Exercise-induced cardiac opioid system activation attenuates apoptosis pathway in obese rats

Alexandre‐Santos, Beatriz; Machado, Marcus Vinícius Ribeiro; Menezes, Ágatha Cristie; Velasco, Larissa Lírio; Sepúlveda-Fragoso, Vinícius; Vieira, Aline Bomfim; Borges, Juliana Pereira; Tibiriçá, Eduardo; Magliano, D’Angelo Carlo; Nóbrega, Antônio Cláudio Lucas da; Frantz, Eliete Dalla Corte

doi:10.1016/j.lfs.2019.06.017

Cited by 10 publications

(2 citation statements)

References 41 publications

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“…Our data are the first to show that DOR activation remarkably inhibits the TGF‐β1‐induced activation of Akt, suggesting that DOR may combat against renal fibrosis partially through Akt pathway. It is needed in future work to clarify whether this phenomenon is unique in renal cells or common in different cell types since there are some studies showing that [56,57].…”

Section: Discussionmentioning

confidence: 99%

Alleviation of TGF‐β1 induced tubular epithelial–mesenchymal transition via the δ‐opioid receptor

Luo

Song

et al. 2020

The FEBS Journal

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Renal fibrosis is a common pathological feature of progressive chronic kidney disease (CKD). It is indicated that transforming growth factor‐β1 (TGF‐β1) plays as a central mediator in renal fibrosis. The present study aimed to investigate the role of δ‐opioid receptor (DOR) on renal fibrosis of the rat renal proximal tubular epithelial cell line (NRK‐52E) induced by TGF‐β1 and to elucidate its underlying mechanism, as well as its involvement in signaling pathways. Cells were treated with TGF‐β1 (10 ng·mL−1), along with a specific DOR agonist (UFP‐512) or naltrindole (a DOR antagonist). Cell viability and morphology, as well as cell migration, were measured after drug administration. Western blotting was employed to examine the extracellular matrix (ECM) protein Fibronectin, and the tubular epithelial–mesenchymal transition (EMT) markers (E‐cadherin and α‐smooth muscle actin (α‐SMA)), signal transducer (p‐Smad3), and EMT‐regulatory gene (Snail). The expression level of phosphorylated Akt and p38 was also examined. Our results showed that TGF‐β1 induced fibroblastic appearance and increased the expression of Fibronectin, α‐SMA, P‐Smad3, and Snail, while it decreased the expression of E‐cadherin in NRK‐52E cells. Moreover, TGF‐β1 induced the activation of Akt and p38 MAPK signaling pathways. DOR activation was found to efficiently block morphological changes and cell migration, as long as the expression changes of Fibronectin, E‐cadherin, α‐SMA, P‐Smad3, Snail, P‐Akt, and P‐p38 were induced by TGF‐β1. These findings suggest that DOR may serve as an antifibrotic factor for renal proximal tubule cells by inhibiting the fibrosis process via TGF‐β/Smad, Akt, and p38 MAPK signaling pathways.

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Section: Discussionmentioning

confidence: 99%

Alleviation of TGF‐β1 induced tubular epithelial–mesenchymal transition via the δ‐opioid receptor

Luo

Song

et al. 2020

The FEBS Journal

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“…В публикации B. Alexandre-Santos и соавт. (2019) продемонстрировано снижение как экспрессии проэнкефалина, так и представительства опиоидных рецепторов в миокарде у крыс, содержащихся на высокожировой диете, что, по-видимому, привело к изменению внутриклеточной регуляции сопряженных с опиоидными рецепторами киназ PI3K, ERK и GSK-3β и к повышению активности каспазы-3, киназы, индуцирующей апоптоз кардиомиоцитов [44]. Вместе с тем в недавнем исследовании под руководством H.H.…”

Section: механизмы снижения эффективности дистантного посткондиционир...unclassified

Remote postconditioning of myocardium: mechanisms, efficacy in metabolic syndrome in experimental and clinical studies (review)

Mukhomedzyanov

Khlestkina

Логвинов

et al. 2023

SJCEM

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Remote postconditioning of the heart (RPost) – performed several periods of short-term ischemia-reperfusion of an remote organ after a long period of ischemia immediately before the resumption or in the early reperfusion, which leads to a reduction in the size at the subsequently formed infarction – represents a great therapeutic potential for clinical practice. The mechanism of remote postconditioning includes a trigger that can be played by adenosine, opioids, cannabinoids, bradykinin, CGRP, and substance P. Protein kinase C, PI3 kinase, Akt kinase, and JAK play an important role in the signaling mechanism of remote postconditioning. Experimental studies found that genetically determined or diet-induced metabolic changes reduce the effectiveness of cardioprotection in RPost. As possible mechanisms of cardioprotection inefficiency, we can suggest a decrease in the release of humoral factors, dysfunction of the receptor and signaling link of RPost, the effect of metabolic disorders on the functioning of KATP channel, mPTP, and on the state of mitochondrial respiration. However, these assumptions need experimental substantiation. The results of clinical studies show both the antinecrotizing and infarct-limiting effect of RPost in AMI and cardiac surgery, and the lack of its effectiveness. The role of metabolic disorders in the absence of the effectiveness of RPost in patients requires substantiation.

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Precursor fractions of neurotensin and enkephalin might point to molecular mechanisms of cancer risk modulation during a lifestyle-intervention in germline BRCA1/2 gene mutation carriers

Grill

Yahiaoui-Doktor

Basrai

et al. 2021

Breast Cancer Res Treat

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Background Germline BRCA1/2 mutation carriers (gBMC) face increased cancer risks that are modulated via non-genetic lifestyle factors whose underlying molecular mechanisms are unknown. The peptides Neurotensin (NT) and Enkephalin (ENK)—involved in tumorigenesis and obesity-related diseases—are of interest. We wanted to know whether these biomarkers differ between gBMC and women from the general population and what effect a 1-year lifestyle-intervention has in gBMC. Methods The stable precursor fragments pro-NT and pro-ENK were measured at study entry (SE), after 3 and 12 months for 68 women from LIBRE-1 (a controlled lifestyle-intervention feasibility trial for gBMC involving structured endurance training and the Mediterranean Diet). The SE values were compared with a cohort of the general population including female subjects with and without previous cancer disease, non-suggestive for hereditary breast and ovarian cancer (OMA-reference). For LIBRE-1, we analysed the association between the intervention-related change in the two biomarkers and certain lifestyle factors. Results At SE, gBMC had a higher median pro-NT than OMA-reference (in the subgroups with previous cancer 117 vs. 91 pmol/L, p = 0.002). Non-diseased gBMC had lower median pro-ENK levels when compared to the non-diseased reference group. VO2peak and pro-NT 1-year change in LIBRE-1 were inversely correlated (r = − 0.435; CI − 0.653 to − 0.151; p = 0.004). Pro-ENK correlated positively with VO2peak at SE (r = 0.323; CI 0.061–0.544; p = 0.017). Regression analyses showed an inverse association of 1-year changes for pro-NT and Omega-6/Omega-3 (Estimate: − 37.9, p = 0.097/0.080) in multivariate analysis. Conclusion Our results give first indications for lifestyle-related modification particularly of pro-NT in gBMC.

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Exercise-induced cardiac opioid system activation attenuates apoptosis pathway in obese rats

Cited by 10 publications

References 41 publications

Alleviation of TGF‐β1 induced tubular epithelial–mesenchymal transition via the δ‐opioid receptor

Alleviation of TGF‐β1 induced tubular epithelial–mesenchymal transition via the δ‐opioid receptor

Remote postconditioning of myocardium: mechanisms, efficacy in metabolic syndrome in experimental and clinical studies (review)

Precursor fractions of neurotensin and enkephalin might point to molecular mechanisms of cancer risk modulation during a lifestyle-intervention in germline BRCA1/2 gene mutation carriers

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