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Article: Evaluation of Parkin in the Regulation of Myocardial Mitochondria-Associated Membranes and Cardiomyopathy During Endotoxemia.

Kim, Matthew / Nikouee, Azadeh / Sun, Yuxiao / Zhang, Qing-Jun / Liu, Zhi-Ping / Zang, Qun Sophia

Frontiers in cell and developmental biology

2022 Volume 10, Page(s) 796061

Abstract: Background: ...

Abstract	Background:
Language	English
Publishing date	2022-02-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2022.796061
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Article ; Online: Histone methylations in heart development, congenital and adult heart diseases.

Zhang, Qing-Jun / Liu, Zhi-Ping

Epigenomics

2015 Volume 7, Issue 2, Page(s) 321–330

Abstract: Heart development comprises myocyte specification, differentiation and cardiac morphogenesis. These processes are regulated by a group of core cardiac transcription factors in a coordinated temporal and spatial manner. Histone methylation is an emerging ... ...

Abstract	Heart development comprises myocyte specification, differentiation and cardiac morphogenesis. These processes are regulated by a group of core cardiac transcription factors in a coordinated temporal and spatial manner. Histone methylation is an emerging epigenetic mechanism for regulating gene transcription. Interplay among cardiac transcription factors and histone lysine modifiers plays important role in heart development. Aberrant expression and mutation of the histone lysine modifiers during development and in adult life can cause either embryonic lethality or congenital heart diseases, and influences the response of adult hearts to pathological stresses. In this review, we describe current body of literature on the role of several common histone methylations and their modifying enzymes in heart development, congenital and adult heart diseases.
MeSH term(s)	Animals ; Cardiomegaly/genetics ; Cardiomegaly/metabolism ; Heart/embryology ; Heart Defects, Congenital/genetics ; Heart Defects, Congenital/metabolism ; Heart Diseases/genetics ; Heart Diseases/metabolism ; Histones/metabolism ; Humans ; Methylation ; Mice ; Myocardium/metabolism
Chemical Substances	Histones
Language	English
Publishing date	2015-05-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2537199-X
ISSN	1750-192X ; 1750-1911
ISSN (online)	1750-192X
ISSN	1750-1911
DOI	10.2217/epi.14.60
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Article ; Online: Inhibition of Jumonji demethylases reprograms severe dilated cardiomyopathy and prolongs survival.

Tran, Tram Anh / Zhang, Qing-Jun / Wang, Lei / Gonzales, Christopher / Girard, Luc / May, Herman / Gillette, Thomas / Liu, Zhi-Ping / Martinez, Elisabeth D

The Journal of biological chemistry

2021 Volume 298, Issue 2, Page(s) 101515

Abstract: Hypertrophic/dilated cardiomyopathy, often a prequel to heart failure, is accompanied by maladaptive transcriptional changes that contribute to arrythmias and contractile misfunction. Transgenic mice constitutively expressing high levels of calcineurin ... ...

Abstract	Hypertrophic/dilated cardiomyopathy, often a prequel to heart failure, is accompanied by maladaptive transcriptional changes that contribute to arrythmias and contractile misfunction. Transgenic mice constitutively expressing high levels of calcineurin are known to develop extreme heart hypertrophy, which progresses to dilated cardiomyopathy, and to die several weeks after birth. Here, we characterized aberrant transcriptional and epigenetic pathways in this mouse model and established a pharmacological approach to treat established cardiomyopathy. We found that H3K4me3 (trimethyl histone 3 lysine 4) and H3K9me3 (trimethyl histone 3 lysine 9) Jumonji histone demethylases are markedly increased at the protein level and show enhanced enzymatic activity in diseased hearts. These epigenetic regulators continued to increase with time, further affecting cardiac gene expression. Our findings parallel the lower H3K4me3 and H3K9me3 levels seen in human patients. Inhibition of Jumonji demethylase activities in vivo results in lower histone demethylase enzymatic function in the heart and higher histone methylation levels and leads to partial reduction of heart size, reversal of maladaptive transcriptional programs, improved heart function, and prolonged survival. At the molecular level, target genes of transcription factor myocyte enhancer factor 2 are specifically regulated in response to pharmacological or genetic inhibition of Jumonji demethylases. Similar transcriptional reversal of disease-associated genes is seen in a second disease model based on cardiac mechanical overload. Our findings validate pharmacological inhibitors of Jumonji demethylases as potential therapeutics for the treatment of cardiomyopathies across disease models and provide evidence of the reversal of maladaptive transcriptional reprogramming leading to partial restoration of cardiac function. In addition, this study defines pathways of therapeutic resistance upregulated with disease progression.
MeSH term(s)	Animals ; Cardiomyopathy, Dilated/drug therapy ; Cardiomyopathy, Dilated/genetics ; Enzyme Inhibitors/pharmacology ; Histone Demethylases/genetics ; Histone Demethylases/metabolism ; Histones/genetics ; Histones/metabolism ; Humans ; Jumonji Domain-Containing Histone Demethylases/antagonists & inhibitors ; Jumonji Domain-Containing Histone Demethylases/metabolism ; Lysine/metabolism ; Mice ; Small Molecule Libraries/pharmacology
Chemical Substances	Enzyme Inhibitors ; Histones ; Small Molecule Libraries ; Histone Demethylases (EC 1.14.11.-) ; Jumonji Domain-Containing Histone Demethylases (EC 1.14.11.-) ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2021-12-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2021.101515
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Article ; Online: The potentials of human adipose tissue derived mesenchymal stem cells in targeted therapy of experimental glioma

FAN Cun-gang / ZHANG Qing-jun

Chinese Journal of Contemporary Neurology and Neurosurgery, Vol 12, Iss 6, Pp 651-

2012 Volume 654

Abstract: Glioblastoma is the most common primary malignant brain tumor in adults. With current standard therapy which includes extensive microsurgical resection along with concurrent chemoradiotherapy and adjuvant temozolomide (TMZ), the median survival of ... ...

Abstract	Glioblastoma is the most common primary malignant brain tumor in adults. With current standard therapy which includes extensive microsurgical resection along with concurrent chemoradiotherapy and adjuvant temozolomide (TMZ), the median survival of glioblastoma patients is only 14.60 months nowadays. Recent studies demonstrated that human adipose tissue derived mesenchymal stem cells (hAT-MSCs) possessed the glioma-trophic migratory capacity. The engineered hAT-MSCs expressing herpes simplex virus-thymidine kinase (HSV-tk), yeast cytosine deaminase::uracil phosphoribosyltransferase (CDy:: UPRT), and rabbit carboxylesterase (rCE) could exert inhibitory effects on glioma when combined with prodrugs, such as ganciclovir (GCV), 5-fluorocytosine (5-FC) and irinotecan (CPT-11), respectively. hAT-MSCs carrying the oncolytic virus or expressing tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) also could inhibit the growth of glioma. This paper summarizes the recent progress in this field to pave the way for hAT-MSCs based targeted therapy of glioma in future.
Keywords	Mesenchymal stem cell transplantation Drug carriers Adipose tissue Neoplasms ; experimental Glioma Review ; Neurology. Diseases of the nervous system ; RC346-429 ; Neurosciences. Biological psychiatry. Neuropsychiatry ; RC321-571 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Neurology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	610
Language	Chinese
Publishing date	2012-12-01T00:00:00Z
Publisher	Tianjin Huanhu Hospital
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Effect and mechanism of miR-34a on proliferation, apoptosis and invasion of laryngeal carcinoma cells.

Wang, Ju-Xiang / Zhang, Qing-Jun / Pei, Shi-Geng / Yang, Bao-Liang

Asian Pacific journal of tropical medicine

2016 Volume 9, Issue 5, Page(s) 494–498

Abstract: Objective: To discuss the effect and mechanism of miR-34a on the proliferation, apoptosis and invasion of laryngeal carcinoma cells.: Methods: The laryngeal squamous carcinoma Hep2 cells were transiently transfected with miR-34a mimics and miR-34a NC. ...

Abstract	Objective: To discuss the effect and mechanism of miR-34a on the proliferation, apoptosis and invasion of laryngeal carcinoma cells. Methods: The laryngeal squamous carcinoma Hep2 cells were transiently transfected with miR-34a mimics and miR-34a NC. The MTT, colony-forming assay, Hoechst staining and AnnexinV-PI double staining flow cytometry were employed to detect the effect of miR-34a on the viability and apoptosis of laryngeal squamous carcinoma Hep2 cells; Transwell assay to defect the effect of miR-34a on the migration and invasion of laryngeal squamous carcinoma Hep2 cells; western blot and RT-PCR assay to defect the effect of miR-34a mimics on the expression of survivin and Ki-67 mRNA in laryngeal squamous carcinoma Hep2 cells. Results: Compared with miR-34a NC group, the cell viability in miR-34 mimics group was significantly decreased (P < 0.01), the cell apoptosis rate was significantly increased (P < 0.01), the abilities of cell migration and invasion were significantly reduced (P < 0.01) and the expression of survivin and Ki-67 mRNA was significantly decreased (P < 0.01). Conclusions: The increased expression of miR-34a can induce the apoptosis of Hep2 laryngeal carcinoma cells and inhibit the cell proliferation and invasion, which is related to the down-regulated expression of survivin and Ki-67.
Language	English
Publishing date	2016-05
Publishing country	China
Document type	Journal Article
ISSN	2352-4146
ISSN (online)	2352-4146
DOI	10.1016/j.apjtm.2016.03.018
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Article ; Online: Age-Independent Cardiac Protection by Pharmacological Activation of Beclin-1 During Endotoxemia and Its Association With Energy Metabolic Reprograming in Myocardium-A Targeted Metabolomics Study.

Kim, Matthew / Nikouee, Azadeh / Zou, Raymond / Ren, Di / He, Zhibin / Li, Ji / Wang, Lu / Djukovic, Danijel / Raftery, Daniel / Purcell, Hayley / Promislow, Daniel / Sun, Yuxiao / Goodarzi, Mohammad / Zhang, Qing-Jun / Liu, Zhi-Ping / Zang, Qun Sophia

Journal of the American Heart Association

2022 Volume 11, Issue 14, Page(s) e025310

Abstract: Background We showed that Beclin-1-dependent autophagy protects the heart in young and adult mice that underwent endotoxemia. Herein, we compared the potential therapeutic effects of Beclin-1 activating peptide, TB-peptide, on endotoxemia-induced cardiac ...

Abstract	Background We showed that Beclin-1-dependent autophagy protects the heart in young and adult mice that underwent endotoxemia. Herein, we compared the potential therapeutic effects of Beclin-1 activating peptide, TB-peptide, on endotoxemia-induced cardiac outcomes in young adult and aged mice. We further evaluated lipopolysaccharide (lipopolysaccharide)-induced and TB-peptide treatment-mediated alterations in myocardial metabolism. Methods and Results C57BL/6J mice that were 10 weeks and 24 months old were challenged by lipopolysaccharide using doses at which cardiac dysfunction occurred. Following the treatment of TB-peptide or control vehicle, heart contractility, circulating cytokines, and myocardial autophagy were evaluated. We detected that TB-peptide boosted autophagy, attenuated cytokines, and improved cardiac performance in both young and aged mice during endotoxemia. A targeted metabolomics assay was designed to detect a pool of 361 known metabolites, of which 156 were detected in at least 1 of the heart tissue samples. Lipopolysaccharide-induced impairments were found in glucose and amino acid metabolisms in mice of all ages, and TB-peptide ameliorated these alterations. However, lipid metabolites were upregulated in the young group but moderately downregulated in the aged by lipopolysaccharide, suggesting an age-dependent response. TB-peptide mitigated lipopolysaccharide-mediated trend of lipids in the young mice but had little effect on the aged. (Study registration: Project DOI: https://doi.org/10.21228/M8K11W). Conclusions Pharmacological activation of Beclin-1 by TB-peptide is cardiac protective in both young and aged population during endotoxemia, suggest a therapeutic potential for sepsis-induced cardiomyopathy. Metabolomics analysis suggests that an age-independent protection by TB-peptide is associated with reprograming of energy production via glucose and amino acid metabolisms.
MeSH term(s)	Amino Acids/metabolism ; Animals ; Beclin-1/metabolism ; Cytokines/metabolism ; Endotoxemia ; Glucose/metabolism ; Lipopolysaccharides ; Mice ; Mice, Inbred C57BL ; Myocardium/metabolism
Chemical Substances	Amino Acids ; Beclin-1 ; Cytokines ; Lipopolysaccharides ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-07-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.122.025310
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Article ; Online: Uncoupling of PARP1 trapping and inhibition using selective PARP1 degradation.

Wang, Shuai / Han, Lei / Han, Jungsoo / Li, Peng / Ding, Qing / Zhang, Qing-Jun / Liu, Zhi-Ping / Chen, Chuo / Yu, Yonghao

Nature chemical biology

2019 Volume 15, Issue 12, Page(s) 1223–1231

Abstract: PARP1 inhibitors (PARPi) are known to kill tumor cells via two mechanisms (PARP1 catalytic inhibition and PARP1 trapping). The relative contribution of these two pathways in mediating the cytotoxicity of PARPi, however, is not well understood. Here we ... ...

Abstract	PARP1 inhibitors (PARPi) are known to kill tumor cells via two mechanisms (PARP1 catalytic inhibition and PARP1 trapping). The relative contribution of these two pathways in mediating the cytotoxicity of PARPi, however, is not well understood. Here we designed a series of small molecule PARP degraders. Treatment with one such compound iRucaparib-AP6 results in highly efficient and specific PARP1 degradation. iRucaparib-AP6 blocks the enzymatic activity of PARP1 in vitro, and PARP1-mediated poly-ADP-ribosylation signaling in intact cells. This strategy mimics PARP1 genetic depletion, which enables the pharmacological decoupling of PARP1 inhibition from PARP1 trapping. Finally, by depleting PARP1, iRucaparib-AP6 protects muscle cells and primary cardiomyocytes from DNA-damage-induced energy crisis and cell death. In summary, these compounds represent 'non-trapping' PARP1 degraders that block both the catalytic activity and scaffolding effects of PARP1, providing an ideal approach for the amelioration of the various pathological conditions caused by PARP1 hyperactivation.
MeSH term(s)	Animals ; Humans ; Mice ; Poly (ADP-Ribose) Polymerase-1/antagonists & inhibitors ; Poly (ADP-Ribose) Polymerase-1/metabolism ; Proteolysis
Chemical Substances	Poly (ADP-Ribose) Polymerase-1 (EC 2.4.2.30)
Language	English
Publishing date	2019-10-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2202962-X
ISSN	1552-4469 ; 1552-4450
ISSN (online)	1552-4469
ISSN	1552-4450
DOI	10.1038/s41589-019-0379-2
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Article ; Online: Hepatic FGF21 preserves thermoregulation and cardiovascular function during bacterial inflammation.

Huen, Sarah C / Wang, Andrew / Feola, Kyle / Desrouleaux, Reina / Luan, Harding H / Hogg, Richard / Zhang, Cuiling / Zhang, Qing-Jun / Liu, Zhi-Ping / Medzhitov, Ruslan

The Journal of experimental medicine

2021 Volume 218, Issue 10

Abstract: Sickness behaviors, including anorexia, are evolutionarily conserved responses to acute infections. Inflammation-induced anorexia causes dramatic metabolic changes, of which components critical to survival are unique depending on the type of inflammation. ...

Abstract	Sickness behaviors, including anorexia, are evolutionarily conserved responses to acute infections. Inflammation-induced anorexia causes dramatic metabolic changes, of which components critical to survival are unique depending on the type of inflammation. Glucose supplementation during the anorectic period induced by bacterial inflammation suppresses adaptive fasting metabolic pathways, including fibroblast growth factor 21 (FGF21), and decreases survival. Consistent with this observation, FGF21-deficient mice are more susceptible to mortality from endotoxemia and polybacterial peritonitis. Here, we report that increased circulating FGF21 during bacterial inflammation is hepatic derived and required for survival through the maintenance of thermogenesis, energy expenditure, and cardiac function. FGF21 signaling downstream of its obligate coreceptor, β-Klotho (KLB), is required in bacterial sepsis. However, FGF21 modulates thermogenesis and chronotropy independent of the adipose, forebrain, and hypothalamus, which are operative in cold adaptation, suggesting that in bacterial inflammation, either FGF21 signals through a novel, undescribed target tissue or concurrent signaling of multiple KLB-expressing tissues is required.
MeSH term(s)	Animals ; Bacterial Infections/mortality ; Bacterial Infections/physiopathology ; Body Temperature Regulation/physiology ; Endotoxemia/chemically induced ; Endotoxemia/metabolism ; Endotoxemia/mortality ; Fibroblast Growth Factors/genetics ; Fibroblast Growth Factors/metabolism ; Heart Rate/genetics ; Heart Rate/physiology ; Inflammation/microbiology ; Inflammation/physiopathology ; Klotho Proteins/genetics ; Klotho Proteins/metabolism ; Lipopolysaccharides/toxicity ; Liver/physiology ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Mice
Chemical Substances	Klb protein, mouse ; Lipopolysaccharides ; fibroblast growth factor 21 ; Fibroblast Growth Factors (62031-54-3) ; Klotho Proteins (EC 3.2.1.31)
Language	English
Publishing date	2021-08-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20202151
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Article ; Online: Cardio-omentopexy Reduces Cardiac Fibrosis and Heart Failure After Experimental Pressure Overload.

Wang, Jian / Zhang, Qing-Jun / Pirolli, Timothy J / Liu, Zhi-Ping / Powell, LaShondra / Thorp, Edward B / Jessen, Michael / Forbess, Joseph M

The Annals of thoracic surgery

2018 Volume 107, Issue 5, Page(s) 1448–1455

Abstract: Background: The pedicled greater omentum has been shown to offer benefit in ischemic heart disease for both animal models and human patients. The impact of cardio-omentopexy in a pressure overload model of left ventricular hypertrophy (LVH) is unknown.!# ...

Abstract	Background: The pedicled greater omentum has been shown to offer benefit in ischemic heart disease for both animal models and human patients. The impact of cardio-omentopexy in a pressure overload model of left ventricular hypertrophy (LVH) is unknown. Methods: LVH was created in rats by banding the ascending aorta after right thoracotomy (n = 23). Sham surgery was performed in 12 additional rats. Six weeks after banding, surviving LVH rats were assigned to cardio-omentopexy by left thoracotomy (LVH+Om, n = 8) or sham left thoracotomy (LVH, n = 8). Sham rats also underwent left thoracotomy for cardio-omentopexy (Sham+Om, n = 6); the remaining rats underwent sham left thoracotomy (Sham, n = 6). Results: Echocardiography 10 weeks after cardio-omentopexy revealed LV end-systolic diameter, cardiomyocyte diamter, and myocardial fibrosis in the LVH group were significantly increased compared with the LVH+Om, Sham+Om, and Sham groups (p < 0.01). LV ejection fraction of the LVH group was lower than the LVH+Om group (p < 0.01). Gene expression analysis revealed significantly lower levels of sarcoendoplasmic reticulum calcium adenosine triphosphatase 2b in LVH rats than in the LVH+Om, Sham+Om, and Sham groups (p < 0.01). In contrast, collagen type 1 α 1 chain, lysyl oxidase-like protein 1, nuclear protein-1, and transforming growth factor- β1 in the LVH group were significantly higher than in the LVH+Om cohort (p < 0.01), consistent with a reduced fibrotic phenotype after omentopexy. Lectin staining showed myocardial capillary density of the LVH group was significantly lower than all other groups (p < 0.01). Conclusions: Cardio-omentopexy reduced cardiac dilation, contractile dysfunction, cardiomyocyte hypertrophy, and myocardial fibrosis, while maintaining other molecular indicators of contractile function in this LVH model.
MeSH term(s)	Animals ; Cardiac Surgical Procedures ; Collagen Type I, alpha 1 Chain ; Disease Models, Animal ; Endomyocardial Fibrosis/etiology ; Endomyocardial Fibrosis/prevention & control ; Heart Failure/etiology ; Heart Failure/prevention & control ; Hypertrophy, Left Ventricular/complications ; Hypertrophy, Left Ventricular/pathology ; Hypertrophy, Left Ventricular/surgery ; Male ; Myocardium ; Omentum/surgery ; Rats ; Rats, Sprague-Dawley ; Stroke Volume
Chemical Substances	Col1a1 protein, rat ; Collagen Type I, alpha 1 Chain
Language	English
Publishing date	2018-12-12
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	211007-6
ISSN	1552-6259 ; 0003-4975
ISSN (online)	1552-6259
ISSN	0003-4975
DOI	10.1016/j.athoracsur.2018.11.019
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Article ; Online: Matricellular Protein Cilp1 Promotes Myocardial Fibrosis in Response to Myocardial Infarction.

Zhang, Qing-Jun / He, Yu / Li, Yongnan / Shen, Huali / Lin, Ling / Zhu, Min / Wang, Zhaoning / Luo, Xiang / Hill, Joseph A / Cao, Dian / Luo, Richard L / Zou, Raymond / McAnally, John / Liao, Jun / Bajona, Pietro / Zang, Qun S / Yu, Yonghao / Liu, Zhi-Ping

Circulation research

2021 Volume 129, Issue 11, Page(s) 1021–1035

Abstract: Figure: see text]. ...

Abstract	[Figure: see text].
MeSH term(s)	Animals ; Cells, Cultured ; Fibrosis ; HEK293 Cells ; Humans ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mice ; Mice, Inbred C57BL ; Myocardial Infarction/metabolism ; Myocardial Infarction/pathology ; Myocardium/metabolism ; Myocardium/pathology ; Myofibroblasts/metabolism ; Myofibroblasts/pathology ; Pyrophosphatases/genetics ; Pyrophosphatases/metabolism
Chemical Substances	Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; CILP protein, mouse (EC 3.6.1.-) ; Pyrophosphatases (EC 3.6.1.-)
Language	English
Publishing date	2021-10-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.121.319482
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