دورية أكاديمية
أعرض في EDS

Macrophage TGF-β signaling is critical for wound healing with heterotopic ossification after trauma.

التفاصيل البيبلوغرافية
العنوان: Macrophage TGF-β signaling is critical for wound healing with heterotopic ossification after trauma.
المؤلفون: Patel NK; Section of Plastic Surgery, Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan, USA., Nunez JH; Department of Surgery, UT Southwestern Medical Center, Dallas, Texas, USA., Sorkin M; Section of Plastic Surgery, Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan, USA., Marini S; Department of Epidemiology and Emerging Pathogens Institute, University of Florida, Gainesville, Florida, USA., Pagani CA; Section of Plastic Surgery, Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan, USA.; Department of Surgery, UT Southwestern Medical Center, Dallas, Texas, USA., Strong AL; Section of Plastic Surgery, Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan, USA., Hwang CD; Section of Plastic Surgery, Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan, USA., Li S; Section of Plastic Surgery, Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan, USA., Padmanabhan KR; Epigenomics Core, University of Michigan Medical School, Ann Arbor, Michigan, USA., Kumar R; Acceleron Pharma, Inc., Cambridge, Massachusetts, USA., Bancroft AC; Department of Surgery, UT Southwestern Medical Center, Dallas, Texas, USA., Greenstein JA; Section of Plastic Surgery, Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan, USA., Nelson R; Section of Plastic Surgery, Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan, USA., Rasheed HA; Section of Plastic Surgery, Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan, USA., Livingston N; Department of Surgery, UT Southwestern Medical Center, Dallas, Texas, USA., Vasquez K; Section of Plastic Surgery, Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan, USA., Huber AK; Section of Plastic Surgery, Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan, USA., Levi B; Section of Plastic Surgery, Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan, USA.; Department of Surgery, UT Southwestern Medical Center, Dallas, Texas, USA.
المصدر: JCI insight [JCI Insight] 2022 Oct 24; Vol. 7 (20). Date of Electronic Publication: 2022 Oct 24.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: American Society for Clinical Investigation Country of Publication: United States NLM ID: 101676073 Publication Model: Electronic Cited Medium: Internet ISSN: 2379-3708 (Electronic) Linking ISSN: 23793708 NLM ISO Abbreviation: JCI Insight Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Ann Arbor, Michigan : American Society for Clinical Investigation, [2016]-
مواضيع طبية MeSH: Ossification, Heterotopic*/metabolism , Transforming Growth Factor beta1*/metabolism, Humans ; Chromatin/metabolism ; Ligands ; Macrophages/metabolism ; Receptor, Transforming Growth Factor-beta Type I/genetics ; Wound Healing ; Transforming Growth Factor beta/metabolism
مستخلص: Transforming growth factor-β1 (TGF-β1) plays a central role in normal and aberrant wound healing, but the precise mechanism in the local environment remains elusive. Here, using a mouse model of aberrant wound healing resulting in heterotopic ossification (HO) after traumatic injury, we find autocrine TGF-β1 signaling in macrophages, and not mesenchymal stem/progenitor cells, is critical in HO formation. In-depth single-cell transcriptomic and epigenomic analyses in combination with immunostaining of cells from the injury site demonstrated increased TGF-β1 signaling in early infiltrating macrophages, with open chromatin regions in TGF-β1-stimulated genes at binding sites specific for transcription factors of activated TGF-β1 (SMAD2/3). Genetic deletion of TGF-β1 receptor type 1 (Tgfbr1; Alk5), in macrophages, resulted in increased HO, with a trend toward decreased tendinous HO. To bypass the effect seen by altering the receptor, we administered a systemic treatment with TGF-β1/3 ligand trap TGF-βRII-Fc, which resulted in decreased HO formation and a delay in macrophage infiltration to the injury site. Overall, our data support the role of the TGF-β1/ALK5 signaling pathway in HO.
References: Nat Rev Mol Cell Biol. 2013 Aug;14(8):467-73. (PMID: 23839578)
Nat Rev Nephrol. 2016 Jun;12(6):325-38. (PMID: 27108839)
J Bone Miner Res. 1997 Oct;12(10):1584-95. (PMID: 9333119)
J Biol Chem. 2005 Mar 4;280(9):8343-50. (PMID: 15623506)
J Biol Chem. 2003 Mar 21;278(12):10304-13. (PMID: 12525489)
Cold Spring Harb Perspect Biol. 2016 May 02;8(5):. (PMID: 27141051)
Bone. 2013 May;54(1):28-34. (PMID: 23314070)
Proc Natl Acad Sci U S A. 2016 Jan 19;113(3):E338-47. (PMID: 26721400)
Proc Natl Acad Sci U S A. 1987 Aug;84(16):5788-92. (PMID: 2886992)
J Exp Med. 1991 May 1;173(5):1121-32. (PMID: 2022923)
J Immunol. 1991 Sep 1;147(5):1600-6. (PMID: 1652608)
Cell. 2020 Feb 6;180(3):490-501.e16. (PMID: 31955848)
Nat Commun. 2015 Jul 22;6:7866. (PMID: 26198319)
Strategies Trauma Limb Reconstr. 2014 Aug;9(2):65-71. (PMID: 24934800)
Biochem Soc Trans. 2006 Dec;34(Pt 6):1141-4. (PMID: 17073770)
Biomaterials. 2019 Mar;196:51-66. (PMID: 29107337)
J Biol Chem. 2001 May 18;276(20):17058-62. (PMID: 11279127)
Ann N Y Acad Sci. 1990;593:188-96. (PMID: 1695824)
Bone Res. 2019 Dec 10;7:36. (PMID: 31840004)
Blood. 2006 Sep 15;108(6):1821-9. (PMID: 16705092)
Nucleic Acids Res. 2016 Jul 8;44(W1):W160-5. (PMID: 27079975)
Acta Biomater. 2019 Apr 15;89:73-83. (PMID: 30844569)
J Biomech. 2013 Mar 15;46(5):890-8. (PMID: 23357697)
Semin Cell Dev Biol. 2020 May;101:123-139. (PMID: 31879265)
Nature. 1992 Oct 22;359(6397):693-9. (PMID: 1436033)
Nat Commun. 2018 Feb 7;9(1):551. (PMID: 29416028)
Nat Commun. 2017 Dec 12;8(1):2070. (PMID: 29234012)
Nature. 2008 May 15;453(7193):314-21. (PMID: 18480812)
J Immunol. 2020 Apr 15;204(8):2203-2215. (PMID: 32161098)
Int J Surg. 2019 Feb;62:74-85. (PMID: 30615954)
J Bone Miner Res. 1999 Nov;14(11):1805-15. (PMID: 10571679)
Br J Haematol. 2008 Jun;142(2):192-201. (PMID: 18492113)
Cardiovasc Res. 2011 Aug 1;91(3):510-8. (PMID: 21478266)
PLoS One. 2015 Dec 31;10(12):e0146124. (PMID: 26720610)
Birth Defects Res C Embryo Today. 2014 Mar;102(1):37-51. (PMID: 24677722)
J Immunol. 2008 Jul 15;181(2):1232-44. (PMID: 18606677)
Mech Ageing Dev. 2018 Jun;172:51-58. (PMID: 29132871)
Science. 2003 Jul 18;301(5631):363-7. (PMID: 12869760)
J Biomed Mater Res B Appl Biomater. 2003 Apr 15;65(1):150-6. (PMID: 12632384)
Am J Physiol Lung Cell Mol Physiol. 2010 Jun;298(6):L735-43. (PMID: 20190033)
Nat Methods. 2012 Jun 28;9(7):676-82. (PMID: 22743772)
Growth Factors. 2007 Apr;25(2):101-7. (PMID: 17891595)
Proc Natl Acad Sci U S A. 2019 Jul 30;116(31):15570-15579. (PMID: 31311865)
J Immunol. 2008 May 15;180(10):6553-65. (PMID: 18453574)
Sci Rep. 2016 Feb 16;6:21176. (PMID: 26880204)
Tissue Eng Part A. 2012 Jun;18(11-12):1140-50. (PMID: 22480213)
J Immunol. 1995 Aug 15;155(4):2077-84. (PMID: 7636258)
Science. 1999 Apr 2;284(5411):143-7. (PMID: 10102814)
Int J Mol Med. 2012 Nov;30(5):1119-25. (PMID: 22922645)
Curr Osteoporos Rep. 2015 Apr;13(2):116-24. (PMID: 25687936)
J Clin Invest. 2020 Oct 1;130(10):5444-5460. (PMID: 32673290)
Biosci Rep. 2020 Mar 27;40(3):. (PMID: 32065217)
J Am Soc Nephrol. 2015 Apr;26(4):896-906. (PMID: 25266072)
J Cell Physiol. 1995 Aug;164(2):334-43. (PMID: 7622580)
J Bone Miner Res. 1991 Sep;6(9):961-8. (PMID: 1789143)
BMC Syst Biol. 2014 May 15;8:55. (PMID: 24886091)
Nat Commun. 2015 Jul 21;6:7802. (PMID: 26193821)
J Exp Med. 2020 Feb 13;217(3):e20190103. (PMID: 32997468)
Nat Biotechnol. 2011 Jan;29(1):24-6. (PMID: 21221095)
Int J Oncol. 2004 Nov;25(5):1375-82. (PMID: 15492828)
Injury. 2005 Dec;36(12):1392-404. (PMID: 16102764)
J Cell Biol. 1993 Jul;122(1):103-11. (PMID: 8314838)
Stem Cells. 2010 Apr;28(4):734-42. (PMID: 20146266)
Microbes Infect. 1999 Dec;1(15):1275-82. (PMID: 10611755)
Cold Spring Harb Perspect Biol. 2017 Jun 1;9(6):. (PMID: 28108486)
Wound Repair Regen. 2016 Mar;24(2):215-22. (PMID: 26704519)
Respir Res. 2004 Nov 30;5:24. (PMID: 15571627)
Nat Commun. 2020 Feb 5;11(1):722. (PMID: 32024825)
Mol Pharm. 2013 Apr 1;10(4):1425-31. (PMID: 23410508)
Chest. 2019 Mar;155(3):534-539. (PMID: 30359615)
Science. 1993 May 28;260(5112):1344-8. (PMID: 8388127)
Dev Biol. 2009 Aug 15;332(2):325-38. (PMID: 19501582)
Mol Ther. 2017 Aug 2;25(8):1974-1987. (PMID: 28716575)
BMC Immunol. 2012 Jun 15;13:31. (PMID: 22703233)
Nat Metab. 2019 Sep;1(9):912-926. (PMID: 31572976)
Brief Bioinform. 2013 Mar;14(2):178-92. (PMID: 22517427)
Growth Factors. 2009 Apr;27(2):114-20. (PMID: 19180355)
Nat Commun. 2019 Jul 18;10(1):3168. (PMID: 31320650)
Proc Natl Acad Sci U S A. 1993 May 15;90(10):4577-81. (PMID: 8506302)
Proc Natl Acad Sci U S A. 1991 Aug 1;88(15):6805-9. (PMID: 1650483)
معلومات مُعتمدة: R01 AR079171 United States AR NIAMS NIH HHS; R01 AR079863 United States AR NIAMS NIH HHS
فهرسة مساهمة: Keywords: Bone Biology; Growth factors; Immunology; Macrophages
المشرفين على المادة: 0 (Chromatin)
0 (Ligands)
EC 2.7.11.30 (Receptor, Transforming Growth Factor-beta Type I)
0 (Transforming Growth Factor beta1)
0 (Transforming Growth Factor beta)
تواريخ الأحداث: Date Created: 20220913 Date Completed: 20221026 Latest Revision: 20230618
رمز التحديث: 20230620
مُعرف محوري في PubMed: PMC9714796
DOI: 10.1172/jci.insight.144925
PMID: 36099022
قاعدة البيانات: MEDLINE
الوصف
تدمد:2379-3708
DOI:10.1172/jci.insight.144925