Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic inflammatory cells are key components in the progression of atherosclerotic plaques and restenosis after coronary angioplasty. Adhesion molecules are fundamental in inflammatory processes. Therefore, the distributions of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule (VCAM) were investigated in directional coronary atherectomy specimens obtained from 14 patients, in 6 with acute coronary syndromes (myocardial infarction and unstable angina within 1 month), 6 with old myocardial infarction and 2 with stable effort angina. There were eight primary lesions and six restenotic lesions. Atherectomy tissue fragments were snap frozen and cut into 4 microns thick cryostat sections for immunohistochemical staining by avidin-biotin complex immunoperoxidase techniques using adhesion molecule specific monoclonal antibodies BBIG-I1 (ICAM-1) and BBIG-V1 (VCAM). The cells of lesions were characterized in sequential sections by macrophage marker KP1 (CD68), endothelial marker JC/70A (CD31), and smooth muscle cell marker 1A4 (alpha-smooth muscle actin). Four restenotic lesions that had undergone a prior balloon angioplasty within a few months consisted of intimal proliferation and the other lesions were atherosclerotic plaque. Macrophage-rich areas were seen in the lesions from acute coronary syndromes and/or early restenotic lesions. Expression of ICAM-1 or VCAM was strongly associated with macrophage-rich areas, but VCAM staining was weaker than ICAM-1 except in one restenotic lesion. Macrophages that express ICAM-1 and/or VCAM may be important in the unstable plaques and restenotic lesions related to disease activity of ischemic heart disease.
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PMID:[Immunohistochemical analysis of adhesion molecules in directional coronary atherectomy specimens]. 747 44

Osteoclasts from a patient affected by osteopetrosis were examined in vivo and in vitro. Iliac crest biopsy revealed an osteosclerotic pattern, with prominent numbers of osteoclasts noted for hypernuclearity and incomplete adherence to the bone surface. A population comprising tartrate-resistant acid phosphatase (TRAP)-positive, multinucleated and mononuclear cells, and alkaline phosphatase-positive stromal fibroblasts was obtained in vitro from bone marrow. Mononuclear TRAP-positive precursors spontaneously fused in culture to form giant osteoclast-like cells. These cells expressed the osteoclast marker MMP-9 and calcitonin receptor, and lacked the macrophage marker, Fc receptor. Expression and distribution of c-src, c-fms, and CD68, and response to steroid hormones relevant to osteoclast differentiation and function were apparently normal, whereas cell retraction in response to calcitonin was impaired. TRAP-positive multinucleated cells did not form osteoclast-specific adhesion structures (clear zone, podosomes, or actin rings). Bone resorption rate was severely reduced in vitro. Focal adhesions and stress fibers were observed en lieu of podosomes and actin rings. Adhesion structures contained low levels of immunoreactive vitronectin receptor, most of this integrin being retained in cytoplasmic vesicles. These data provide the first characterization of abnormal differentiation and function of human osteopetrotic osteoclast-like cells.
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PMID:Mechanisms of osteoclast dysfunction in human osteopetrosis: abnormal osteoclastogenesis and lack of osteoclast-specific adhesion structures. 1062 70

In osteoarthritis (OA), cartilage and bone fragments have been described within the synovial tissue which are surrounded by synovial cells (i.e. detritus synovitis). These cells appear to attach actively to the cartilage and bone fragments. In rheumatoid arthritis (RA), on the other hand, synovial fibroblasts (SF) have also been shown to be localized at sites of invasion into cartilage and bone and to degrade extracellular matrix (ECM) by secreting proteolytic enzymes. One prerequisite for exerting their aggressive properties is the attachment to cartilage and bone ECM. This attachment appears to be mediated by the expression of different adhesion molecules for which corresponding binding sites on ECM components are known. As it has not been addressed to which ECM proteins SF adhere and with which affinity this process takes place, we investigated the adherence of SF from patients with OA and RA to different cartilage and bone matrix proteins. Synovial tissue samples were obtained during synovectomy or arthroplastic surgery and used for isolating and culturing SF. Synovial cells attaching to cartilage/bone fragments were characterized using immunohistochemistry. The adherence of SF to ECM proteins was examined using an adhesion assay with the following proteins coated on 96-well plates: aggrecan (AGG), bone sialoprotein (BSP), cartilage oligomeric matrix protein (COMP), collagen type I, II and VI, proline arginine-rich, end leucine-rich repeat protein (PRELP), osteopontin (OPN) and recombinant chondroadherin (CHAD). Bovine serum albumin was used as negative control. In addition, adhering fibroblasts were photographed using a phase-contrast microscope. As compared with RA-SF, significantly higher numbers of OA-SF adhering to collagen type II, OPN and CHAD could be detected (P < 0.05). In contrast, RA-SF showed increased attachment to collagen type II, OPN and BSP. Adhesion to AGG, COMP and PRELP appeared not to be significantly increased and differed widely among the SF samples, and, apart from one exception (BSP), OA-SF adhered in higher numbers to the matrix proteins than did RA-SF. Using immunohistochemistry, synovial cells attached to cartilage/bone fragments could be shown to predominantly express CD68 (>/=50%). The CD68-negative population was of the fibroblast phenotype (AS02 positive). The study demonstrates that the binding pattern of OA-SF and RA-SF to ECM proteins differs considerably and therefore provides novel insights into the difficult pathophysiology of OA and RA. In general, it appeared that SF adhere primarily to ECM proteins that contain known binding sites for adhesion molecules (e.g. integrins: collagen/integrin alpha(2)beta(1)) and that higher numbers of OA-SF adhered to the cartilage and bone matrix proteins than did RA-SF.
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PMID:Differential adherence of osteoarthritis and rheumatoid arthritis synovial fibroblasts to cartilage and bone matrix proteins and its implication for osteoarthritis pathogenesis. 1554 Oct 45

Adhesion of inflammatory cells to vascular endothelium is mediated by specific cell adhesion receptors on both leukocytes and endothelial cells. One of the adhesion molecules on the endothelium is P-selectin. Decreased vascular P-selectin expression has been associated with tumor progression in melanoma patients. We now report on the expression of endothelial P-selectin in colorectal cancer (CRC). We studied a colorectal tissue specimen series ranging from normal colorectal tissue via unmetastasized primary tumors to tumors with the same depth of invasion at the primary site but with liver metastases. Moreover, P-selectin expression levels in liver metastases were determined. The number of P-selectin positive vessels as a fraction of the total number of vessels, both intra- and peritumorally, was determined by staining for CD62P and CD34, respectively. Furthermore, by immunostaining for leukocytes (CD45) and macrophages (CD68), it was evaluated whether levels of P-selectin expression influenced infiltrate density and composition. The results showed that levels of peritumoral P-selectin expression were reciprocal to the degree of progression in CRC. This relation was even more pronounced intratumorally: in metastasized primary tumors and in the metastatic lesions, P-selectin expression was virtually absent. This distribution pattern was reflected in the numbers of leukocytes that accumulated in the various tissues, since in the primary tumors with metastases, and in the metastatic lesions, hardly any infiltrating cells were observed. In these lesions, leukocytes were present in the peritumoral zone, but seemed unable to enter the tumor tissue. In primary tumors without metastasis, the intratumoral leukocyte infiltration density was significantly higher. Recruitment levels of macrophages remained constant throughout the different tissues. We suggest that downregulation of endothelial P-selectin expression is a mechanism by which CRC lesions evade inflammatory regression and, thereby, progress to a more advanced stage of malignancy.
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PMID:Progressive loss of endothelial P-selectin expression with increasing malignancy in colorectal cancer. 1564 Aug 34

Joint immobilization is commonly used for the treatment of joint injuries and diseases, but it also causes unfavorable outcomes such as joint contracture. The purpose of this study was to examine the morphological changes of the synovial membrane that is suspected as a cause of joint contracture, and localization of type A (macrophage-like) and type B (fibroblast-like) synoviocytes in the capsule after joint immobilization. Male Sprague-Dawley rats were used in this study. Unilateral knee joints were rigidly immobilized at 150 degrees of flexion with internal fixators for 3 days, 1, 2, 4, 8, and 16 weeks (7 rats/each immobilized group), while 42 rats were sham-operated. Sagittal sections of 5 mum were prepared from the medial midcondylar region of the knee joints and assessed with histological, histomorphometric, and immunohistochemical methods. Adhesions were observed both in the anterior and posterior synovial membranes in the immobilized group after 2 weeks. In the adhesion area, the cells were mainly composed of type A synoviocytes that were positive for CD68 and type B synoviocytes positive for prolyl 4-hydroxylase subunit beta. The length of synovial membrane in the immobilized group was significantly shorter than that in the control group after 2 and 4 weeks. After 8 weeks, the adhesion area in the immobilized group became fibrous and hypocellular. The staining intensity of hyaluronic acid-binding protein was increased after 16 weeks. Adhesion and shortening of the synovial membrane and the structural changes of the adhesion area may contribute to the development of joint contracture.
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PMID:Distribution of type A and B synoviocytes in the adhesive and shortened synovial membrane during immobilization of the knee joint in rats. 2050 69

Mild skin rejection is a common observation in reconstructive transplantation. To enlighten the role of this inflammatory reaction we investigated markers for cellular and antibody mediated rejection, adhesion molecules and tolerance markers. Forty-seven skin biopsies (rejection grade I) of human hand allografts were investigated by immunohistochemistry (CD3, CD4, CD8, CD20, CD68, C4d, LFA-1, ICAM-1, E-selectin, P-selectin, VE-cadherin, HLA-DR, IDO, and Foxp3). Expression was read with respect to time after transplant. The infiltrate was mainly comprised of CD3+T-lymphocytes. Among these, CD8+cells were more prominent than CD4+cells. CD20+B-lymphocytes were sparse and CD68+macrophages were found in some, but not all samples (approximately 10% of the infiltrate). The CD4/CD8-ratio was increased after the first year. C4d staining was mainly positive in samples at time-points later than 1 year. Adhesion molecules LFA-1, ICAM-1, E-selectin, P-selectin, and VE-cadherin were found upregulated, and for P-selectin, expression increased with time after transplant. IDO expression was strongest at 3 months-1 year post-transplant and a tendency toward more Foxp3+ cells at later time points was observed. Mild skin rejection after hand transplantation presents with a T-cell dominated dermal cell infiltrate and upregulation of adhesion molecules. The role of C4d expression after year one remains to be elucidated.
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PMID:Histopathologic characterization of mild rejection (grade I) in skin biopsies of human hand allografts. 2198 70