Ronald H. Goldstein's research while affiliated with Boston University and other places

... FN is a major constituent of the ECM [61][62][63][64]. It is synthesized as a soluble protein and assembled into an insoluble fibrillar matrix outside of cells [44,65,66]. ...

... Although emphysema is defined by the destruction of distal air spaces, with or without fibrosis [97], the majority of clinical studies have described an increase in the amount of ECM fiber deposition in the airways and the lung parenchyma [112][113][114][115]. However, it is important to emphasize that these evaluations were usually performed in patients who were in advanced stages of the disease and in experimental models, after a few days of disease induction [104,[116][117][118]. ...

... 5 μm sections were cut and slides were stained with H&E. Mean linear intercept (MLI), a measurement of airspace destruction and a metric used in experimental models of emphysema, was measured as previously described [25,56]. MLI was determined by selecting 10 fields from an H&E stained slide of the left lung by a blinded reviewer. ...

... To determine the role of protein synthesis and prostaglandins on hypoxia-induced suppression of methyl-AIB uptake, cells were treated with 0% O 2 in the presence and absence of cycloheximide or indomethacin. Cycloheximide at 5 M inhibits 85% of protein synthesis in human lung fibroblasts (17). As reported in these cells (16), cycloheximide alone decreased methyl-AIB uptake (Fig. 6), suggesting the constitutive expression of an activating protein. ...

... There are certainly major differences between the two type I promoters and there may be species differences between human and murine promoters. We employed transgenic animals to examine the function of the collagen ␣1(I) promoter fragment in vivo [Agarwal et al., 1996]. When transgenic mice carrying 3.6 kb of rat collagen promoter driving CAT reporter gene (ColCAT3.6) ...

... The enzymes treatment of cancer has a long history, first in 1902 with the work of Dr John Beard; a professor at the University of Edinburgh proposed that the pancreatic proteolytic enzyme trypsin represent powerful anti-cancer tool phenotypic revertants [14] . L-lysine alpha-oxidase was also recognized as a target for the anti-oncogenic transcription factor, interferon regulatory element-1 (IRE-1), which manifests tumor suppressor activity and contributes to the development of human hematopoietic malignancies [15] . [16] reported that malignant human breast carcinomas and broncho-pulmonary carcinomas LOX was highly expressed in hypertrophic scar-like stroma, surrounding the in situ tumor which forms a peritumor barrier, type I, III, and IV collagens and elastin were found to be co-distributed. ...

... Transforming growth factor-beta 1 (TGF-β1), which plays a very important role in collagen expression [19], has also been widely implicated in the development of tissue fibrosis. Certainly, in both human and animal models of post-traumatic joint contracture, TGF-β1 expression is increased in the joint capsule [20]. ...

... These genes belong to interferonstimulated genes, related closely to interferon signaling (Schneider et al., 2014). Previous studies suggested that interferon (IFN) and IFN-stimulated genes might be involved in pulmonary fibrosis (Neville et al., 1997;Berkmana et al., 2001;Christmann et al., 2014). The low dose of IFN-α could promote bleomycin-induced lung fibrosis in mice and hamsters, though this effect was complicated and might also be influenced by IFN preparations (Neville et al., 1997;Berkmana et al., 2001). ...

... It was suggested that PGE2 was produced in response to the TGF~ and this was mediating the anti-proliferative effects. PGE2 has been shown to decrease the expression ofTGF~ RI and RII and also has the effect of decreasing the binding ofTGF~ to TGF~ RI and RII by 50% (304). Indomethacin, an inhibitor ofPGE2 overcame the inhibitory effects observed in the 1997 McAnulty study (140) and restored the proliferative effects seen previously using low concentrations of ligand. ...

... Furthermore, fibroblasts derived from the aged mouse heart respond to pathophysiological levels of insulin by upregulating an already elevated ERK phosphorylation and increasing collagen type I expression even further (42). Insulin-dependent ERK activation has also been reported by others (101,103). It is not known whether there is cross talk between any of these pathways (TGF-␤, PDGF, EGF, and insulin) in aging cardiac fibroblasts, although weak synergism between insulin and EGF has been reported in other models (22). ...