2011
DOI: 10.1007/s00296-011-1891-1
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Increased expression of IL-1 receptors in response to IL-1β may produce more IL-6, IL-8, VEGF, and PGE2 in senescent synovial cells induced in vitro than in presenescent cells

Abstract: Primary synovial cells with high passage number demonstrate increased production of proinflam-

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Cited by 9 publications
(5 citation statements)
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References 14 publications
(16 reference statements)
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“…RA-derived FLS, which undergo replicative senescence induced by serial passage, produce significantly more IL-6, IL-8, vascular endothelial growth factor (VEGF) and prostaglandin E2 (PGE2) in response to IL-1β, when compared to early-passage FLS [202]. Analysis of the molecular mechanisms underlying SASP revealed a critical role of persistent DNA damage response involving increased levels of proteins from the ATM pathway (ATM, NBS1, CHK2) [203, 204].…”
Section: The Nine Hallmarks Of Aging and Ramentioning
confidence: 99%
“…RA-derived FLS, which undergo replicative senescence induced by serial passage, produce significantly more IL-6, IL-8, vascular endothelial growth factor (VEGF) and prostaglandin E2 (PGE2) in response to IL-1β, when compared to early-passage FLS [202]. Analysis of the molecular mechanisms underlying SASP revealed a critical role of persistent DNA damage response involving increased levels of proteins from the ATM pathway (ATM, NBS1, CHK2) [203, 204].…”
Section: The Nine Hallmarks Of Aging and Ramentioning
confidence: 99%
“…Interleukin‐1β (IL‐1β) is a cytokine released by activated macrophages and monocytes during the acute phase of the inflammatory response . IL‐1β is a potent stimulator of the HPA axis by releasing CRH, adrenocorticotropic hormone (ACTH), and glucocorticoids . Although there is strong evidence supporting the influence of altered neuroendocrine and immune responses in mood disorders, the neurobiological factors involved in suicidal behavior have been scarcely researched.…”
mentioning
confidence: 99%
“…TNF-α may directly promote osteoclast maturation and differentiation by inducing the expression of macrophage colony-stimulating factor and receptor activator of nuclear factor κB ligand (RANKL) in osteoblasts (50). Additionally, TNF-α may directly promote RANKL-exposed precursor cells to differentiate into osteoclasts, activate mature osteoclasts and inhibit osteoclast apoptosis (51). According to the present results, CGRP pretreatment inhibited PgLPS-induced osteoblast apoptosis; however, this phenomenon was reversed by the addition of TNF-α.…”
Section: Discussionmentioning
confidence: 99%