TY - JOUR
T1 - Cellular and molecular alterations in spinal cord injury patients with pressure ulcers
T2 - A preliminary report
AU - Cruse, J. M.
AU - Wang, H.
AU - Lewis, R. E.
AU - Cespedes, J.
AU - Morrison, R. S.
AU - Lineaweaver, W. C.
AU - Dilioglou, S.
N1 - Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 2002/4
Y1 - 2002/4
N2 - The study was designed to investigate the changes, both numerically and functionally, of the molecules critical to wound healing in spinal cord injury (SCI) patients. Spinal cord injury patients who demonstrated delayed healing of their pressure ulcers were used as study subjects. Age-matched healthy individuals served as controls. Adhesion molecule expression of the peripheral blood leukocytes, including lymphocytes and granulocytes, was measured by flow cytometric analysis. Binding capacity of the lymphocytes was evaluated using human umbilical cord vein endothelial cells (HUVECs) as the binding matrix. Samples from pressure ulcers of the patients were immunostained to define fibronectin, kalinin, β4 integrin, α2β1, α3β1, α5β1, and CD138 expression. Compared to healthy controls, there was decreased expression of CD11a, CD11b, CD18, CD49b, CD49c, CD49d, CD54, and CD8 in patients' lymphocyte populations and CD11a, CD18, CD49c, CD49d, and CD8 in patients' granulocyte populations. The binding capacity, expressed as percentage binding of the lymphocytes to the HUVEC matrix, was greatly diminished in the patients. There was markedly diminished immunohistochemical staining of fibronectin in pressure ulcers. These findings showed that delayed healing of pressure ulcers in SCI patients can be attributed to reduced adhesion molecule expression, impaired cell-cell interaction, and lack of extracellular matrix structural and functional protein.
AB - The study was designed to investigate the changes, both numerically and functionally, of the molecules critical to wound healing in spinal cord injury (SCI) patients. Spinal cord injury patients who demonstrated delayed healing of their pressure ulcers were used as study subjects. Age-matched healthy individuals served as controls. Adhesion molecule expression of the peripheral blood leukocytes, including lymphocytes and granulocytes, was measured by flow cytometric analysis. Binding capacity of the lymphocytes was evaluated using human umbilical cord vein endothelial cells (HUVECs) as the binding matrix. Samples from pressure ulcers of the patients were immunostained to define fibronectin, kalinin, β4 integrin, α2β1, α3β1, α5β1, and CD138 expression. Compared to healthy controls, there was decreased expression of CD11a, CD11b, CD18, CD49b, CD49c, CD49d, CD54, and CD8 in patients' lymphocyte populations and CD11a, CD18, CD49c, CD49d, and CD8 in patients' granulocyte populations. The binding capacity, expressed as percentage binding of the lymphocytes to the HUVEC matrix, was greatly diminished in the patients. There was markedly diminished immunohistochemical staining of fibronectin in pressure ulcers. These findings showed that delayed healing of pressure ulcers in SCI patients can be attributed to reduced adhesion molecule expression, impaired cell-cell interaction, and lack of extracellular matrix structural and functional protein.
KW - Cellular adhesion molecules
KW - Fibronectin
KW - Pressure ulcers
KW - Spinal cord injury
KW - Wound healing
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U2 - 10.1006/exmp.2002.2420
DO - 10.1006/exmp.2002.2420
M3 - Article
C2 - 11890721
AN - SCOPUS:0036343408
SN - 0014-4800
VL - 72
SP - 124
EP - 131
JO - Experimental and Molecular Pathology
JF - Experimental and Molecular Pathology
IS - 2
ER -