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Keywords {🔍}

trex, article, pubmed, group, fig, analysis, mice, chondrocyte, staining, chondrocytes, macrophages, macrophage, expression, cartilage, google, scholar, quantitative, cas, apoptosis, polarization, lps, role, osteoarthritis, lpsinduced, levels, groups, cfos, representative, protein, matrix, dna, data, oxidative, central, inflammation, stress, protective, blue, dmm, treatment, bar, progression, inflammatory, effect, sicfos, cell, colii, images, significantly, effects,

Topics {✒️}

tpa-modulated trans-acting factor ap-1-dependent c-fos activation sa-β-gal staining kit lps + si-c-fos treated quantitative real-time rt-pcr trex1-mediated anti-inflammatory effects cytoplasmic double-stranded dna cyclic gmp-amp synthase si-c-fos treated inflammation-driven chondrocyte injury lps-induced inflammatory conditions hydrochloric acid/ethanol solution including aicardi-goutières syndrome molecular alterations post-surgery si-c-fos reversed quantitative real-time pcr reduced glycosaminoglycan content endothelial-macrophage coculture models article download pdf full size image dmm-induced oa progression sa-β-gal activity phorbol ester-inducible genes macrophage-mediated inflammatory responses parametric kruskal-wallis tests c57bl/6 jcya-trex1em1/cya tumor necrosis factor-alpha c-fos protein expression anti-inflammatory m2 phenotypes enzyme-linked immunosorbent assay treatment significantly rescued hrp-conjugated secondary antibodies trex1-deficient mice compared central nervous system c-fos expression levels sham-operated trex1−/− mice trex1−/− mice post-dmm late apoptotic/necrotic cells spinal cord injury lps-driven senescence ap-1 inhibition attenuates mitigates osteoarthritis progression lps-induced suppression lps-induced reductions lps-induced injury sa-β-gal sham-operated wt mice si-c-fos lps-induced inflammation c-terminal truncations

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         headline:AP-1-dependent c-Fos activation by TREX1 drives M2 macrophage polarization and mitigates osteoarthritis progression
         description:Inflammation significantly contributes to the pathogenesis of osteoarthritis (OA). Recent studies have elucidated the critical role of the three-prime repair exonuclease 1 (TREX1) in regulating inflammatory responses and oxidative stress. The aim of the study was to investigate the regulatory function of TREX1 in maintaining joint homeostasis subsequent to the destabilization of the medial meniscus (DMM) in a murine model. Trex1-KO mice on a C57BL/6J background were utilized to investigate the role of Trex1 in OA. The DMM-induced OA model demonstrated histological and molecular alterations post-surgery, with immunofluorescence and Western blot analyses employed to assess chondrocyte characteristics and protein expression, respectively. In vitro experiments have been conducted where we established a co-culture system of macrophages and chondrocytes to investigate the regulatory role of Trex1 in macrophage polarization and its subsequent biological effects on chondrocytes, as well as the underlying mechanisms of these regulatory actions. TREX1 deficiency intensifies OA progression in DMM mice, marked by increased oxidative stress, inflammation, and cartilage damage. TREX1 pretreatment in macrophages mitigates LPS-induced chondrocyte apoptosis and oxidative stress, an effect attenuated by si-c-Fos. AP-1 inhibition counters TREX1’s protective impact on chondrocytes. TREX1 modulates macrophage polarization, influencing chondrocyte differentiation and matrix homeostasis in OA pathogenesis. Overall, TREX1’s influence on macrophage polarization affects chondrocyte function and cartilage homeostasis, making it a potential therapeutic target for OA treatment.
         datePublished:2025-06-25T00:00:00Z
         dateModified:2025-06-25T00:00:00Z
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            Mcrophage
            Chondrocyte
            Osteoathritis
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            Biomedicine
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      headline:AP-1-dependent c-Fos activation by TREX1 drives M2 macrophage polarization and mitigates osteoarthritis progression
      description:Inflammation significantly contributes to the pathogenesis of osteoarthritis (OA). Recent studies have elucidated the critical role of the three-prime repair exonuclease 1 (TREX1) in regulating inflammatory responses and oxidative stress. The aim of the study was to investigate the regulatory function of TREX1 in maintaining joint homeostasis subsequent to the destabilization of the medial meniscus (DMM) in a murine model. Trex1-KO mice on a C57BL/6J background were utilized to investigate the role of Trex1 in OA. The DMM-induced OA model demonstrated histological and molecular alterations post-surgery, with immunofluorescence and Western blot analyses employed to assess chondrocyte characteristics and protein expression, respectively. In vitro experiments have been conducted where we established a co-culture system of macrophages and chondrocytes to investigate the regulatory role of Trex1 in macrophage polarization and its subsequent biological effects on chondrocytes, as well as the underlying mechanisms of these regulatory actions. TREX1 deficiency intensifies OA progression in DMM mice, marked by increased oxidative stress, inflammation, and cartilage damage. TREX1 pretreatment in macrophages mitigates LPS-induced chondrocyte apoptosis and oxidative stress, an effect attenuated by si-c-Fos. AP-1 inhibition counters TREX1’s protective impact on chondrocytes. TREX1 modulates macrophage polarization, influencing chondrocyte differentiation and matrix homeostasis in OA pathogenesis. Overall, TREX1’s influence on macrophage polarization affects chondrocyte function and cartilage homeostasis, making it a potential therapeutic target for OA treatment.
      datePublished:2025-06-25T00:00:00Z
      dateModified:2025-06-25T00:00:00Z
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         Trex1
         Mcrophage
         Chondrocyte
         Osteoathritis
         AP-1
         Cell Biology
         Biomedicine
         general
         Life Sciences
         Biochemistry
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            address:
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               type:PostalAddress
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      name:Enning Cui
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      name:Lei Zhang
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      name:Department of Joint Bone Disease Surgery, Changhai Hospital, Naval Medical University, Shanghai, China
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      name:Department of Orthopedics, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing City, China
      name:Department of Orthopedics, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing City, China
      name:Department of Orthopedics, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing City, China
      name:Department of Orthopedics, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing City, China
      name:Department of Orthopedics, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing City, China
      name:Department of Orthopedics, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing City, China
      name:Department of Orthopedics, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing City, China

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