellular and intracellular extracts prepared as described (Canty et al., 2004). A significant decrease in [¹⁴C]-collagen relative to β-actin (detected by western blotting) in the intracellular extracts was observed in the KO samples (*p < 0.01, t-test).

DOI: http://dx.doi.org/10.7554/eLife.09345.004