C57bl 6j bl6

10-week-old male C57Bl/6J (BL6) (Jackson Laboratory Bar Harbor, ME, USA; Stock No: 000664) or Trem2^-/- mice (C57BL/6J-Trem2^em2Adiuj/J; Jackson Laboratory Bar Harbor, ME, USA; Stock No: 027197) were subjected to an ACL injury using a non-invasive single dynamic tibial compressive overload model previously described by Christiansen et al. (21 (link)). Briefly, the mouse knee was placed between two vertically aligned plates positioned using an electromagnetic material testing system (ElectroForce 3200, TA Instruments, New Castle, DE, USA) and a compressive force was applied (21 (link)). ACL rupture occurred after a total compressive force, between 12N-18N, was administered. For pain relief, buprenorphine (0.01 mg/kg) and sterile saline were administered intraperitoneally immediately post-injury. All animal experiments were approved by the Lawrence Livermore National Laboratory and University of California, Davis Institutional Animal Care and Use Committee and conformed to the Guide for the care and use of laboratory animals.

C57BL/6J (BL6), B6;129-Sirt1^tm1Ygu/J(Sirt1^f/f), and C57BL/6J-Tg (Itgax-Cre-EGFP) 4097Ach/J (CD11c-Cre-GFP) mice were purchased at 6–7 weeks of age from the Jackson Laboratory (Bar Harbor, ME). Sirt1^f/f mice, in which two loxP sites flank Sirt1 exon 4, were crossed to CD11c-Cre-GFP transgenic mice. As the Sirt1^f/f mice were on a mixed C57BL/6J;129 background, we backcrossed the Sirt1^f/f-CD11c-Cre progeny to a C57BL/6J background for six generations. Deletion of exon 4 produces an internally truncated protein that lacks catalytic activity, causing a Sirt1-null genotype [64 ]. Thus, Cre+ mice lack a functional SIRT1 in CD11c^high cells. Sirt1^f/f-CD11c-Cre (SIRT1-/-) mouse breeding took place in-house at the University of Michigan (Ann Arbor, MI).

Wild‐type (WT) C57BL/6 J (BL6) and NOD.Cg‐Prkdc^scidIl2rg^tm1Wj1/SzJ [nonobese diabetic/severe combined immunodeficiency (NOD/SCID)/IL2Rγ KO, NSG] mice were purchased from Jackson Laboratory, maintained under specific pathogen‐free conditions and given food and water ad libitum. Age‐ and sex‐matched mice at least 8 weeks old were used. All studies were approved by our Institutional Animal Care and Use Committee.

The care and use of animals for all experiments described conformed to NIH guidelines. Experimental mice were housed with a 12:12 h light:dark cycle with free access to chow and water, in standard laboratory cages located in a temperature and humidity-controlled vivarium. The protocols for care and use of animals was approved by the Institutional Animal Care and Use Committees at the University of Virginia, the University of Colorado Denver and at the National Institute on Deafness and Other Communication Disorders. All above-mentioned institutions accredited by the American Association for the Accreditation of Laboratory Animal Care. C57BL/6J (Bl6, from Jackson Laboratory, ME, USA) mice and sibling mice served as control mice for this study. Neonatal mouse pups [postnatal day 0 (P0)–P5] were sacrificed by rapid decapitation, and mature mice were euthanized by CO₂ asphyxiation followed by cervical dislocation. The Myo7a::beta-actin:GFP mouse line expressing beta-actin-GFP from a Myo7a BAC transgene^{29 (link),30 (link)} was a gift from Dr Haydn Prosser (Wellcome Trust Sanger Institute, UK).

Male and female wild-type (WT) C57BL/6J (BL6) and NOD.Cg-Prkdc^scidIl2rg^tm1Wj1/SzJ (non-obese diabetic/severe combined immunodeficiency (NOD/SCID)/interleukin-2Rγ KO, NSG) mice were purchased from Jackson Laboratory (Bar Harbor, ME, USA), maintained under specific pathogen-free conditions and given food and water ad libitum. Eight- to ten-week-old age- and sex-matched mice were used for experiments. All animal studies were approved by our Institutional Animal Care and Use Committee.