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4. Cell lineage tracing and functional assessment of supraspinatus tendon healing in an acute repair murine model.

Author

Moser, Helen L., Abraham, Adam C., Howell, Kristen, Laudier, Damien, Zumstein, Matthias A., Galatz, Leesa M., and Huang, Alice H.

Subjects
*FATE mapping (Genetics), *SUPRASPINATUS muscles, *ROTATOR cuff, *TENDON injuries, *FUNCTIONAL assessment, TENDON injury healing
Abstract

Rotator cuff supraspinatus tendon injuries are common with high rates of anatomic failure after surgical repair. The purpose of the study was to define clinically relevant features of a mouse model of supraspinatus tendon injury to determine painful, functional, and structural outcomes; we further investigated two cell populations mediating healing using genetic lineage tracing after full detachment and repair of the supraspinatus tendon in mice. The pain was assessed using the mouse grimace scale and function by gait analysis and tensile testing. Histological and microCT analyses were used to determine enthesis/tendon and bone structure, respectively. Lineage tracing was carried out using inducible Cre lines for ScxCreERT2 (tendon cells) and αSMACreERT2 (myofibroblasts and mesenchymal progenitors). Mice only expressed pain transiently after surgery despite long‐term impairment of functional and structural properties. Gait, tensile mechanical properties, and bone properties were significantly reduced after injury and repair. Lineage tracing showed relatively few Scxlin tendon cells while αSMAlin cells contributed strongly to scar formation. Despite surgical reattachment of healthy tendon, lineage tracing revealed poor preservation of supraspinatus tendon after acute injury and loss of tendon structure, suggesting that tendon degeneration is also a key impediment of successful rotator cuff repair. Scar formation after surgery is mediated largely by αSMAlin cells and results in permanently reduced functional and structural properties. [ABSTRACT FROM AUTHOR]

Published
2021
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5. Six Proven Practices for Backbone Organizations

Author

Moser, Helen and Crespin, Richard

Abstract

Collaborations among multiple organizations are simple in theory, but difficult in practice. Making them work requires a backbone organization that pays close attention to the needs of all participants.

Published
2018
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6. Genetic lineage tracing of targeted cell populations during enthesis healing

Author

Moser, Helen Laura, Doe, Anton P, Meier, Kristen, Garnier, Simon, Laudier, Damien, Akiyama, Haruhiko, Zumstein, Matthias, Galatz, Leesa M, and Huang, Alice H

Subjects
musculoskeletal system, 610 Medicine & health
Abstract

Rotator cuff supraspinatus tendon injuries are clinically challenging due to the high rates of failure after surgical repair. One key limitation to functional healing is the failure to regenerate the enthesis transition between tendon and bone, which heals by disorganized scar formation. Using two models of supraspinatus tendon injury in mouse (partial tear and full detachment/repair), the purpose of the study was to determine functional gait outcomes and identify the origin of the cells that mediate healing. Consistent with previous reports, enthesis injuries did not regenerate; partial tear resulted in a localized scar defect adjacent to intact enthesis, while full detachment with repair resulted in full disruption of enthesis alignment and massive scar formation between tendon and enthesis fibrocartilage. Although gait after partial tear injury was largely normal, gait was permanently impaired after full detachment/repair. Genetic lineage tracing of intrinsic tendon and cartilage/fibrocartilage cells (Scx and Sox9 , respectively), myofibroblasts (αSMA ), and Wnt-responsive stem cells (Axin2 ) failed to identify scar-forming cells in partial tear injury. Unmineralized enthesis fibrocartilage was strongly labeled by Sox9 while Axin2 labeled a subset of tendon cells away from the skeletal insertion site. In contrast to the partial tear model, Axin2 labeling showed considerable contribution of Axin2 cells to the scar after full detachment/repair. Clinical Significance: Clinically relevant models of rotator cuff tendon injuries in mouse enable the use of genetic tools; lineage tracing suggests that distinct mechanisms of healing are activated with full detachment/repair injuries versus partial tear. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:3275-3284, 2018.

Published
2018
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11. Biologics and stem cell‐based therapies for rotator cuff repair.

Author

Bianco, Spencer T., Moser, Helen L., Galatz, Leesa M., and Huang, Alice H.

Subjects
*ROTATOR cuff, *BIOLOGICALS, *SUPRASPINATUS muscles, *TENDON injuries, *CHRONIC pain, *ANIMAL models in research
Abstract

The rotator cuff is composed of several distinct muscles and tendons that function in concert to coordinate shoulder motion. Injuries to these tendons frequently result in permanent dysfunction and persistent pain. Despite considerable advances in operation techniques, surgical repair alone still does not fully restore rotator cuff function. This review focuses on recent research in the use of biologics and stem cell‐based therapies to augment repair, highlighting promising avenues for future work and remaining challenges. While a number of animal models are used for rotator cuff studies, the anatomy of the rotator cuff varies dramatically between species. Since the rodent rotator cuff shares the most anatomical features with the human, this review will focus primarily on rodent models to enable consistent interpretation of outcome measures. [ABSTRACT FROM AUTHOR]

Published
2019
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20. Abstracts of papers Minneapolis Fall Meeting

Author

Litchfield, C. C., Rakoff, Henry, Maire, René, Holman, R. T., Subbaram, M. R., Youngs, C. G., McCarthy, M. J., Kuksis, A., Trowbridge, J. R., Herrick, A. B., Bauman, R. A., Craig, B. M., Bhatty, M. K., Sen, N., Schlenk, H., Gellerman, J. L., Emken, E. A., Butterfield, R. O., Blank, M. L., Farquhar, Margaret, Reiser, Raymond, Luddy, F. E., Barford, R. A., Herb, S. F., Riemenschneider, R. W., Peifer, J. J., Muesing, R., Janssen, F., Schmit, J. A., Buchnea, Dmytro, Dufek, E. J., DeJarlais, W. J., Feuge, R. O., Zarins, Zigrida, Kircher, H. W., Johnston, A. E., Glass, C. A., Schmolka, I. R., Cenker, M., Kokorudz, M., Mangold, H. K., Houle, C. R., Bistline, Jr., R. G., Stirton, A. J., Berglund, E. D., Crecelius, S. B., Cohen, Irving, Economou, Peter, Spangler, W. G., Watanabe, Henry, Groves, W. L., Netzel, D. A., Stanley, C. W., Rathburn, D. W., Reck, R. A., Molnar, N. M., Baron, S., Horning, E. C., Holmes, W. L., Hamilton, J. G., Muldrey, J. E., Goldsmith, Grace A., Shulman, G. P., Link, W. E., Lew, H. Y., Desmond, C. T., Borden, W. T., Gildenberg, L., Lundgren, D. P., Keily, H. J., Knaggs, E. A., Varenyi, L., Yeager, J. A., Fischer, E., Weil, J. K., Stirton, A. J., Morrisroe, J., Atwood, R. W., Temple, R. E., Malins, D. C., Wekell, J. C., Morrissette, R. A., Ven Horst, Helen, Rohwedder, W. K., Selke, E., Scholfield, C. R., Tulloch, A. P., Schmid, H. H. O., Lundberg, W. O., Harris, J. A., Magne, F. C., Skau, E. L., Mehrens, J. E., Smullin, C. F., Cooper, A. D., Tuna, N., Heimberg, M., Fizette, N. B., Klausner, H., Horning, M., Mayer, S. E., Swoboda, P. A. T., Lea, C. H., Chipault, J. R., Mizuno, G. R., Anderson, R. H., Huntley, T. E., Moser, Helen A., Evans, C. D., Kwolek, W. F., Hill, F. D., Hammond, E. G., Pohle, W. D., Gregory, R. L., Van Giessen, B., Pohle, W. D., Weiss, T. J., Taylor, J. R., Ahern, J. J., Rolker, Jr., J. H., Rheineck, A. E., Shulman, Sol, Brand, B. G., Schoen, H. O., Gast, L. E., Cowan, J. C., Peng, S. C. S., Wood, D. L., Hopper, Jr., L. L., Dollear, F. G., Zimmerman, D. D., Therriault, D. G., Taylor, J. F., Westphal, U., Mullen, J. D., Smith, D. E., Riser, G. R., Bloom, F. W., Witnauer, L. P., Mod, R. R., Magne, F. C., Bell, E. W., Friedrich, J. P., Gast, L. E., Maerker, G., Haeberer, E. T., Ault, W. C., Kenney, H. E., Komanowsky, Daria, Wrigley, A. N., Eisner, Abner, Perlstein, Theodore, Beal, R. E., Fitton, P., Pryde, E. H., Mayland, B. J., Harvin, R. L., Trimarke, C. R., Frankel, E. N., Davison, V. L., Emken, E., Mabrouk, A. F., Selke, E., Rohwedder, W. K., Lavery, H., Oakley, H. B., Lovegren, N. V., Bradshaw, B., Scott, W. E., Krewson, C. F., Oswald, J., Crauer, L. S., Pennington, H., Carter, Fairie Lyn, Frampton, V. L., McGhee, J. E., Kirk, L. D., Mustakas, G. C., Scott, W. E., Griffin, Jr., E. L., Allen, L. E., Smith, O. B., Downey, R. K., Black, L. T., Jurbergs, K. A., Dowling, D. J., Szutowicz, Walter, McKillican, Mary E., Bell, J. M., Rahm, J. J., Kaunitz, Hans, Johnson, Ruth Ellen, Blank, Merle, Privett, O. S., Mahadevan, V., Cubero, E., Lundberg, W. O., Sand, D., and Feldman, G. L.

Published
1963
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44. LETTERS TO THE EDITORS.

Author

Moser, Helen Lambarth, Loch, P. L., Cole, Fred F., Francis, J. M., Savage, J. R., McKinney, M. I., Chamberlin, John R., Jelenko, Delia M., O'Brien, R. C., Melanson, Joseph I., Paull, Joseph T., Girardot, Lawrence E., Moody, George B., Knickles, Chester A., and Lindley, Sandy

Subjects
*LETTERS to the editor, *DIETITIANS, *HOSPITAL personnel, *COMMUNISTS
Abstract

Several letters to the editor are presented in response to articles in previous issues including "They Didn't Know What They Started," by Steven M. Spencer in the February 24, 1951 issue, "The Man Who Looks Like Truman," by Maurice Zolotow in the February 17, 1951 issue and "The Communist's Dearest Friend," by Craig Thompson in the February 17, 1951 issue.

Published
1951

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