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. Author manuscript; available in PMC: 2020 Dec 8.
Published in final edited form as: Matrix Biol. 2020 Sep 17;94:77–94. doi: 10.1016/j.matbio.2020.09.001

Fig. 7.

Fig. 7.

The absence of Col11a1 expression results in abnormal FDL fibrils in mature Col11a1Δten/Δten mice. FDLs from mature male Col11a1Δten/Δten mice (day 60) have a severe disruption in collagen fibril structure and diameter distributions compared to control tendons. (A,B) Electron microscopic analysis demonstrates a substantial increase in small diameter fibrils as well as overall smaller diameters in the FDLs from Col11a1Δten/Δten compared to control FDLs. (C-E) The fibril distributions from wild type and Col11a1Δten/Δten tendons are significantly different (KS p<0.0001). In the Col11a1Δten/Δten mice there is a significant shift to small diameter fibrils and a virtual absence of large diameter fibrils characteristic of the mature FDL. The mature day 60 mice show the same trends as seen in maturing day 30 mice (Fig. 4). (F) Fibril density is significantly increased in the Col11a1Δten/Δten FDLs compared to controls, consistent with the significant shift to small diameter fibrils observed in this genotype. (n=3 mice for each genotype).