Il‐1β and prostaglandins regulate integrin mRNA expression

Milam, Stephen B.; Magnuson, Victoria L.; Steffensen, Bjørn; Chen, Dali; Klebe, Robert J.

doi:10.1002/jcp.1041490202

Cited by 49 publications

(29 citation statements)

References 69 publications

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“…Increased ultrastructural localization of p-1 integrin at areas of morphological specialization and greatest mechanical stress, such as 2-bands and in areas where collagen attaches to cardiac myocytes, emphasizes the relationship between integrins and ECM components and the role mechanical stimulation may play in the expression and distribution of these components . Chemical factors, including metalloproteinases, growth factors, and cyrokines, also regulate the organization and interactions of ECM components, integrins, and intracellular development (Nakagawa et al, in press;Milam et al, 1991;Werb et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

Distribution of beta-1 integrin in the developing rat heart.

Carver

Price

Raso

et al. 1994

J Histochem Cytochem.

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Cell-cell and cell-matrix interactions play critical roles in various developmental processes including differentiation, proliferation, and migration. Members of the integrin family of cell surface components are important mediators of these cell-extracellular matrix (ECM) contacts or interactions.The ECM provides signals to individual cells essential for development and differentiation and plays essential roles in establishing and maintaining the complex structure of the vertebrate heart. Integrins provide a fundamental link for transduction of developmental signals to cells. Integrin expression by cardiac myqtes is altered during neonatal heart development and disease; however, little is known regarding the spatial and temporal patterns of integrin expression during embryonic and fetal heart development. Essential to understanding the role of integrins in the organization of the heart, the present studies have localized 0-1 integrin protein and mRNA in fetal and neonatal rat hearts. b1 integrin is predominantly found in regions of remodeling (trabeculae) in the early heart (10-13 days of gestation). Later in development (15 days of gestation onward), b1 integrin is abundant in regions containing an elaborate ECM, such as the valves. These studies further support the hypothesis that the expressions of integrins and ECM are coordinately regulated in the developing heart. ( J Hisrochem Cytochem

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Section: Discussionmentioning

confidence: 99%

Distribution of beta-1 integrin in the developing rat heart.

Carver

Price

Raso

et al. 1994

J Histochem Cytochem.

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“…17 and 62). There is also evidence that NO mediates the catabolic effects of IL-1 (63) and modulation of integrins (45,64) in OA cartilage. The overproduction of COX-2 and PGE 2 in OA may contribute to the pain experienced in this disease, because inhibitors of COX-2 provide symptomatic improvement in the clinic (65).…”

Section: Regulation Of No and Pge 2 Production By Il-18 In Human Oaafmentioning

confidence: 99%

Functional Genomic Analysis in Arthritis-Affected Cartilage: Yin-Yang Regulation of Inflammatory Mediators by α5β1 and αVβ3 Integrins

Attur

Dave

Clancy

et al. 2000

The Journal of Immunology

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Osteoarthritis-affected cartilage exhibits enhanced expression of fibronectin (FN) and osteopontin (OPN) mRNA in differential display and bioinformatics screen. Functional genomic analysis shows that the engagement of the integrin receptors α5β1 and αvβ3 of FN and OPN, respectively, have profound effects on chondrocyte functions. Ligation of α5β1 using activating mAb JBS5 (which acts as agonist similar to FN N-terminal fragment) up-regulates the inflammatory mediators such as NO and PGE2 as well as the cytokines, IL-6 and IL-8. Furthermore, up-regulation of these proinflammatory mediators by α5β1 integrin ligation is mediated via induction and autocrine production of IL-1β, because type II soluble IL-1 decoy receptor inhibits their production. In contrast, αvβ3 complex-specific function-blocking mAb (LM609), which acts as an agonist similar to OPN, attenuates the production of IL-1β, NO, and PGE2 (triggered by α5β1, IL-1β, IL-18, or IL-1β, TNF-α, plus LPS) in a dominant negative fashion by osteoarthritis-affected cartilage and activated bovine chondrocytes. These data demonstrate a cross-talk in signaling mechanisms among integrins and show that integrin-mediated “outside in” and “inside out” signaling very likely influences cartilage homeostasis, and its deregulation may play a role in the pathogenesis of osteoarthritis.

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“…These a-subunits may form heterodimers with other a subunits to provide unique cell-extracellular matrix relationships. These alterations may be important for cell migration, cellular responses to inflammation, and cell-mediated turnover of affected articular tissues (Cutolo et al, 1993;Milam et al, 1991a;Ruoslahti, 1991;Stoolman, 1989;Takahashirtfl!., 1992;Tremble etal, 1994;Wallet al, 1994).…”

Section: (4) Integrinsmentioning

confidence: 99%

Pathogenesis of Degenerative Joint Disease in the Human Temporomandibular Joint

Haskin

Milam²,

Cameron

1995

Critical Reviews in Oral Biology & Medicine

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136

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ABSTRACT:The wide range of disease prevalences reported in epidemiological studies of temporomandibular degenerative joint disease reflects the fact that diagnoses are frequently guided by the presence or absence of non-specific signs and symptoms. Treatment is aimed at alleviating the disease symptoms rather than being guided by an understanding of the underlying disease processes. Much of our current understanding of disease processes in the temporomandibular joint is based on the study of other articular joints. Although it is likely that the molecular basis of pathogenesis is similar to that of other joints, additional study of the temporomandibular joint is required due to its unique structure and function. This review summarizes the unique structural and molecular features of the temporomandibular joint and the epidemiology of degenerative temporomandibular joint disease. As is discussed in this review, recent research has provided a better understanding of the molecular basis of degenerative joint disease processes, including insights into: the regulation of cytokine expression and activation, arachidonic acid metabolism, neural contributions to inflammation, mechanisms of extracellular matrix degradation, modulation of cell adhesion in inflammatory states, and the roles of free radicals and heat shock proteins in degenerative joint disease. Finally, the multiple cellular and molecular mechanisms involved in disease initiation and progression, along with factors that may modify the adaptive capacity of the joint, are presented as the basis for the rational design of new and more effective therapy.

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Il‐1β and prostaglandins regulate integrin mRNA expression

Cited by 49 publications

References 69 publications

Distribution of beta-1 integrin in the developing rat heart.

Distribution of beta-1 integrin in the developing rat heart.

Functional Genomic Analysis in Arthritis-Affected Cartilage: Yin-Yang Regulation of Inflammatory Mediators by α5β1 and αVβ3 Integrins

Pathogenesis of Degenerative Joint Disease in the Human Temporomandibular Joint

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