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• Research Paper Volume 12, Issue 4 pp 3682-3693

  Exosomes isolated from the plasma of remote ischemic conditioning rats improved cardiac function and angiogenesis after myocardial infarction through targeting Hsp70

  Relevance score: 7.6882896

  Qin Chen, Minghan Huang, Jiayi Wu, Qiong Jiang, Xingchun Zheng

  Keywords: exosomes, remote ischemic conditioning, myocardial infarction, Hsp70

  Published in Aging on February 18, 2020

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  Remote ischemic conditioning (RIC) is a promising therapeutic strategy to protect heart against ischemic-reperfusion injury. Exosomes have been proved to be an important regulator in many pathological processes. Whether the exosomes derived from RIC could improve cardiac remodeling and function after myocardial infarction (MI) has not been reported. MI animal model was established by ligating the left coronary artery. The bilateral hindlimbs of rats were subjected to RIC treatment using tourniquets. Exosomes were isolated from the plasma of RIC rats and identified by transmission electron microscope. The proliferation, migration, and apoptosis of endothelial cells were measured by CCK8, traswell, and flow cytometry. Western blotting, and qRT-PCR were applied to measure the expression of angiogenesis-related molecules, and immunohistochemistry staining was used to observe the expression of vWF. RIC and RIC exosomes remarkably facilitated cardiac function, cardiac cell remodeling, and angiogenesis. RIC exosomes markedly increased the cell ratio in the G1 phase, cell migration, cell proliferation, tube formation, and inhibited cell apoptosis through Hsp70. The expression of eNOS, iNOS, HIF-1α, Ang-1, and VEGF was markedly increased by RIC exosomes. RIC exosomes significantly improved cardiac function, cardiac remodeling, and angiogenesis after MI, and they accelerated angiogenesis through increasing the levels of angiogenesis-related molecules.

  

  RIC remarkably promoted cardiac remodeling and angiogenesis after myocardial infarction. (A) Histopathological analysis of heart tissues by HE, Masson, vWF IHC staining, respectively (scale bar= 100 μm); (B) RIC treatment significantly decreased the infarction ratio; (C) RIC treatment significantly increased left ventricular ejection fraction; (D) RIC treatment significantly increased left ventricular fractional shortening. Data were shown as the mean ± SD (n = 5/each group), * P<0.05 compared with the group MI.

  
  
  

  

  Isolation of exosomes from RIC rats. (A) Exosomes identification by TEM; (B) Measurement of exosomes particle size; (C) Measurement of exosomes concentration by flow cytometry; (D) Identification of CD9 and CD81 by western blotting.

  
  
  

  

  Exosomes from RIC rats significantly promoted cardiac remodeling and angiogenesis after myocardial infarction. (A) Histopathological analysis of heart tissues by HE and Masson (scale bar= 100 μm); (B) Investigation of angiogenesis after RIC exosomes treatment by vWf IHC staining (scale bar= 100 μm); (C) RIC exosomes treatment significantly decreased the infarction ratio; (D) RIC treatment significantly elevated left ventricular ejection fraction; (E) RIC treatment significantly promoted left ventricular fractional shortening. Data were shown as the mean ± SD (n = 3/each group), * P<0.05 compared with respective time point in the control group, # P<0.05 compared with 7 days’ time point in the group RIC exosomes.

  
  
  

  

  Exosomes from RIC markedly improved the cell viability and angiogenesis through promoting Hsp70. (A) RIC exosomes remarkably elevated the expression of Hsp70; (B) RIC exosomes significantly accelerated cell proliferation; (C) RIC exosomes remarkably increased the ratio of cell in G1 stage; (D) RIC exosomes significantly inhibited cell apoptosis; (E) RIC exosomes remarkably promoted cell migration (scale bar= 500 μm); (F) RIC exosomes significantly increased tube formation (scale bar= 500 μm). * P<0.05 compared with the control group. # P<0.05 compared with group si-Hsp70+ RIC exosomes.

  
  
  

  

  The expression increase of angiogenesis-related molecules after incubation with exosomes through targeting Hsp70. (A) Western analysis of angiogenesis-related molecule after treatment with si-Hsp70 and RIC exosomes; (B) Protein quantitative analysis of angiogenesis-related molecule after treatment with si-Hsp70 and RIC exosomes; (C) mRNA expression of angiogenesis-related molecule after treatment with si-Hsp70 and RIC exosomes. * P<0.05 compared with the control group. # P<0.05 compared with group si-Hsp70+RIC exosomes.

  
  
  

• Research Paper pp undefined-undefined

  The regulatory mechanism of HSP70 in endoplasmic reticulum stress in pepsin-treated laryngeal epithelium cells and laryngeal cancer cells

  Relevance score: 7.3175

  Wei Chen, Zhiyi Wang, Junfeng Ji, Tao Shi, Hong ye Jiao, You Cheng, Li Xu, Rui Wang

  Keywords: HSP70, endoplasmic reticulum stress, laryngeal cancer, apoptosis, autophagy

  Published in Aging on Invalid Date

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  Backgrounds: Excessive pepsin can damage both normal laryngeal epithelial cells and laryngeal cancer (LC) cells. Heat shock protein 70 (HSP70) is closely related to pepsin. In this paper, we will explore the different significance of the regulatory role of HSP70 in endoplasmic reticulum stress (ERS) level in pepsin-treated laryngeal epithelial cells and LC cells.

  Methods: In cell experiments, laryngeal epithelial cells and LC cells were selected and induced by different concentrations of pepsin. Cell activity was detected by CCK8, cell apoptosis was detected by flow cytometry, and autophagy was detected by autophagy detection kit. The expression of ER)-related proteins was detected by immunofluorescence (IF) and Western blot. Cell transfection was used to inhibit HSP70 expression in both cells, and ERS, apoptosis, and autophagy were measured using related techniques. In animal experiments, a mouse model bearing LC was established. TUNEL assay detected apoptosis, autophagy kit detected autophagy, and ER-related protein expression was detected by Western blot.

  Results: HSP70 was increased in pepsin-stimulated laryngeal epithelial cells and LC cells, thereby inhibiting ER and ER-induced apoptosis and autophagy. Inhibition of HSP70 reduced the expression of glucose regulated protein 78 (GRP78) in pepsin-stimulated laryngeal epithelial cells and LC cells, and only inhibited downstream apoptosis-related pathways in laryngeal epithelial cells rather than in LC cells. Inhibition of HSP70 and ER could significantly promote apoptosis and inhibit tumor growth in the absence of pepsin stimulation in vivo.

  Conclusion: ER level regulated by HSP70 had different significance in laryngeal epithelial cells and LC cells treated with pepsin.