Experimental Tracheal Replacement: Angiogenesis and Null Apoptosis Promote Stenosis
Background: Tracheal replacement is a challenge for thoracic surgeons due to stenosis in the trachea-prosthesis anastomosis. We propose that stenosis occurs due to fibrosis as a result of an abnormal healing process, characterized by an increased expression of wound healing growth factors (vascular...
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doaj-f8b643fa903747e6b58bfdae417b61422021-06-04T02:12:58ZengKorean Society for Thoracic & Cardiovascular SurgeryJournal of Chest Surgery2765-16062765-16142021-06-0154319119910.5090/jcs.20.146Experimental Tracheal Replacement: Angiogenesis and Null Apoptosis Promote StenosisJ. Alfredo Santibáñez-Salgado0https://orcid.org/0000-0002-7632-9158Avelina Sotres-Vega1https://orcid.org/0000-0002-1873-4243Miguel O. Gaxiola-Gaxiola2https://orcid.org/0000-0002-2945-9793Jaime Villalba-Caloca3https://orcid.org/0000-0001-9499-1930Karen Bobadilla Lozoya4https://orcid.org/0000-0001-9948-4065Joaquín A. Zúñiga-Ramos5https://orcid.org/0000-0002-7143-0281Instituto Nacional de Enfermedades Respiratorias “Ismael Cosio Villegas”Instituto Nacional de Enfermedades Respiratorias “Ismael Cosio Villegas”Instituto Nacional de Enfermedades Respiratorias “Ismael Cosio Villegas”Instituto Nacional de Enfermedades Respiratorias “Ismael Cosio Villegas”Instituto Nacional de Enfermedades Respiratorias “Ismael Cosio Villegas”Tecnológico de MonterreyBackground: Tracheal replacement is a challenge for thoracic surgeons due to stenosis in the trachea-prosthesis anastomosis. We propose that stenosis occurs due to fibrosis as a result of an abnormal healing process, characterized by an increased expression of wound healing growth factors (vascular endothelial growth factor [VEGF], survivin, and CD31), which promote angiogenesis and decrease apoptosis. We analyzed the immunoreactivity of VEGF, survivin, CD31, and caspase-3 in the development of fibrotic stenosis in prosthetic tracheal replacement. Methods: Fourteen dogs were operated on: group I (n=7) received a 6-ring cervical tracheal segment autograft, while in group II (n=7), a 6-ring segment of the cervical trachea was resected and tracheal continuity was restored with a Dacron prosthesis. The follow-up was 3 months. Immunoreactivity studies for VEGF, survivin, CD31, and caspase-3 were performed. A statistical analysis was done using the Wilcoxon signed rank test. Results: Four animals in group I were euthanized on the 10th postoperative day due to autograft necrosis. Three animals completed the study without anastomotic stenosis. Moderate expression of VEGF (p=0.038), survivin (p=0.038), and CD31 (p=0.038) was found. All group II animals developed stenosis in the trachea-prosthesis anastomotic sites. Microscopy showed abundant collagen and neovascularization vessels. Statistically significant immunoreactive expression of VEGF (p=0.015), survivin (p=0.017), and CD31 (p=0.011) was observed. No expression of caspase-3 was found. Conclusion: We found a strong correlation between fibrosis in trachea-prosthesis anastomoses and excessive angiogenesis, moderate to intense VEGF, CD31, and survivin expression, and null apoptotic activity. These factors led to uncontrolled collagen production.tracheaprosthesisangiogenesisapoptosisfibrosis |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
J. Alfredo Santibáñez-Salgado Avelina Sotres-Vega Miguel O. Gaxiola-Gaxiola Jaime Villalba-Caloca Karen Bobadilla Lozoya Joaquín A. Zúñiga-Ramos |
spellingShingle |
J. Alfredo Santibáñez-Salgado Avelina Sotres-Vega Miguel O. Gaxiola-Gaxiola Jaime Villalba-Caloca Karen Bobadilla Lozoya Joaquín A. Zúñiga-Ramos Experimental Tracheal Replacement: Angiogenesis and Null Apoptosis Promote Stenosis Journal of Chest Surgery trachea prosthesis angiogenesis apoptosis fibrosis |
author_facet |
J. Alfredo Santibáñez-Salgado Avelina Sotres-Vega Miguel O. Gaxiola-Gaxiola Jaime Villalba-Caloca Karen Bobadilla Lozoya Joaquín A. Zúñiga-Ramos |
author_sort |
J. Alfredo Santibáñez-Salgado |
title |
Experimental Tracheal Replacement: Angiogenesis and Null Apoptosis Promote Stenosis |
title_short |
Experimental Tracheal Replacement: Angiogenesis and Null Apoptosis Promote Stenosis |
title_full |
Experimental Tracheal Replacement: Angiogenesis and Null Apoptosis Promote Stenosis |
title_fullStr |
Experimental Tracheal Replacement: Angiogenesis and Null Apoptosis Promote Stenosis |
title_full_unstemmed |
Experimental Tracheal Replacement: Angiogenesis and Null Apoptosis Promote Stenosis |
title_sort |
experimental tracheal replacement: angiogenesis and null apoptosis promote stenosis |
publisher |
Korean Society for Thoracic & Cardiovascular Surgery |
series |
Journal of Chest Surgery |
issn |
2765-1606 2765-1614 |
publishDate |
2021-06-01 |
description |
Background: Tracheal replacement is a challenge for thoracic surgeons due to stenosis in the trachea-prosthesis anastomosis. We propose that stenosis occurs due to fibrosis as a result of an abnormal healing process, characterized by an increased expression of wound healing growth factors (vascular endothelial growth factor [VEGF], survivin, and CD31), which promote angiogenesis and decrease apoptosis. We analyzed the immunoreactivity of VEGF, survivin, CD31, and caspase-3 in the development of fibrotic stenosis in prosthetic tracheal replacement.
Methods: Fourteen dogs were operated on: group I (n=7) received a 6-ring cervical tracheal segment autograft, while in group II (n=7), a 6-ring segment of the cervical trachea was resected and tracheal continuity was restored with a Dacron prosthesis. The follow-up was 3 months. Immunoreactivity studies for VEGF, survivin, CD31, and caspase-3 were performed. A statistical analysis was done using the Wilcoxon signed rank test.
Results: Four animals in group I were euthanized on the 10th postoperative day due to autograft necrosis. Three animals completed the study without anastomotic stenosis. Moderate expression of VEGF (p=0.038), survivin (p=0.038), and CD31 (p=0.038) was found. All group II animals developed stenosis in the trachea-prosthesis anastomotic sites. Microscopy showed abundant collagen and neovascularization vessels. Statistically significant immunoreactive expression of VEGF (p=0.015), survivin (p=0.017), and CD31 (p=0.011) was observed. No expression of caspase-3 was found.
Conclusion: We found a strong correlation between fibrosis in trachea-prosthesis anastomoses and excessive angiogenesis, moderate to intense VEGF, CD31, and survivin expression, and null apoptotic activity. These factors led to uncontrolled collagen production. |
topic |
trachea prosthesis angiogenesis apoptosis fibrosis |
work_keys_str_mv |
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