Erythropoietin (EPO) attenuates the immunohistochemical expression of tumor growth factor-ß (TGF-ß) in bleomycin (BLM)-induced pulmonary fibrosis (PF) in rats

Tsavlis, Drosos; Anestakis, Doxakis; Tzoumaka, Anna; Symeonidou, Constantina; Koliakou, Kokona Kouzi; Tektonidou, Anastasia; Spandou, Evangelia

doi:10.1183/13993003.congress-2018.pa996

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“…Regarding ER stress-triggered apoptosis downstream, increased Ca 2+ leakage into the cytoplasm mediated by TG activates the TGF-β/Smad3 pathway [60,61], which induces intrinsic apoptosis in the affected cells [62,63]. In addition, activated caspase-3 (a cysteine protease) triggers DNA fragmentation in cells undergoing apoptosis [27,50].…”

Section: Discussionmentioning

confidence: 99%

Erythropoietin Nanobots: Their Feasibility for the Controlled Release of Erythropoietin and Their Neuroprotective Bioequivalence in Central Nervous System Injury

Nguyen

Koo

et al. 2022

Applied Sciences

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Background: Erythropoietin (EPO) plays important roles in neuroprotection in central nervous system injury. Due to the limited therapeutic time window and coexistence of hematopoietic/extrahematopoietic receptors displaying heterogenic and phylogenetic differences, fast, targeted delivery agents, such as nanobots, are needed. To confirm the feasibility of EPO-nanobots (ENBs) as therapeutic tools, the authors evaluated controlled EPO release from ENBs and compared the neuroprotective bioequivalence of these substances after preconditioning sonication. Methods: ENBs were manufactured by a nanospray drying technique with preconditioning sonication. SH-SY5Y neuronal cells were cotreated with thapsigargin and either EPO or ENBs before cell viability, EPO receptor activation, and endoplasmic reticulum stress-related pathway deactivation were determined over 24 h. Results: Preconditioning sonication (50–60 kHz) for 1 h increased the cumulative EPO release from the ENBs (84% versus 25% at 24 h). Between EPO and ENBs at 24 h, both neuronal cell viability (both > 65% versus 15% for thapsigargin alone) and the expression of the proapoptotic/apoptotic biomolecular markers JAK2, PDI, PERK, GRP78, ATF6, CHOP, TGF-β, and caspase-3 were nearly the same or similar. Conclusion: ENBs controlled EPO release in vitro after preconditioning sonication, leading to neuroprotection similar to that of EPO at 24 h.

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