Serum Heat Shock Protein Levels and the Relationship of Heat Shock Proteins with Various Parameters in Chronic Obstructive Pulmonary Disease Patients

Ünver, Ramazan; Deveci, Figen; Kırkıl, Gamze; Telo, Selda; Kaman, Dilara; Kuluöztürk, Mutlu

doi:10.5578/ttj.30518

Cited by 9 publications

(5 citation statements)

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“…COPD is accompanied by hypoxia and increased cellular stress in addition to increased inflammation. High expression of matrix metalloproteases (MMPs), including MMP-2, MMP-8, MMP-9, and MMP-12, and chaperone heat shock protein-27 (HSP-27) have been confirmed in both lung tissues of COPD rat models and in COPD patients (9)(10)(11)(12)(13)(14)(15). These markers are also closely correlated with COPD development (11,16,17).…”

Section: Introductionmentioning

confidence: 99%

Role of Pneumocystis jirovecii infection in chronic obstructive pulmonary disease progression in an immunosuppressed rat Pneumocystis pneumonia model

Xue

Chen

2020

Exp Ther Med

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Pneumocystis jirovecii (P. jirovecii), an opportunistic fungal pathogen, is the primary cause of Pneumocystis pneumonia (PCP), which affects immunocompromised individuals and leads to high morbidity and mortality. P. jirovecii colonization is associated with development of chronic obstructive pulmonary disease (COPD) in patients with HIV infection, and also non-sufferers, and in primate models of HIV infection. However, the mechanisms underlying P. jirovecii infection in the pathogenesis of COPD have yet to be fully elucidated. To investigate the pathogenicity of P. jirovecii infection and its role in COPD development, the present study established a PCP rat model induced by dexamethasone sodium phosphate injection. Expression of COPD-related biomarkers, including matrix metalloproteinases (MMPs) MMP-2, MMP-8, MMP-9, and MMP-12, and heat shock protein-27 (HSP-27), were quantified in the rat PCP model using reverse transcription-quantitative polymerase chain reaction, ELISA, western blot analysis, immunohistochemistry and gelatin zymography. Body weight, COPD symptoms, and pulmonary histopathology were assessed. Inflammatory cell counts in splenic tissues were measured using flow cytometry. It was identified that MMP and HSP-27 expression increased in the PCP rats, which was in agreement with previous literature. Therefore, it was hypothesized that P. jirovecii infection may have an important role in COPD development.

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Section: Introductionmentioning

confidence: 99%

Role of Pneumocystis jirovecii infection in chronic obstructive pulmonary disease progression in an immunosuppressed rat Pneumocystis pneumonia model

Xue

Chen

2020

Exp Ther Med

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“…COPD has both pulmonary and extrapulmonary manifestations, and systemic chronic inflammation has been identified as a potential COPD endotype [4]. It is considered that the persistent low-grade inflammation in stable COPD might be caused by increased levels of many inflammatory mediators [5], reactive oxygen and nitrogen species [6], and pathogen-associated molecular patterns or damage-associated molecular patterns (DAMPs) such as extracellular heat shock protein 70 (eHsp70) [7][8][9]. eHsp70 is thought to activate proinflammatory responses by binding to Toll-like receptors (TLRs) 2 and 4, leading to increased cytokines concentrations [10].…”

Section: Introductionmentioning

confidence: 99%

Increased HSP70 and TLR2 Gene Expression and Association of HSP70 rs6457452 Single Nucleotide Polymorphism with the Risk of Chronic Obstructive Pulmonary Disease in the Croatian Population

et al. 2021

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Heat shock protein 70 (Hsp70) engages Toll-like receptors (TLR) 2 and 4 when found in the extracellular compartment and contributes to inflammation in chronic obstructive pulmonary disease (COPD). Since there is growing evidence for the genetic risk factors for COPD, the gene expression of HSP70, TLR2 and TLR4 was determined, as well as the association between HSP70, TLR2 and TLR4 single nucleotide polymorphisms, (SNPs) and COPD. The gene expression was assessed in peripheral blood cells of 137 COPD patients and 95 controls by a quantitative polymerase chain reaction (qPCR), while a total of nine SNPs were genotyped by TaqMan allelic discrimination real-time PCR. HSP70 and TLR2 gene expression was increased in COPD patients compared to the controls, regardless of the disease severity and smoking status of participants. The rs6457452 SNP of HSP70 was associated with COPD, indicating the protective role of the T allele (OR = 0.46, 95% CI = 0.24–0.89, p = 0.022). Furthermore, COPD C/T heterozygotes showed a decreased HSP70 mRNA level compared to COPD C/C homozygotes. In conclusion, HSP70 and TLR2 may have a role in the pathogenesis of COPD, and the HSP70 rs6457452 variant might influence the genetic susceptibility to COPD in the Croatian population.

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“…At the same time, there is a greater ease of onset of lung cancer in patients with a severe level of airway obstruction. e ability of extracellularly released HSPs to modulate the secretions of proinflammatory cytokines probably plays a key role in the progression of COPD itself and in its potential evolution to a carcinogenic level [61][62][63][64].…”

Section: Hsp 60mentioning

confidence: 99%

Role of HSP60/HSP10 in Lung Cancer: Simple Biomarkers or Leading Actors?

Fucarino

Pitruzzella

2020

Journal of Oncology

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Cancers are one of the major challenges faced by modern medicine both because of their impact in terms of the amount of cases and of the ineffectiveness of therapies used today. A concrete support to the fight against them can be found in the analysis and understanding of the molecular mechanisms involving molecular chaperones. In particular, HSP60 and HSP10 seem to play an important role in carcinogenesis, supporting tumours in their proliferation, survival, and metastasis. Efforts must be directed toward finding ways to eliminate or block this “mistaken” chaperone. Therefore, the scientific community must develop therapeutic strategies that consider HSP60 and HSP10 as the possible target of an anti-tumoural treatment and not only as diagnostic biomarkers, since they contribute to the evolution of pre-cancerous respiratory pathologies in lung tumours. HSP60 acts at the mitochondrial, cytoplasmic, and extracellular levels in the development of cancer pathologies. The molecular mechanisms in which these chaperones are involved concern cell survival, the restoration of a condition of absence of replicative senescence, the promotion of pro-inflammatory environments, and an increase in the ability to form metastases. In this review, we will also present examples of interactions between HSP60 and HSP10 and different molecules and ways to exploit this knowledge in anticancer therapies for lung tumours. In order to improve not only chances for an earlier diagnosis but also treatments for patients suffering from this type of disease, chaperones must be considered as key agents in carcinogenesis and primary targets in therapeutics.

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Serum Heat Shock Protein Levels and the Relationship of Heat Shock Proteins with Various Parameters in Chronic Obstructive Pulmonary Disease Patients

Cited by 9 publications

References 0 publications

Role of Pneumocystis jirovecii infection in chronic obstructive pulmonary disease progression in an immunosuppressed rat Pneumocystis pneumonia model

Role of Pneumocystis jirovecii infection in chronic obstructive pulmonary disease progression in an immunosuppressed rat Pneumocystis pneumonia model

Increased HSP70 and TLR2 Gene Expression and Association of HSP70 rs6457452 Single Nucleotide Polymorphism with the Risk of Chronic Obstructive Pulmonary Disease in the Croatian Population

Role of HSP60/HSP10 in Lung Cancer: Simple Biomarkers or Leading Actors?

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