scholarly journals Cellular Physiology of Articular Cartilage in Health and Disease

10.5772/28379 ◽  
2012 ◽  
Author(s):  
Peter I. ◽  
Robert J. ◽  
John S.
Keyword(s):  
Articular Cartilage ◽  
Cellular Physiology ◽  
Health And Disease

scholarly journals The ciliary protein IFT88 controls post-natal cartilage thickness and influences development of osteoarthritis

2020 ◽  
Author(s):  
CR Coveney ◽  
L Zhu ◽  
J Miotla-Zarebska ◽  
B Stott ◽  
I Parisi ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Cell Biology ◽  
Articular Chondrocytes ◽  
Skeletal Development ◽  
Cartilage Degradation ◽  
Cartilage Thickness ◽  
Tissue Growth ◽  
Calcified Cartilage ◽  
Health And Disease

AbstractMechanical forces are known to drive cellular signalling programmes in cartilage development, health, and disease. Proteins of the primary cilium, implicated in mechanoregulation, control cartilage formation during skeletal development, but their role in post-natal cartilage is unknown. Ift88fl/fl and AggrecanCreERT2 mice were crossed to create a cartilage specific inducible knockout mouse AggrecanCreERT2;Ift88fl/fl. Tibial articular cartilage thickness was assessed, through adolescence and adulthood, by histomorphometry and integrity by OARSI score. In situ cell biology was investigated by immunohistochemistry (IHC) and qPCR of micro-dissected cartilage. OA was induced by destabilisation of the medial meniscus (DMM). Some mice were provided with exercise wheels in their cage. Deletion of IFT88 resulted in a reduction in medial articular cartilage thickness (atrophy) during adolescence from 102.57μm, 95% CI [94.30, 119.80] in control (Ift88fl/fl) to 87.36μm 95% CI [81.35, 90.97] in AggrecanCreERT2;Ift88fl/fl by 8-weeks p<0.01, and adulthood (104.00μm, 95% CI [100.30, 110.50] in Ift88fl/fl to 89.42μm 95% CI [84.00, 93.49] in AggrecanCreERT2;Ift88fl/fl, 34-weeks, p<0.0001) through a reduction in calcified cartilage. Thinning in adulthood was associated with spontaneous cartilage degradation. Following DMM, AggrecanCreERT2;Ift88fl/fl mice had increased OA (OARSI scores at 12 weeks Ift88fl/fl = 22.08 +/− 9.30, and AggrecanCreERT2;Ift88fl/fl = 29.83 +/− 7.69). Atrophy was not associated with aggrecanase-mediated destruction or chondrocyte hypertrophy. Ift88 expression positively correlated with Tcf7l2 and connective tissue growth factor. Cartilage thickness was restored in AggrecanCreERT2;Ift88fl/fl by voluntary wheel exercise. Our results demonstrate that ciliary IFT88 regulates cartilage thickness and is chondroprotective, potentially through modulating mechanotransduction pathways in articular chondrocytes.

Amphiregulin in cellular physiology, health, and disease: Potential use as a biomarker and therapeutic target

2021 ◽  
Author(s):  
Siddharth S. Singh ◽  
Shashi B. Chauhan ◽  
Awnish Kumar ◽  
Shashi Kumar ◽  
Christian R. Engwerda ◽  
...  
Keyword(s):  
Therapeutic Target ◽  
Cellular Physiology ◽  
Health And Disease ◽  
Potential Use

Automated Indentation Demonstrates Structural Stiffness of Femoral Articular Cartilage and Temporomandibular Joint Mandibular Condylar Cartilage Is Altered in FgF2KO Mice

Cartilage ◽  
2020 ◽  
pp. 194760352096256
Author(s):  
Paige S. Woods ◽  
Alyssa A. Morin ◽  
Po-Jung Chen ◽  
Sarah Mahonski ◽  
Liping Xiao ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Temporomandibular Joint ◽  
Functional Characterization ◽  
Structural Stiffness ◽  
Motion Controller ◽  
Condylar Cartilage ◽  
Spatially Resolved ◽  
Mandibular Condylar Cartilage ◽  
Fgf2 Expression ◽  
Health And Disease

Objective Employ an automated indentation technique, using a commercially available machine, to assess the effect of fibroblast growth factor 2 (FGF2) expression on structural stiffness over the surface of both murine femoral articular cartilage (AC) and temporomandibular joint (TMJ) mandibular condylar cartilage (MCC). Design Experiments were performed using 3-month-old female homozygote Fgf2KO mice with wild type (WT) littermates. After euthanization, isolated mandibles and hindlimbs were either processed for histology or subjected to automated indentation on a Biomomentum Mach-1 v500csst with a 3-axis motion controller in a phosphate buffered saline bath using a 0.3 mm spherical tip indenter. The effect of indentation depth on normal force was characterized, then structural stiffness was calculated and mapped at multiple positions on the AC and MCC. Results Automated indentation of the AC and TMJ MCC was successfully completed and was able to demonstrate both regional variation in structural stiffness and differences between WT and Fgf2KO mice. Structural stiffness values for Fgf2KO AC were significantly smaller than WT at both the medial/anterior ( P < 0.05) and medial/posterior ( P < 0.05) positions. Global Fgf2KO also lead to a decrease in MCC thickness of the TMJ compared with WT ( P < 0.05) and increased structural stiffness values for Fgf2KO at both the posterior and anterior location ( P < 0.05). Conclusions Automated indentation spatially resolved differences in structural stiffness between WT and Fgf2KO tissue, demonstrating FGF2 expression affects femoral AC and TMJ MCC. This quantitative method will provide a valuable approach for functional characterization of cartilage tissues in murine models relevant to knee joint and TMJ health and disease.

scholarly journals Chondrocyte heterogeneity: immunohistologically defined variation of integrin expression at different sites in human fetal knees.

1995 ◽  
Vol 43 (4) ◽  
pp. 447-457 ◽  
Author(s):  
D M Salter ◽  
J L Godolphin ◽  
M S Gourlay
Keyword(s):  
Articular Cartilage ◽  
Growth Plate ◽  
Articular Chondrocytes ◽  
Knee Joints ◽  
Matrix Composition ◽  
Epiphyseal Growth Plate ◽  
Surface Receptors ◽  
Cartilage Differentiation ◽  
Health And Disease ◽  
And Function

During development and at maturity different forms of cartilage vary in morphology and macromolecular content. This reflects heterogeneity of chondrocyte activity, in part involving differential interactions with the adjacent extracellular matrix via specialized cell surface receptors such as integrins. We undertook an immunohistological study on a series of human fetal knee joints to assess variation in the expression of integrins by chondrocytes and potential matrix ligands in articular, epiphyseal, growth plate, and meniscal cartilage. The results show that articular chondrocytes (beta 1+, beta 5 alpha V+, alpha 1+, alpha 2+/-, alpha 5+, weakly alpha 6+, alpha V+) differed from epiphyseal (beta 1+, beta 5 alpha V+, alpha 1+/-, alpha 2+/-, alpha 5+, alpha 6+, alpha V+) growth plate (beta 1+, beta 5 alpha V+, alpha 1-, alpha 2-, alpha 5+, alpha 6+, alpha V+), and meniscal cells (beta 1+, beta 5 alpha V+, alpha 1+, strongly alpha 2+, alpha 5+, alpha 6+, alpha V+ in expression of integrin subunits. There was no expression of beta 3, beta 4, beta 6, or alpha 3 by chondrocytes. These results differ from previous reports on the expression of integrins by adult articular cartilage, where alpha 2 and alpha 6 are not seen. Variation in distribution of matrix ligands was also seen. Fibronectin, laminin and Type VI collagen were expressed in all cartilages but there was restricted expression of tenascin, ED-A and ED-B fibronectin isoforms (articular cartilage and meniscus), and vitronectin (absent from growth plate cartilage). Regulated expression of integrins by chondrocytes, associated with changes in the pericellular matrix composition, is of potential importance in control of cartilage differentiation and function in health and disease.

scholarly journals GSK3 as a Regulator of Cytoskeleton Architecture: Consequences for Health and Disease

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 2092
Author(s):  
Daria Hajka ◽  
Bartosz Budziak ◽  
Łukasz Pietras ◽  
Przemysław Duda ◽  
James A. McCubrey ◽  
...  
Keyword(s):  
Growth And Development ◽  
Glycogen Synthase ◽  
Vital Role ◽  
Cell Polarization ◽  
Glycogen Synthase Kinase 3 ◽  
Directional Migration ◽  
Cellular Physiology ◽  
A Cell ◽  
Health And Disease ◽  
Migration Of Cells

Glycogen synthase kinase 3 (GSK3) was initially isolated as a critical protein in energy metabolism. However, subsequent studies indicate that GSK-3 is a multi-tasking kinase that links numerous signaling pathways in a cell and plays a vital role in the regulation of many aspects of cellular physiology. As a regulator of actin and tubulin cytoskeleton, GSK3 influences processes of cell polarization, interaction with the extracellular matrix, and directional migration of cells and their organelles during the growth and development of an animal organism. In this review, the roles of GSK3–cytoskeleton interactions in brain development and pathology, migration of healthy and cancer cells, and in cellular trafficking of mitochondria will be discussed.

scholarly journals The cellular physiology of articular cartilage

1996 ◽  
Vol 81 (3) ◽  
pp. 535-545 ◽  
Author(s):  
AC Hall ◽  
ER Horwitz ◽  
RJ Wilkins
Keyword(s):  
Articular Cartilage ◽  
Cellular Physiology

Clinical Application of the Basic Science of Articular Cartilage Pathology and Treatment

2020 ◽  
Vol 33 (11) ◽  
pp. 1056-1068
Author(s):  
Anna J. Schreiner ◽  
Aaron M. Stoker ◽  
Chantelle C. Bozynski ◽  
Keiichi Kuroki ◽  
James P. Stannard ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Basic Science ◽  
Treatment Strategies ◽  
Cartilage Defects ◽  
Treatment Algorithms ◽  
Relative Paucity ◽  
Health And Disease ◽  
And Function ◽  
Surgical Treatments ◽  
Articular Cartilage Defects

AbstractThe joint is an organ with each tissue playing critical roles in health and disease. Intact articular cartilage is an exquisite tissue that withstands incredible biologic and biomechanical demands in allowing movement and function, which is why hyaline cartilage must be maintained within a very narrow range of biochemical composition and morphologic architecture to meet demands while maintaining health and integrity. Unfortunately, insult, injury, and/or aging can initiate a cascade of events that result in erosion, degradation, and loss of articular cartilage such that joint pain and dysfunction ensue. Importantly, articular cartilage pathology affects the health of the entire joint and therefore should not be considered or addressed in isolation. Treating articular cartilage lesions is challenging because left alone, the tissue is incapable of regeneration or highly functional and durable repair. Nonoperative treatments can alleviate symptoms associated with cartilage pathology but are not curative or lasting. Current surgical treatments range from stimulation of intrinsic repair to whole-surface and whole-joint restoration. Unfortunately, there is a relative paucity of prospective, randomized controlled, or well-designed cohort-based clinical trials with respect to cartilage repair and restoration surgeries, such that there is a gap in knowledge that must be addressed to determine optimal treatment strategies for this ubiquitous problem in orthopedic health care. This review article discusses the basic science rationale and principles that influence pathology, symptoms, treatment algorithms, and outcomes associated with articular cartilage defects in the knee.

Importance of Subchondral Bone to Articular Cartilage in Health and Disease

1999 ◽  
Vol 10 (3) ◽  
pp. 180-192 ◽  
Author(s):  
H Imhof ◽  
M Breitenseher ◽  
F Kainberger ◽  
T Rand ◽  
S Trattnig
Keyword(s):  
Articular Cartilage ◽  
Subchondral Bone ◽  
Health And Disease
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