Angiotensin (1-7) Inhibits Transforming Growth Factor-Β1–Induced Epithelial-Mesenchymal Transition of Human Keratinocyte Hacat Cells in vitro

References

• Marneros AG, Krieg T. Keloids – clinical diagnosis, pathogenesis, and treatment options. J Dtsch Dermatol Ges. 2004;2(11):905–913. doi:10.1046/j.1439-0353.2004.04077.x
   PubMedGoogle Scholar
• Atiyeh BS, Costagliola M, Hayek SN. Keloid or hypertrophic scar: the controversy: review of the literature. Ann Plast Surg. 2005;54(6):676–680. doi:10.1097/01.sap.0000164538.72375.93
   PubMed Web of Science ®Google Scholar
• Ding J, Tredget EE. The Role of Chemokines in Fibrotic Wound Healing. Adv Wound Care. 2015;4(11):673–686. doi:10.1089/wound.2014.0550
   PubMed Web of Science ®Google Scholar
• Satish L, Evdokiou A, Geletu E, Hahn JM, Supp DM. Pirfenidone inhibits epithelial–mesenchymal transition in keloid keratinocytes. Burns Trauma. 2020;8. doi:10.1093/burnst/tkz007
   PubMed Web of Science ®Google Scholar
• Bock (Seifert) O, Yu H, Zitron S, Bayat A, Ferguson MW, Mrowietz U. Studies of Transforming Growth Factors Beta 1–3 and their Receptors I and II in Fibroblast of Keloids and Hypertrophic Scars. Acta Dermato-Venereologica. 2005;85(3):216–220. doi:10.1080/00015550410025453
   PubMed Web of Science ®Google Scholar
• Tamaoki M, Imanaka-Yoshida K, Yokoyama K, et al. Tenascin-C regulates recruitment of myofibroblasts during tissue repair after myocardial injury. Am J Pathol. 2005;167(1):71–80. doi:10.1016/S0002-9440(10)62954-9
   PubMed Web of Science ®Google Scholar
• Nangole FW, Agak GW. Keloid pathophysiology: fibroblast or inflammatory disorders? JPRAS Open. 2019;22:44–54. doi:10.1016/j.jpra.2019.09.004
   PubMedGoogle Scholar
• Kuwahara H, Tosa M, Egawa S, Murakami M, Mohammad G, Ogawa R. Examination of Epithelial Mesenchymal Transition in Keloid Tissues and Possibility of Keloid Therapy Target. Plast Reconstr Surg Glob Open. 2016;4(11):e1138. doi:10.1097/GOX.0000000000001138
   PubMedGoogle Scholar
• Hahn JM, McFarland KL, Combs KA, Supp DM. Partial epithelial-mesenchymal transition in keloid scars: regulation of keloid keratinocyte gene expression by transforming growth factor-β1. Burns Trauma. 2016;4:30. doi:10.1186/s41038-016-0055-7
   PubMed Web of Science ®Google Scholar
• Yang C-E, Moon SJ, Kim SJ, et al. Epithelial-mesenchymal transition in keloid tissue. Arch Plast Surg. 2018;45(06):600–601. doi:10.5999/aps.2017.01214
   PubMedGoogle Scholar
• Kong D, Li Y, Wang Z, Sarkar FH. Cancer Stem Cells and Epithelial-to-Mesenchymal Transition (EMT)-Phenotypic Cells: are They Cousins or Twins? Cancers. 2011;3(1):716–729. doi:10.3390/cancers30100716
   PubMedGoogle Scholar
• Wendt MK, Schiemann WP. Therapeutic targeting of the focal adhesion complex prevents oncogenic TGF-beta signaling and metastasis. Breast Cancer Res. 2009;11(5):R68. doi:10.1186/bcr2360
   PubMed Web of Science ®Google Scholar
• Ma X, Chen J, Xu B, et al. Keloid-derived keratinocytes acquire a fibroblast-like appearance and an enhanced invasive capacity in a hypoxic microenvironment in vitro. Int J Mol Med. 2015;35(5):1246–1256. doi:10.3892/ijmm.2015.2135
   PubMed Web of Science ®Google Scholar
• Hahn JM, McFarland KL, Combs KA, Supp DM. Partial epithelial-mesenchymal transition in keloid scars: regulation of keloid keratinocyte gene expression by transforming growth factor-β1. Burns Trauma. 2016;4:s41038-016-0055–7.
   PubMed Web of Science ®Google Scholar
• Zhang M, Liu S, Guan E, et al. Hyperbaric oxygen therapy can ameliorate the EMT phenomenon in keloid tissue. Medicine. 2018;97(29):e11529. doi:10.1097/MD.0000000000011529
   PubMed Web of Science ®Google Scholar
• Do DV, Ong CT, Khoo YT, et al. Interleukin-18 system plays an important role in keloid pathogenesis via epithelial-mesenchymal interactions. Br J Dermatol. 2012;166(6):1275–1288. doi:10.1111/j.1365-2133.2011.10721.x
   PubMed Web of Science ®Google Scholar
• Jiang X, Zhang Z, Song C, et al. Glaucocalyxin A reverses EMT and TGF-β1-induced EMT by inhibiting TGF-β1/Smad2/3 signaling pathway in osteosarcoma. Chem Biol Interact. 2019;307:158–166. doi:10.1016/j.cbi.2019.05.005
   PubMed Web of Science ®Google Scholar
• Xu J, Lamouille S, Derynck R. TGF-β-induced epithelial to mesenchymal transition. Cell Res. 2009;19(2):156–172. doi:10.1038/cr.2009.5
   PubMed Web of Science ®Google Scholar
• Rygiel KA, Robertson H, Marshall HL, et al. Epithelial–mesenchymal transition contributes to portal tract fibrogenesis during human chronic liver disease. Lab Invest. 2008;88(2):112–123. doi:10.1038/labinvest.3700704
   PubMed Web of Science ®Google Scholar
• Lee JH, Massagué J. TGF-β in developmental and fibrogenic EMTs. Semin Cancer Biol. 2022;86:136–145. doi:10.1016/j.semcancer.2022.09.004
   PubMed Web of Science ®Google Scholar
• U T, S A, N U, C P, Y N, P V. Molecular signalings in keloid disease and current therapeutic approaches from natural based compounds. Pharm Biol. 2015;53.
   Web of Science ®Google Scholar
• Hong Y-K, Chang Y-H, Lin Y-C, Chen B, Guevara BEK, Hsu C-K. Inflammation in Wound Healing and Pathological Scarring. Adv Wound Care. 2023;12(5):288–300. doi:10.1089/wound.2021.0161
   Web of Science ®Google Scholar
• Yan L, Cao R, Wang L, et al. Epithelial–mesenchymal transition in keloid tissues and TGF-β1 –induced hair follicle outer root sheath keratinocytes. Wound Repair Regener. 2015;23(4):601–610. doi:10.1111/wrr.12320
   PubMed Web of Science ®Google Scholar
• Grande MT, Sánchez-Laorden B, López-Blau C, et al. Snail1-induced partial epithelial-to-mesenchymal transition drives renal fibrosis in mice and can be targeted to reverse established disease. Nature Med. 2015;21(9):989–997. doi:10.1038/nm.3901
   PubMed Web of Science ®Google Scholar
• A M, A G-P, M N, P A, C E. The expression of the renin-angiotensin-aldosterone system in the skin and its effects on skin physiology and pathophysiology. J Physiol Pharmacol. 2019;70.
   Web of Science ®Google Scholar
• Ghatage T, Goyal SG, Dhar A, Bhat A. Novel therapeutics for the treatment of hypertension and its associated complications: peptide- and nonpeptide-based strategies. Hypertens Res. 2021;44(7):740–755. doi:10.1038/s41440-021-00643-z
   PubMed Web of Science ®Google Scholar
• Sumners C, Peluso AA, Haugaard AH, Bertelsen JB, Steckelings UM. Anti-fibrotic mechanisms of angiotensin AT 2 -receptor stimulation. Acta Physiol (Oxf). 2019;227(1):e13280. doi:10.1111/apha.13280
   PubMed Web of Science ®Google Scholar
• Simões e Silva A, Silveira K, Ferreira A, Teixeira M. ACE2, angiotensin-(1-7) and M as receptor axis in inflammation and fibrosis. Br J Pharmacol. 2013;169(3):477–492. doi:10.1111/bph.12159
   PubMed Web of Science ®Google Scholar
• Bernasconi R, Thriene K, Romero‐Fernández E, et al. Pro‐inflammatory immunity supports fibrosis advancement in epidermolysis bullosa: intervention with Ang‐(1‐7). EMBO Mol Med. 2021;13(10). doi:10.15252/emmm.202114392
   PubMed Web of Science ®Google Scholar
• Okamura K. Angiotensin(1–7) attenuated Angiotensin II-induced hepatocyte EMT by inhibiting NOX-derived H2O2-activated NLRP3 inflammasome/IL-1β/Smad circuit. Free Radic Biol Med. 2016;97:531–543. doi:10.1016/j.freeradbiomed.2016.07.014.
   PubMed Web of Science ®Google Scholar
• Zhou JP, Tang W, Feng Y, et al. Angiotensin-(1–7) decreases the expression of collagen I via TGF-β1/Smad2/3 and subsequently inhibits fibroblast–myofibroblast transition. Clin Sci. 2016;130(21):1983–1991. doi:10.1042/CS20160193
   PubMed Web of Science ®Google Scholar
• Marty P, Chatelain B, Lihoreau T, et al. Halofuginone regulates keloid fibroblast fibrotic response to TGF-β induction. Biomed. Pharmacother. 2021;135:111182. doi:10.1016/j.biopha.2020.111182
   PubMed Web of Science ®Google Scholar
• Miyake Y, Nagaoka Y, Okamura K, Takeishi Y, Tamaoki S, Hatta M. SNAI2 is induced by transforming growth factor‑β1, but is not essential for epithelial‑mesenchymal transition in human keratinocyte HaCaT cells. Exp Ther Med. 2021;22(4):1–10. doi:10.3892/etm.2021.10558
   Web of Science ®Google Scholar
• Wang T, Zhang L, Shi C, et al. TGF-β-induced miR-21 negatively regulates the antiproliferative activity but has no effect on EMT of TGF-β in HaCaT cells. Int J Biochem Cell Biol. 2012;44(2):366–376. doi:10.1016/j.biocel.2011.11.012
   PubMed Web of Science ®Google Scholar
• Krause G, Winkler L, Mueller SL, Haseloff RF, Piontek J, Blasig IE. Structure and function of claudins. Biochimica et Biophysica Acta. 2008;1778(3):631–645. doi:10.1016/j.bbamem.2007.10.018
   PubMed Web of Science ®Google Scholar
• Rybinski B, Franco-Barraza J, Cukierman E. The wound healing, chronic fibrosis, and cancer progression triad. Physiol Genom. 2014;46(7):223–244. doi:10.1152/physiolgenomics.00158.2013
   PubMed Web of Science ®Google Scholar
• Kalluri R, Weinberg RA. The basics of epithelial-mesenchymal transition. J Clin Invest. 2009;119(6):1420–1428. doi:10.1172/JCI39104
   PubMed Web of Science ®Google Scholar
• Liu F, Gu L-N, Shan B-E, Geng C-Z, Sang M-X. Biomarkers for EMT and MET in breast cancer: an update. Oncol Lett. 2016;12(6):4869–4876. doi:10.3892/ol.2016.5369
   PubMed Web of Science ®Google Scholar
• Reinke LM, Xu Y, Cheng C. Snail represses the splicing regulator epithelial splicing regulatory protein 1 to promote epithelial-mesenchymal transition. J Biol Chem. 2012;287(43):36435–36442. doi:10.1074/jbc.M112.397125
   PubMed Web of Science ®Google Scholar
• Conacci-Sorrell M, Simcha I, Ben-Yedidia T, Blechman J, Savagner P, Ben-Ze’ev A. Autoregulation of E-cadherin expression by cadherin–cadherin interactions. J Cell Biol. 2003;163(4):847–857. doi:10.1083/jcb.200308162
   PubMed Web of Science ®Google Scholar
• Vincent T, Neve EPA, Johnson JR, et al. A SNAIL1-SMAD3/4 transcriptional repressor complex promotes TGF-β mediated epithelial-mesenchymal transition. Nat Cell Biol. 2009;11(8):943–950. doi:10.1038/ncb1905
   PubMed Web of Science ®Google Scholar
• Guo H, Jian Z, Liu H, et al. TGF-β1-induced EMT activation via both Smad-dependent and MAPK signaling pathways in Cu-induced pulmonary fibrosis. Toxicol Appl Pharmacol. 2021;418:115500. doi:10.1016/j.taap.2021.115500
   PubMed Web of Science ®Google Scholar
• Chen Y, Fan J, Cao L, et al. Unique mechanistic insights into the beneficial effects of angiotensin-(1-7) on the prevention of cardiac fibrosis: a metabolomic analysis of primary cardiac fibroblasts. Exp Cell Res. 2019;378(2):158–170. doi:10.1016/j.yexcr.2019.03.006
   PubMed Web of Science ®Google Scholar
• Liu M-L, Xing S-J, Liang X-Q, et al. Reversal of Hypoxic Pulmonary Hypertension by Hypoxia-Inducible Overexpression of Angiotensin-(1-7) in Pulmonary Endothelial Cells. Mol Ther Methods Clin Dev. 2020;17:975–985. doi:10.1016/j.omtm.2020.04.008
   PubMed Web of Science ®Google Scholar
• Choi HS, Kim IJ, Kim CS, et al. Angiotensin-[1–7] attenuates kidney injury in experimental Alport syndrome. Sci Rep. 2020;10(1):4225. doi:10.1038/s41598-020-61250-5
   PubMed Web of Science ®Google Scholar
• Touyz RM, Montezano AC. Angiotensin-(1–7) and Vascular Function. Hypertension. 2018;71(1):68–69. doi:10.1161/HYPERTENSIONAHA.117.10406
   PubMed Web of Science ®Google Scholar