https://ogma.newcastle.edu.au/vital/access/ /manager/Index en-au 5 Fibulin-1c regulates transforming growth factor-beta activation in pulmonary tissue fibrosis https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:48369 Fbln1c-deficient (Fbln1c–/–) mice had reduced pulmonary remodeling/fibrosis and improved lung function after bleomycin challenge. Fbln1c interacted with fibronectin, periostin, and tenascin-C in collagen deposits following bleomycin challenge. In a potentially novel mechanism of fibrosis, Fbln1c bound to latent TGF-β–binding protein 1 (LTBP1) to induce TGF-β activation and mediated downstream Smad3 phosphorylation/signaling. This process increased myofibroblast numbers and collagen deposition. Fbln1c and LTBP1 colocalized in lung tissues from patients with IPF. Thus, Fbln1c may be a novel driver of TGF-β–induced fibrosis involving LTBP1 and may be an upstream therapeutic target.]]> Wed 15 Mar 2023 13:12:38 AEDT ]]> A cGAS-dependent response links DNA damage and senescence in alveolar epithelial cells: a potential drug target in IPF https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49742 Tue 30 May 2023 15:22:46 AEST ]]> Circulating RNA differences between patients with stable and progressive idiopathic pulmonary fibrosis https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:38777 Tue 08 Feb 2022 12:17:52 AEDT ]]> A senescence bystander effect in human lung fibroblasts https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45373 2O2 or etoposide; (ii) LFs derived from IPF patients (IPF-LFs) with a high baseline of senescence; or (iii) senescence-induced A549 cells, an AEC line. Additionally, ratios of non-senescent Ctrl-LFs and senescence-induced Ctrl-LFs (100:0, 0:100, 50:50, 90:10, 99:1) were co-cultured and their effect on induction of senescence measured. We demonstrated that exposure of naïve non-senescent Ctrl-LFs to CM from senescence-induced Ctrl-LFs and AECs and IPF-LFs increased the markers of senescence including nuclear localisation of phosphorylated-H2A histone family member X (H2AXγ) and expression of p21, IL-6 and IL-8 in Ctrl-LFs. Additionally, co-cultures of non-senescent and senescence-induced Ctrl-LFs induced a senescent-like phenotype in the non-senescent cells. These data suggest that the phenomenon of “senescence-induced senescence” can occur in vitro in primary cultures of human LFs, and provides a possible explanation for the abnormal abundance of senescent cells in the lungs of IPF patients]]> Thu 27 Oct 2022 12:28:40 AEDT ]]> The fibrogenic actions of lung fibroblast-derived urokinase: a potential drug target in IPF https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30970 Thu 24 Mar 2022 11:31:57 AEDT ]]> Fibulin-1 predicts disease progression in patients with idiopathic pulmonary fibrosis https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:19841 Sat 24 Mar 2018 07:57:07 AEDT ]]>