The Role of Soft Connective Tissue in the Response of Pig Articular Cartilage in Organ Culture to Excess of Retinol

1973 ◽  
Vol 13 (1) ◽  
pp. 205-219
Author(s):  
M. E. J. BARRATT
Keyword(s):  
Articular Cartilage ◽  
Connective Tissue ◽  
Organ Culture ◽  
Growing Pigs ◽  
Cartilage Matrix ◽  
Normal Medium ◽  
Chondroid Tissue ◽  
Extensive Degradation

The action of excess retinol on articular cartilage from growing pigs was studied in organ culture. Retinol had little or no effect on explants of articular cartilage alone, but if the explants were cut so as to include some of the marrow tissue in the invasion cavities, or were cultivated near or in contact with capsular tissue, retinol caused extensive degradation of the cartilage matrix, as indicated by loss of metachromatic staining properties. Many chondrocytes were released from their capsules and assumed a fibroblast-like form. Two types of regeneration were seen. In control explants that included part of the invasion zone, cells below the explant laid down a metachromatic matrix; in similar explants cultured in the presence of retinol, a non-metachromatic osteoid-like tissue was formed at this site. There was little recovery when retinol-treated explants were transferred to normal medium, although both osteoid and chondroid tissue were sometimes regenerated.

Endocytosis of Sugars in Embryonic Skeletal Tissues in Organ Culture

1969 ◽  
Vol 4 (1) ◽  
pp. 139-154
Author(s):  
J. T. DINGLE ◽  
HONOR B. FELL ◽  
AUDREY M. GLAUERT
Keyword(s):  
Organ Culture ◽  
Lysosomal Enzymes ◽  
Articular Chondrocytes ◽  
Appreciable Amount ◽  
Neutral Salt ◽  
Normal Medium ◽  
Limb Bone ◽  
Cytoplasmic Vacuolation ◽  
Golgi Region

Cultivation of limb-bone rudiments in medium containing various non-metabolizable or poorly metabolizable sugars caused vacuolation of the perichondrial and articular cells and was accompanied by an increased synthesis and profuse secretion of lysosomal enzymes. Experiments with [14C] dextran indicated that the cytoplasmic vacuolation was due not to a higher rate of endocytosis, but rather to an abnormally long persistence of the pinocytotic vacuoles. Metachromatic material was lost from the cartilage only in the immediate vicinity of the vacuolated articular chondrocytes and the amount of hexosamine and hydroxyproline released into the medium was not much increased. However, the hexosamine and hydroxyproline of the sucrose treated rudiments was much more susceptible to extraction with neutral salt than those of paired controls. Sucrose taken up by the cells was liberated when the rudiments were returned to normal medium; this release, unlike the secretion of lysosomal enzymes, was unaffected by the presence of hydrocortisone. It is probable that the primary lysosornes, formed in the enlarged Golgi region, are the vehicles for the secretion of lysosomal enzymes. No appreciable amount of enzyrnic activity was released into the medium from rudiments grown in the presence of 0.08 M sucrose, before 36 h; at, or just before this time, however, a net increase in synthesis of enzyme was observed. The role of endocytosis in the resorption of skeletal matrix is discussed.

Influence of the pericellural environment of the cells: The role of mucopolysaccharides in the protection of cartilage cells against immune reactions

1975 ◽  
Vol 271 (912) ◽  
pp. 325-341 ◽  
Keyword(s):  
Rheumatoid Arthritis ◽  
Articular Cartilage ◽  
Connective Tissue ◽  
Cartilage Degradation ◽  
Superficial Layer ◽  
Culture Technique ◽  
Cartilage Matrix ◽  
Control Medium ◽  
Igg Antibodies ◽  
The Matrix

Problems related to rheumatoid arthritis have been investigated by a group at Cambridge using the organ culture technique. Since auto-allergic reactions may be concerned in the chronicity of the disease, the effects of reactive complement- sufficient antisera (AS + C') on embryonic and post-foetal cartilage were examined. The cartilaginous limb bone rudiments enlarged to several times their original volume in control medium, but in the presence of AS + C' they gradually disintegrated, owing to the breakdown of the cartilage matrix; only the superficial cells of the enveloping soft connective tissue were killed, however. Provided breakdown had not advanced too far, the effects of AS + C' were reversible. It was not clear how AS + C' produced these changes, since cartilage matrix is impermeable to molecules as large as the immunoglobulins. To find whether there was a difference in permeability between embryonic and post-foetal cartilage, similar experiments were made on the articular cartilage of young pigs. AS + C' had no effect on pure articular cartilage, and it was shown immunohistochemically that IgG did not penetrate beyond the most superficial layer of cartilage. When, however, the explant was associated with soft connective tissue either as invading marrow or as an adjacent explant of synovium, the cartilage matrix was depleted of proteoglycan; IgG antibodies then entered the cartilage and reacted with the chondrocytes. After a lapse of 8-10 days, collagen also began to break down. If the degradation of collagen was not too extensive, the changes were reversible. Pure cartilage was depleted of proteoglycan by trypsinization and then cultivated in AS + C'. All the chondrocytes reacted with the IgG antibodies. The peripheral cells were killed, but those in the interior survived and rapidly secreted pericellular capsules rich in proteoglycan, which shielded them from further contact with antibodies. In other experiments, pure cartilage was associated with a synovial explant and cultivated in AS + C' for 10 days; this caused severe depletion of the matrix. The synovial tissue was then removed and the isolated cartilage cultured for a further 10 days in either AS + C' or control medium. If mainly proteoglycan had been lost during the primary culture period, breakdown did not continue in AS + C', and sometimes a little new matrix was regenerated, though less than in control medium; if, however, the collagen had been extensively degraded, breakdown continued even in control medium. It is suggested that in both the embryonic and post-foetal cartilage, degradation of the cartilage matrix was due to the enzymatic activity of the associated soft connective tissue which caused a loss first of proteoglycan, which enabled antibodies to reach the chondrocytes, and then of collagen. The possible relevance of these results to the pathogenesis of rheumatoid arthritis is discussed.

Banded aggregates containing fibrillin are present in the cartilage matrix adjacent to chondrocytes in individuals affected with scoliosis

1992 ◽  
Vol 50 (1) ◽  
pp. 892-893
Author(s):  
Douglas R. Keene ◽  
Magaret Fairhurst ◽  
Catherine C. Ridgway ◽  
Lynn Y. Sakai
Keyword(s):  
Connective Tissue ◽  
Marfan Syndrome ◽  
Cross Section ◽  
Immunoelectron Microscopy ◽  
Cartilage Matrix ◽  
Negative Stain ◽  
Gene Coding ◽  
Rotary Shadowing

Matrix microfibrils are present in the connective tissue matrices of all tissues. Following standard TEM processing, they appear in cross section as cylindrical fibrils 8-10 nm in diameter, often associated with amorphous elastin. They are also seen in the absence of amorphous elastin, for example in the shallow papillary layer of skin, and also in cartilage matrix (Figure 1). Negative stain and rotary shadowing studies suggest that microfibrils are composed of laterally associated globular structures connected by fine filamentous strands (“ beaded strings”), and that they are extendable. Immunoelectron microscopy has demonstrated that fibrillin, a 350 Kd glycoprotein, is distributed along all microfibrils with a relaxed periodicity of about 54 nm The gene coding for fibrillin has recently been identified and is defective in the Marfan syndrome.

scholarly journals AB0026 DECREASE OF ANGIOGENIC T CELLS IN CONNECTIVE TISSUE DISEASE-ASSOCIATED INTERSTITIAL LUNG DISEASE

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1046.3-1047
Author(s):  
V. Pulito-Cueto ◽  
S. Remuzgo Martinez ◽  
F. Genre ◽  
B. Atienza-Mateo ◽  
V. M. Mora-Cuesta ◽  
...  
Keyword(s):  
T Cells ◽  
Interstitial Lung Disease ◽  
Connective Tissue ◽  
Lung Disease ◽  
Cell Subset ◽  
Vascular Damage ◽  
Type I ◽  
Research Support ◽  
Angiogenic T Cells

Background:Interstitial lung disease (ILD) is one of the most significant complications of connective tissue diseases (CTD), leading to an increase of the morbidity and mortality in patients with CTD [1]. A specific T cell subset termed angiogenic T cells (TAng), that promote endothelial repair and revascularization, have been involved in the pathogenesis of CTD [2-4]. However, to the best of our knowledge, no information regarding the role of TAng in CTD-ILD+ is available.Objectives:To study, for the first time, the potential role of TAng related to vascular damage in CTD-ILD+.Methods:Peripheral venous blood was collected from 40 patients with CTD-ILD+ and three comparative groups: 44 CTD-ILD- patients, 21 idiopathic pulmonary fibrosis (IPF) patients and 20 healthy controls (HC). All subjects were recruited from the Rheumatology and Pneumology departments of Hospital Universitario Marqués de Valdecilla, Santander, Spain. Quantification of TAng was performed by flow cytometry. TAng were considered as triple-positive for CD3, CD31 and CXCR4.Results:Patients with CTD-ILD+ exhibited a significantly lower TAng frequency than CTD-ILD- patients (p<0.001). Similar results were obtained when patients with CTD-ILD+ were compared with HC (p=0.004) although no difference was observed between CTD-ILD+ and IPF. In addition, a significant increase of TAng frequency was shown in patients with CTD-ILD- in relation to IPF patients (p<0.001), while no difference was observed between CTD-ILD- and HC.Conclusion:Our results reveal a decrease of TAng frequency related to vascular damage in CTD-ILD+. Furthermore, we disclose that the presence of ILD is associated with lower TAng frequency.References:[1]Expert Rev Clin Immunol 2018;14(1):69-82.[2]Circulation 2007;116(15):1671-82.[3]Ann Rheum Dis 2015 74(5):921-7.[4]PLoS One 2017;12(8):e0183102.Acknowledgements:Personal funds, VP-C: PREVAL18/01 (IDIVAL); SR-M: RD16/0012/0009 (ISCIII-ERDF); LL-G: INNVAL20/06 (IDIVAL); RP-F: START PROJECT (FOREUM); RL-M: Miguel Servet type I CP16/00033 (ISCIII-ESF).Disclosure of Interests:Verónica Pulito-Cueto: None declared, Sara Remuzgo Martinez: None declared, Fernanda Genre: None declared, Belén Atienza-Mateo: None declared, Victor Manuel Mora-Cuesta: None declared, David Iturbe-Fernández: None declared, Leticia Lera-Gómez: None declared, Raquel Pérez-Fernández: None declared, Pilar Alonso Lecue: None declared, Javier Rodriguez Carrio: None declared, Diana Prieto-Peña: None declared, Virginia Portilla: None declared, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Grant/research support from: Abbvie, MSD and Roche, Alfonso Corrales: None declared, Jose Manuel Cifrián-Martínez: None declared, Raquel López-Mejías: None declared, Miguel A González-Gay Speakers bureau: Pfizer, Abbvie, MSD, Grant/research support from: Pfizer, Abbvie, MSD

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