Induction of the 32-kD human stress protein by auranofin and related triethylphosphine gold analogs

Caltabiano, Madelyn M.; Poste, George; Greig, Russell

doi:10.1016/0006-2952(88)90100-1

Cited by 11 publications

(1 citation statement)

References 15 publications

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“…In parallel, different groups identified a 32 kDa stress-responsive protein, whose expression was highly upregulated in different cell lines in response to challenges such as hyperthermia, heavy metals and oxidative stress. This protein, referred to as Heat-Shock Protein 32 (HSP-32) at that time [5][6][7][8][9][10], was later shown to be identical to HO-1 [11,12]. A third isoform, heme oxygenase-3 (HO-3), was characterized in 1997 in a number of different rat tissues, but displayed poor enzymatic activity [13] and its physiological role remains largely uncharacterized to this day.…”

Section: Introductionmentioning

confidence: 99%

Modulation of Inflammation and Immune Responses by Heme Oxygenase-1: Implications for Infection with Intracellular Pathogens

et al. 2020

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Heme oxygenase-1 (HO-1) catalyzes the degradation of heme molecules releasing equimolar amounts of biliverdin, iron and carbon monoxide. Its expression is induced in response to stress signals such as reactive oxygen species and inflammatory mediators with antioxidant, anti-inflammatory and immunosuppressive consequences for the host. Interestingly, several intracellular pathogens responsible for major human diseases have been shown to be powerful inducers of HO-1 expression in both host cells and in vivo. Studies have shown that this HO-1 response can be either host detrimental by impairing pathogen control or host beneficial by limiting infection induced inflammation and tissue pathology. These properties make HO-1 an attractive target for host-directed therapy (HDT) of the diseases in question, many of which have been difficult to control using conventional antibiotic approaches. Here we review the mechanisms by which HO-1 expression is induced and how the enzyme regulates inflammatory and immune responses during infection with a number of different intracellular bacterial and protozoan pathogens highlighting mechanistic commonalities and differences with the goal of identifying targets for disease intervention.

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