Heat shock proteins in pulmonary fibrosis: pawns of cell homeostasis

Barboza, Willy Roque

doi:10.1152/ajpcell.00073.2022

Cited by 5 publications

(4 citation statements)

References 27 publications

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“…HSP90 is similarly involved in promoting TGF-β signaling via direct stabilization of the TGFβ receptor [42], assistance to ERK, via CDC37, and regulating the nuclear translocation of Smad proteins [43,44]. For these reasons, multiple investigators have hypothesized that treatment with HSP90 inhibitors may represent a novel strategy for the management of pulmonary fibrosis [25,45,46]. However, it is not clear if this protective effect is mediated by the upregulation of HSP70, a common mechanism observed during HSP90 inhibition [18], and more importantly, if the association of HSP70 inducers with HSP90 inhibitors may result in an enhanced beneficial effect.…”

Section: Discussionmentioning

confidence: 99%

HSP70 Is a Critical Regulator of HSP90 Inhibitor’s Effectiveness in Preventing HCl-Induced Chronic Lung Injury and Pulmonary Fibrosis

Colunga Biancatelli,

Solopov,

Day

et al. 2024

IJMS

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Exposure to hydrochloric acid (HCl) can provoke acute and chronic lung injury. Because of its extensive production for industrial use, frequent accidental exposures occur, making HCl one of the top five chemicals causing inhalation injuries. There are no Food and Drug Administration (FDA)-approved treatments for HCl exposure. Heat shock protein 90 (HSP90) inhibitors modulate transforming growth factor-β (TGF-β) signaling and the development of chemical-induced pulmonary fibrosis. However, little is known on the role of Heat Shock Protein 70 (HSP70) during injury and treatment with HSP90 inhibitors. We hypothesized that administration of geranylgeranyl-acetone (GGA), an HSP70 inducer, or gefitinib (GFT), an HSP70 suppressant, alone or in combination with the HSP90 inhibitor, TAS-116, would improve or worsen, respectively, HCl-induced chronic lung injury in vivo and endothelial barrier dysfunction in vitro. GGA, alone, improved HCl-induced human lung microvascular endothelial cells (HLMVEC) barrier dysfunction and, in combination with TAS-116, improved the protective effect of TAS-116. In mice, GGA reduced HCl toxicity and while TAS-116 alone blocked HCl-induced chronic lung injury, co-administration with GGA, resulted in further improvement. Conversely, GFT potentiated HCl-induced barrier dysfunction and impaired the antidotal effects of TAS-116. We conclude that combined treatments with HSP90 inhibitors and HSP70 inducers may represent a novel therapeutic approach to manage HCl-induced chronic lung injury and pulmonary fibrosis.

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Section: Discussionmentioning

confidence: 99%

HSP70 Is a Critical Regulator of HSP90 Inhibitor’s Effectiveness in Preventing HCl-Induced Chronic Lung Injury and Pulmonary Fibrosis

Colunga Biancatelli,

Solopov,

Day

et al. 2024

IJMS

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“…This finding of better outcomes in smokers may be partly explained by smoking-induced upregulation of heat shock proteins (HSPs), particularly HSP70 [ 33 ]. HSP70, known for its protective effects, including inhibition of transforming growth factor-beta-β (TGF-β)-dependent epithelial-mesenchymal transition and anti-inflammatory properties [ 34 ], may delay IPF progression. In addition, smoking has been reported to upregulate autophagy markers, such as microtubule-associated protein 1 A/1B light chain 3B (LC3B) [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

Smoking status and clinical outcome in idiopathic pulmonary fibrosis: a nationwide study

Yoon,

Kim,

Bae

et al. 2024

Respir Res

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Background Smoking status has been linked to the development of idiopathic pulmonary fibrosis (IPF). However, the effect of smoking on the prognosis of patients with IPF is unclear. We aimed to investigate the association between smoking status and all-cause mortality or hospitalisation by using national health claims data. Methods IPF cases were defined as people who visited medical institutions between January 2002 and December 2018 with IPF and rare incurable disease exempted calculation codes from the National Health Insurance Database. Total 10,182 patients with available data on smoking status were included in this study. Ever-smoking status was assigned to individuals with a history of smoking ≥ 6 pack-years. The multivariable Cox proportional hazard model was used to evaluate the association between smoking status and prognosis. Results In the entire cohort, the mean age was 69.4 years, 73.9% were males, and 45.2% were ever smokers (current smokers: 14.2%; former smokers: 31.0%). Current smokers (hazard ratio [HR]: 0.709; 95% confidence interval [CI]: 0.643–0.782) and former smokers (HR: 0.926; 95% CI: 0.862–0.996) were independently associated with all-cause mortality compared with non-smokers. Current smokers (HR: 0.884; 95% CI: 0.827–0.945) and former smokers (HR: 0.909; 95% CI: 0.862–0.959) were also associated with a reduced risk of all-cause hospitalisation compared with non-smokers. A non-linear association between smoking amount and prognosis was found in a spline HR curve and showed increasing risk below 6 pack-years. Conclusion Ever-smoking status may be associated with favourable clinical outcomes in patients with IPF.

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“…Their function under normal physiological conditions is to help proteins fold, assemble, operate, and degrade properly. Under stress conditions, they stabilize protein and membrane structures, prevent denatured protein aggregation, and help proteins refold (Androvitsanea et al 2021; Liu et al 2022b; Roque 2022). To date, only a few studies have examined the heat shock protein family as reference proteins.…”

Section: Discussionmentioning

confidence: 99%

Preparation and Application Analysis of a Polyclonal Antibody as Reference Protein in Helicoverpa armigera (Lepidoptera: Noctuidae)

Tan

Jin

Xiao

et al. 2023

Journal of Entomological Science

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A stable and specific heat shock protein 27.2 (HSP27.2) antibody was prepared and analyzed for protein level research in Helicoverpa armigera (Hübner) (Lepidoptera: Noctuidae). The full-length hsp27.2 was amplified from H. armigera larvae and constructed into the prokaryotic expression vector. The purified His-tag fused protein was used to immunize rabbits for the antibody preparation. Western blot analysis indicated that this antibody specifically recognized the HSP27.2 encoded by H. armigera and detected the HSP27.2 encoded by other noctuid larvae. Further analysis of HSP27.2 expression in H. armigera under infection by different pathogenic microorganisms and in different tissues showed that the expression of HSP27.2 is continually stable. The HSP27.2 antibody is efficient and capable as a reference antibody for functional studies involving genes and proteins in H. armigera and other lepidopteran insects.

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Heat shock proteins in pulmonary fibrosis: pawns of cell homeostasis

Cited by 5 publications

References 27 publications

HSP70 Is a Critical Regulator of HSP90 Inhibitor’s Effectiveness in Preventing HCl-Induced Chronic Lung Injury and Pulmonary Fibrosis

HSP70 Is a Critical Regulator of HSP90 Inhibitor’s Effectiveness in Preventing HCl-Induced Chronic Lung Injury and Pulmonary Fibrosis

Smoking status and clinical outcome in idiopathic pulmonary fibrosis: a nationwide study

Preparation and Application Analysis of a Polyclonal Antibody as Reference Protein in Helicoverpa armigera (Lepidoptera: Noctuidae)

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