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Responses to Muscular Exercise, Heat Shock Proteins as Regulators of Inflammation, and Mitochondrial Quality Control
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Alex T. Von Schulze, Paige C. Geiger
As mentioned previously, exercise is an acute bioenergetic and metabolic stress; thus, it is not surprising that stress proteins such as HSPs up-regulate after exercise. It is well known that the HSP70 and HSP20 families increase transcription and content after bouts of physical exercise (18, 43, 47, 84, 85). Importantly, HSP70 is responsive to both high-intensity endurance (59) and resistance training (62), whereas HSP20 is more responsive to resistance training (eccentric) (23). This response is critical for exercise adaptation and recovery (32, 40).
Zearalenone: Insights into New Mechanisms in Human Health
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Cornelia Braicu, Alina Andreea Zimta, Ioana Berindan-Neagoe
This mycotoxin leads to increased oxidative stress in the cellular environment, seen as the overproduction of the carcinogenic, anti-apoptotic chaperons Hsp70 and Hsp20. Moreover, Hsp70 is upregulated in the majority of malignant tumors, with Hsp70-2 having an important role in breast cancer development [13,81,82]. ZEA upregulates mRNA and the protein level of BCL-2 and causes downregulation of BAX, one of the apoptosis essential promoters [78].
Responses to iron oxide and zinc oxide nanoparticles in echinoderm embryos and microalgae: uptake, growth, morphology, and transcriptomic analysis
Published in Nanotoxicology, 2020
Anne-Marie Genevière, Evelyne Derelle, Marie-Line Escande, Nigel Grimsley, Christophe Klopp, Christine Ménager, Aude Michel, Hervé Moreau
Of the 918 DE genes specific to ENPs (common to Fe2O3 and ZnO, not responding to ions), 7 (0.2%) were highly induced, with 3 having a predicted annotation: SfsA, a transcription factor involved in maltose metabolism, MFS1, a transporter of the Major Facilitator Superfamily and RCC1 a Regulator of Chromosome Condensation (Figure S7). Only one gene, MDH5, orthologous of the C. reinhardtii NADP-dependent malate dehydrogenase (EC 1.1.1.37) was highly repressed. In addition, the hsp90 genes encoding stress chaperone proteins were either specifically or more intensively altered by ENPs than their corresponding ions while ENPs specifically induced hsp20 expression. Two essential cell-cycle genes were also preferentially repressed in response to ENPs, albeit to a lesser extent (lower LFC), CDKD, the CDK activating kinase, and APC3 a subunit of the Anaphase Promoting Complex (Figure S7).
Extracellular vesicles in type 2 diabetes mellitus: key roles in pathogenesis, complications, and therapy
Published in Journal of Extracellular Vesicles, 2019
Yongwei Xiao, Lei Zheng, Xiaofeng Zou, Jigang Wang, Jianing Zhong, Tianyu Zhong
DCM and DR are common complications of T2DM. However, only few studies have focused on EVs as therapy for DCM and DR currently. Wang et al. [100] showed that the HSP20-engineered EVs might be a novel therapeutic agent for DCM. The over-expressed HSP20-containing EVs from cardiomyocytes of HSP20-transgenic mice might be able to attenuate cardiac dysfunction, apoptosis, and fibrosis significantly, improving cardiovascular function in diabetic mice. Notably, some EVs have been applied in the therapy of other heart disease, including acute myocardial ischemic injury [101], myocardial infarction [102], and myocardial contractility [103]. Using EVs in the treatment of DCM or DR may be a promising research direction in both animal models and humans.
MiR-33a-5p targets NOMO1 to modulate human cardiomyocyte progenitor cells proliferation and differentiation and apoptosis
Published in Journal of Receptors and Signal Transduction, 2021
Wang Xing, Tiangang Li, Yixuan Wang, Yi Qiang, Chencheng Ai, Hanbo Tang
Several studies have shown the effect of different miRNAs in cardiac tissue. For example, it has been reported that down-regulation of endogenous miR-320 supplies protection against ischemia/reperfusion (I/R)-induced cardiomyocyte death and apoptosis via targeting Hsp20 [25]. And overexpression of miR-1 could facilitate H2O2-induced apoptosis in cardiomyocytes by targeting Bcl-2 in accordance with the previous study [26]. Meanwhile, there are complex molecular networks based on the proliferation and differentiation of hCMPCs, among which miRNA plays a critical role. For instance, Liang et al. [27] found that hCMPCs proliferation was inhibited by miR-10a via restraining its cell cycle progression, and they also discovered that decreased hCMPCs proliferation by miR-10a is not involved in cell apoptosis. However, in line with the experimental data in the present study, hCMPCs proliferation was restrained by up-regulation of miR-33a-5p but apoptosis was enhanced by up-regulation of miR-33a-5p, and down-regulation of miR-33a-5p did the opposite function. Besides, the Bcl-2 family can be categorized into the anti-apoptotic proteins, and the pro-apoptotic proteins such as Bax, and Caspase is a family of single-chain synthesized zymogens playing central roles in apoptotic signaling and execution [28]. And in the present study, expressions of Bax and Cleaved(C) caspase-3 were promoted while Bcl-2 expression was inhibited by up-regulation of miR-33a-5p. Progression through the cell cycle is tightly regulated and checkpoints at phase transitions during the cell cycle ensure that only healthy cells progress and proliferate [29]. And the data in the present study uncovered that hCMPCs cell cycle G0/S transition was suppressed by up-regulation of miR-33a-5p.