S100A1 as a Potential Diagnostic Biomarker for Assessing Cardiotoxicity and Implications for the Chemotherapy of Certain Cancers

Eryılmaz, Ufuk; Demirci, Buket; Aksun, Saliha; Boyacıoğlu, Murat; Akgüllü, Çağdaş; İlgenli, T. Fikret; Yalinkilinc, Hande Sultan; Bilgen, Mehmet

doi:10.1371/journal.pone.0145418

Cited by 17 publications

(11 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The crucial role of S100A1 for cardiac performance and contractility was reported (20,21). In our study, reduced release of S100A1 from injured cardiomyocytes to serum after CIS exposure was demonstrated, which was concordant with our previous study (22). Lapatinib and Trastuzumab decreased S100A1 expression in a ratio of %75.…”

Section: Discussionsupporting

confidence: 93%

Protective Effect of Pycnogenol<sup>®</sup> on Cisplatin Induced-Cardiotoxicity in Rats

Eryılmaz¹,

Aksun²,

Demirci³

2018

meandros

Self Cite

View full text Add to dashboard Cite

Anah tar Ke li me ler Kardiyo-onkoloji, Pycnogenol Öz AbstractObjective: This study investigated the cardiotoxicity of cisplatin (CIS) on rat heart by using the oxidative damage of the rat myocardium, Troponin I and serum S100A1 levels. Previous studies have reported that cell-protective effect of Pycnogenol® (PYC) depended on its antioxidant and anti-inflammatory properties. Hence, the myocardial protective effect of PYC was investigated in this study. Materials and Methods: Rats were randomly assigned to four groups with 5 per group. The experimental groups were as follows: Control Group, Pycnogenol Group: 10 mg/kg Pycnogenol intraperitoneally for 7 days, Cisplatin Group: 15 mg/kg single injection of cisplatin on the 5 th day intraperitoneally, Cisplatin + Pycnogenol Group: 10 mg/kg Pycnogenol for 7 days intraperitoneally, plus 15 mg/kg single injection of cisplatin on the 5 th day. The heart and serum samples were obtained on the 8 th day. Results: CIS and PYC Co-treatment group had increased catalase level (from 43.61±15.16 to 60.80±21.36, p< 0.019) and prevented Troponin I elevation (from 7.34±6.20 to 3.03±1.36). The S100A1 level was significantly reduced by CIS (from 10.25 ±8.8 to 3.99 ± 2.87, p< 0.035) and was restored by PYC treatment (32.07±29.23). Conclusion: Injured cardiomyocytes released Troponin I after exposure to CIS and PYC, which can protect the cells from CIS cardiotoxicity,increased the tissue catalase level. Additionally, PYC treatment increased serum level of S100A1.Amaç: Bu çalışma sıçan kalbi üzerinde sisplatin (CIS) kardiyotoksisitesini, sıçan miyokardı oksidatif hasarını, Troponin I ve serum S100A1 düzeylerini kullanarak araştırmıştır. Önceki çalışmalar, Pycnogenol®'in (PYC) hücre koruyucu etkisinin antioksidan ve anti-inflamatuar özelliklerine bağlı olduğunu bildirmiştir. Bu nedenle, bu çalışmada PYC'nin miyokardiyal koruyucu etkisi araştırılmıştır. Gereç ve Yöntem: Sıçanlar randomize olarak grup başına 5 olacak şekilde dört gruba ayrıldı. Kontrol grupları, pycnogenol grubu: 10 mg/kg 7 gün boyunca intraperitoneal pycnogenol, 5 gün intraperitoneal olarak sisplatin'in 15 mg/kg tek doz enjeksiyonu, Cisplatin + Pycnogenol Grubu: 10 mg/kg Pycnogenol Intraperitoneal olarak 7 gün boyunca, artı beşinci günde 15 mg/kg tek sisplatin enjeksiyonu. Kalp ve serum örnekleri 8. günde elde edildi. Bulgular: CIS ve PYC eş-tedavi grubunda katalaz seviyesi artmış (43,61±15,16'dan 60,80±21,36'ya, p<0,019) ve Troponin I yükselmesini (7,34±6,20'den 3,03±1,36'ya)

show abstract

Section: Discussionsupporting

confidence: 93%

Protective Effect of Pycnogenol<sup>®</sup> on Cisplatin Induced-Cardiotoxicity in Rats

Eryılmaz¹,

Aksun²,

Demirci³

2018

meandros

Self Cite

View full text Add to dashboard Cite

show abstract

“…Various heart diseases are related to S100 proteins which are considered as new markers for cardiac toxicity [13]. S100A1 protein improves cardiac contractility and its expression is reduced following cardiac damage [14]. Human cardiomyopathy exhibited down-regulation of S100A1 expression that decreased the performance of myocardial contraction as documented by Remppis et al [15].…”

Section: Introductionmentioning

confidence: 99%

Liposomal Resveratrol and/or Carvedilol Attenuate Doxorubicin-Induced Cardiotoxicity by Modulating Inflammation, Oxidative Stress and S100A1 in Rats

et al. 2020

View full text Add to dashboard Cite

Doxorubicin (DOX) is a cytotoxic anthracycline antibiotic and one of the important chemotherapeutic agents for different types of cancers. DOX treatment is associated with adverse effects, particularly cardiac dysfunction. This study examined the cardioprotective effects of carvedilol (CAR) and/or resveratrol (RES) and liposomal RES (LIPO-RES) against DOX-induced cardiomyopathy, pointing to their modulatory effect on oxidative stress, inflammation, S100A1 and sarco/endoplasmic reticulum calcium ATPase2a (SERCA2a). Rats received CAR (30 mg/kg) and/or RES (20 mg/kg) or LIPO-RES (20 mg/kg) for 6 weeks and were challenged with DOX (2 mg/kg) twice per week from week 2 to week 6. DOX-administered rats exhibited a significant increase in serum creatine kinase-MB (CK-MB), troponin-I and lactate dehydrogenase (LDH) along with histological alterations, reflecting cardiac cell injury. Cardiac toll-like receptor 4 (TLR-4), inducible nitric oxide synthase (iNOS), tumor necrosis factor (TNF)-α and interleukin (IL)-6 protein expression were up-regulated, and lipid peroxidation was increased in DOX-administered rats. Treatment with CAR, RES or LIPO-RES as well as their alternative combinations ameliorated all observed biochemical and histological alterations with the most potent effect exerted by CAR/LIPO-RES. All treatments increased cardiac antioxidants, and the expression of S100A1 and SERCA2a. In conclusion, the present study conferred new evidence on the protective effects of CAR and its combination with either RES or LIPO-RES on DOX-induced inflammation, oxidative stress and calcium dysregulation.

show abstract

“…It has been reported that S100A1 is most abundant in cardiomyocytes [17] and finds in the extracellular compartment after heart ischemia [18]. In our previous study, we have shown the disruption of S100 A1 after exposure of lapatinib or trastuzumab therapy [19]. Beside of the Troponin I and MDA levels, S100 A1 level did not give any significant changing value.…”

Section: Discussionmentioning

confidence: 62%

The effect of oxaliplatin on heart tissue of the rats

Eryılmaz¹

2018

Ann Clin Anal Med

View full text Add to dashboard Cite

Aim: This study investigates the cardiotoxicity of Oxaliplatin (OXA) on rat heart by using oxidative stress parameters on myocardium and troponin I and S100A1 levels of serum. Material and Method: Acute OXA treatment (4 mg/kg/1 st , 3 rd and 5 th days) has been administered to the 6-8 months old rats. The heart and serum samples were obtained at 7 th and 14 th days of the study. Chronic OXA treatment was (4 mg/kg/two days of week/4 weeks) administered, rats were sacrificed and heart and serum samples were obtained at the 28 th day and at the 2 st day following the completing administration of drugs. Results: The results of all OXA treatment group's antioxidant levels and serum cardiotoxicity markers; troponin I and S100 A1 levels were not significantly different compared to the control group (p>0.05). Discussion: OXA did not produce significant oxidative myocardial damage when given 4 mg/kg in acute and chronic administration.Oxa treatment seems safe in terms of cardiotoxicity.

show abstract

S100A1 as a Potential Diagnostic Biomarker for Assessing Cardiotoxicity and Implications for the Chemotherapy of Certain Cancers

Cited by 17 publications

References 40 publications

Protective Effect of Pycnogenol<sup>®</sup> on Cisplatin Induced-Cardiotoxicity in Rats

Protective Effect of Pycnogenol<sup>®</sup> on Cisplatin Induced-Cardiotoxicity in Rats

Liposomal Resveratrol and/or Carvedilol Attenuate Doxorubicin-Induced Cardiotoxicity by Modulating Inflammation, Oxidative Stress and S100A1 in Rats

The effect of oxaliplatin on heart tissue of the rats

Contact Info

Product

Resources

About